title: Phloridzin reduces blood glucose levels and alters hepatic gene expression in normal BALB/c mice

status: Public on May 18 2012

first: Masuko

last: Kobori

summary:
We previously showed that a diet containing phloridzin suppressed the blood glucose levels in streptozotocin-induced diabetic mice most likely by inhibiting glucose absorption from the small intestine. In this study, we showed that 0.5% and 1% phloridzin diets significantly reduce the blood glucose levels in healthy normal BALB/c mice after 7 days of feeding.
To understand the effect of the high continuing intake of dietary phloridzin on normal mouse livers, we analyzed the hepatic gene expressions in mice fed diets containing 0%, 0.1%, 0.5%, or 1% phloridzin for 14 days using DNA microarrays.

overall_design: Six-week-old male mice were divided into 4 groups of 6 mice each, housed in groups of 3 per cage, and fed a standard purified AIN-93G diet containing 0% (Con), 0.1% (Phlorizin0.1), 0.5% (Phlorizin0.5), or 1% phloridzin (purity > 97%)  (Phlorizin1.0) for 2 weeks.


title: Gene expression profile in peritoneal macrophage stimulated with B-DNA or CpG-B

status: Public on May 20 2012

city: Meguro-ku, Tokyo

first: hideo

last: negishi

address: Komaba 4-6-1

department: Molecular Immunology

country: Japan

institute: University of Tokyo

summary:
Toll-like receptor and RIG-I-like receptor classs may evoke or instruct a distinct type of response that is more reflective of the pathogen encountered.  Although this issue may be critical to a better understanding of the regulation of immune responses to microbial infections, it has not been addressed through a direct, side-by-side comparison of the two receptor classes.
To address this, we performed microarray analysis of mRNAs from peritoneal macrophages stimulated with a synthetic B-form DNA, poly(dA-dT)・poly(dT-dA) ( B-DNA) or a CpG-B oligonucleotide, which respectively activates RLRs or TLR9, and identified B-DNA inducible genes and CpG-B inducible genes.

overall_design: Peritoneal macrophages from B6 mice were stimulated with B-DNA (10μg/ml) or CpG-B(3μM) for 4 hous, and then subjected to microarray analysis.

first: Hideo

last: Negishi

first: Tadatsugu

last: Taniguchi


title: Expression data from murine hematopoietic cells expressing BCR-ABL alone, NUP98-HOXA9 alone, BCR-ABL and NUP98-HOXA9, or null for both oncogenes

status: Public on May 11 2012

city: Rochester

first: John

last: Ashton

state: NY

address: 575 Elmwood Ave

country: USA

institute: University of Rochester

summary:
Leukemia is a complex malignancy with hundreds of distinct mutations associated with disease development.  Studies have shown that oncogenes cooperate to promote leukemia transformation, however, the downstream effectors of this cooperation are largely unknown.
Using a genetically defined mouse model of acute leuekmia, we investigated the regulated of genes downstream of the cooperative oncogenic interaction between BCR-ABL and NUP98-HOXA9 and identified a unique gene signature abberrantly expression in leukemia.

overall_design: Total RNA was isolated from hematopoietic cells transduced with BCR-ABL and Nup98-HOXA9 retroviruses and transplanted into recipient mice.  Bone marrow cells were purified by GFP (BCR-ABL) and YFP (NUP98-HOXA9) using FACS.

middle: M

first: Craig

middle: T

last: Jordan


title: Transcription-associated Loading and Translocation of Condensin II on Chromosome Arms in Embryonic Stem Cells (RNA)

status: Public on May 30 2012

city: Cambridge

first: Richard

middle: A

last: Young

state: MA

address: 9 Cambridge Center

institute: Whitehead Institute for Biomedical Research

summary:
The precise control of gene expression programs is critical for maintenance of cell state in emryonic stem cells.  Cohesin has been shown to play an important role in maintaining gene expression programs by contributing to DNA loops between enhancers and promoters of active genes. The influence of condensin on gene expression is not well understood.
We used microarrays to detail the changes to the global gene expression program of mouse embryonic stem cells upon depletion of cohesin or condensin II.

overall_design: Mouse embryonic stem cells were treated with shRNA constructs targeting CapH2 (2 hairpins), Smc2 (2 hairpins), Smc1 (1 hairpin, 2 biological replicates) and GFP control (1 hairpin, 2 biological replicates) for a total of 8 samples.  After 5 days RNA was extracted from the depleted cells and hybridized to Affymetrix microarrays.

first: Steve

last: Bilodeau

first: Jill

last: Dowen

first: David

last: Orlando


title: Expression data from reactive astrocytes acutely purified from young adult mouse brains

status: Public on May 02 2012

city: Stanford

first: Jennifer

middle: L

last: Zamanian

state: CA

address: 299 Campus Drive

department: Neurobiology

institute: Stanford University

summary: Reactive astrogliosis is characterized by a profound change in astrocyte phenotype in response to all CNS injuries and diseases. To better understand the reactive astrocyte state, we used Affymetrix GeneChip arrays to profile gene expression in populations of reactive astrocytes isolated at various time points after induction using two different mouse injury models, ischemic stroke and neuroinflammation.

overall_design: Young adult male mice underwent middle cerebral artery occlusion (MCAO) to produce ischemic stroke or control sham surgery. Young adult mice were injected intraperitoneally with 5 mg/kg lipopolysaccharide (LPS) to produce neuroinflammation or saline for control. Astrocytes were acutely purified from control and injured brains at 1 day after injury for LPS/saline injection and 1, 3 days and 7 days after MCAO/sham surgeries.

first: Lijun

last: Xu

first: Lynette

middle: C

last: Foo

first: Navid

last: Nouri

first: Lu

last: Zhou

first: Rona

middle: G

last: Giffard

first: Ben

last: Barres


title: Expression data from CD8+ Central memory T cells after different time periods of Concanavalin A  in vitro activation.

city: New York

first: Alan

middle: B

last: Frey

address: 550 First Avenue

department: Cell Biology

institute: NYUMC

summary:
CD8+ tumor infiltrating T cells (TIL) lack effector-phase functions due to defective proximal TCR-mediated signaling shown to result from inactivation of p56lck kinase. We identify a novel interacting partner for p56lck in nonlytic TIL, Protocadherin-18 (‘pcdh18’), and show that pcdh18 is transcribed upon in vitro or in vivo activation of CD8+ central memory T cells (CD44+CD62LhiCD127+) coincident with conversion into effector memory cells (CD44+CD62LloCD127+). Expression of pcdh18 in primary CD8+ effector cells induces the phenotype of nonlytic TIL: defective; proximal TCR signaling, cytokine secretion, and cytolysis; and enhanced AICD. pcdh18 contains a motif (centered at Y505) shared with src kinases (QGQYQP) which is required for the inhibitory phenotype. Thus, pcdh18 is a novel marker of CD8+ effector memory T cells expressed upon cell activation that can function as a negative regulator by restricting the effector phase.
We used microarrays to detail the global programme of gene expression underlying CD8+ 'Central memory' T cells activation and identified distinct transcriptional pattern clusters.

overall_design: Ten spleens were pooled from 62 week old C57BL/6 male mice and enriched for CD8+ T cells by negative selection using a cocktail of biotinylated antibodies to deplete CD4, CD11c, CD11b, MHC-II, B220, and NK cells.  Cells were then stained for CD8, CD44, CD62L, and CD127 and sorted (using a iCyt Reflection parallel cell sorter). Cells were collected and cultured (0.5 x106 cells/well) in 10% complete RPMI media supplemented with 0.005 ugr Con A and RNA prepared using TRIZOL and the 'RNeasy clean-up kit' (Invitrogen) after activation for different times.   We established single transcriptional profiles for 6 time points after T cell activation (4, 6, 8, 16, 20, 24 h) including a control zero h time point (prior to activation). RNA was isolated by standard procedures and its quality was assessed by the NYU Center for Health Informatics and Bioinformatics. cDNAs were hybridized to GeneSpring arrays using the mouse genome MOE430 2.0 array (Affymetrix) which interrogates ~45,000 transcripts.

first: Edwin

middle: J

last: Vazquez-Cintron

first: Ngozi

middle: R

last: Monu

first: Jeremy

last: Burns

first: Roy

last: Blum

first: Gregory

last: Chen

first: Peter

last: Lopez

last: Ma

first: Sasa

last: Radoja


title: Influence of exposure time on gene expression of human intestinal epithelial cells exposed to Lactobacillus acidophilus

status: Public on May 09 2012

city: Raleigh

first: Todd

middle: Robert

last: Klaenhammer

state: NC

department: Department of Food, Bioprocessing, and Nutrition Sciences

institute: North Carolina State University

summary: The Caco-2 epithelial cell line was exposed to the probiotic bacterium L. acidophilus cells for a 1-, 4- or 8-hour exposure time or phosphate-buffered saline (PBS) for 1 hour to study the impact on gene expression levels. The results indicated the effect of exposure time on gene expression levels.

overall_design: Total RNA was isolated from the Caco-2 epithelial cell line after the required exposure time to L. acidophilus NCFM or PBS.

first: Sarah

last: O'Flaherty


title: Differential expression of genes after treatment with DAMTC in human lung adenocarcinoma cells (A549)

status: Public on May 01 2012

city: Delhi

first: Neeru

last: Saini

address: Mall Road

department: FGU

country: India

institute: IGIB

summary: The experiment was designed to identify the genes which get altered after the treatment with DAMTC in A549 cells. The A549 cells plated in T25 flask were treated with DAMTC at a concentration of 160 microgram/ml for 24 h.

overall_design: Biological triplicates of 2 samples were used viz. control A549 cells (Control), A549 cells treated with DAMTC (160 micrograms/ml) for 24 h (Treated)

first: Anita

last: Goel

first: Ravindresh

last: Chhabra


title: Gene expression alteration by macrophage depletion in IKKα mutant mice

city: frederick

first: Qun

last: Jiang

state: Maryland

address: 1050 boyles street

institute: NCI-Frederick

summary:
We generated Ikkα-KA/KA knock-in mice (KA/KA), in which an ATP binding site of Ikkα Lys 44 was replaced by alanine. The knock-in mice develop severe skin lesions and begin to die after 6 to 10 months. We also found lung SCCs in some of the mice. To study lung SCC development, we stabilize the skin condition by crossing  KA/KA with Lori.Ikkα transgenic mice to generate KA/KA-Lori.Ikkα mice, which 100% spontaneously developed lethal lung SCC at 4 to 6 months of age.
Clodronate-liposomes obtained from Dr. N. van Rooijen (Vrije Universiteit, Amsterdam, Netherlands) were intravenously injected into mice twice every week, started in 4 weeks old mice, and continued for 3 months. The dose of clodronate-liposomes was 100µl during the first month and elevated to 150 100µl after that. The depletion efficacy was confirmed by detecting pulmonary macrophages with Flow Cytometry. Depletion of macrophages in these KA/KA-Lori.Ikkα mice could significantly reduce inflammation and prevent lung SCC developmrnt. This aim of this microarray assay is to identify differentially expressed genes among Wild type, KA/KA-Lori.Ikkα, and macophage-depleted KA/KA-Lori.Ikkα mice, which may highlight the important genes or parthways involved in inflammation-associated lung SCC carcinogenesis.

overall_design: Three samples were analyzed: 1. WT (lung tissue from wild type mouse); 2. KA2 (mixture tissue of lung SCC and tumor neighbor from KA/KA-Lori-Ikkα mouse ); 3. KAT (lung tissue from KA/KA-Lori-Ikkα mouse with macrophage depletion treatment)

first: Zuoxiang

last: Xiao

first: Raina

last: Kumar


title: Effect of Nrf2 deletion in postnatal lung development and BPD phenotype in newborn mice

status: Public on May 25 2012

city: Research Triangle Park

first: Steven

last: Kleeberger

address: 111 TW Alexander Dr., Building 101, MD D-201

institute: National Institute of Environmental Health Sciences, NIH

summary:
Background: Nrf2 is an essential cytoprotective transcription factor. However, association of Nrf2 in organ development and neonatal disease is rarely examined. Hyperoxia exposure to newborn rodents generates pulmonary phenotypes which resemble bronchopulmonary dysplasia (BPD) of prematurity.
Methods: To investigate the role of Nrf2 in lung maturation and BPD pathogenesis, Nrf2-deficient (Nrf2-/-) and wild-type (Nrf2+/+) neonates were exposed to air or hyperoxia (O2). Transcriptome analysis determined Nrf2-directed mechanisms in premature lung. Lung injury was assessed by bronchoalveolar lavage analysis and histopathology.
Results: In Nrf2-/- neonates, basal expression of cell cycle machinery, redox balance, and lipid/carbohydrate metabolism genes were suppressed while immunity genes were overexpressed compared to Nrf2+/+ pups. O2-induced mortality and pulmonary inflammation/injury were significantly higher in Nrf2-/- than in Nrf2+/+. Lung DNA lesion and oxidation were greater in Nrf2-/- than in Nrf2+/+, constitutively and after O2. Nrf2-dependent genes modulated cellular growth/proliferation, defense, immunity, and lipid metabolism against hyperoxia. Bioinformatic elucidation of Nrf2 binding motifs and augmented O2-induced inflammation in genetically deficient neonates validated Gpx2 and Marco as Nrf2 effectors.
Conclusion: Overall, Nrf2 in underdeveloped lungs orchestrated cell cycle, morphogenesis, and immunity as well as cellular defense constitutively and under oxidant stress. Results provide putative molecular mechanisms of Nrf2-directed lung alveolarization and BPD of prematurity.

overall_design: PARALLEL study design with 42 samples comparing 14 groups  of age (P1 to P4 corresponding to day 0 to day 3 animals),  gene, and exposure: (4 groups Nrf+/+ wild type P1-P4 air exposure)  (4 groups Nrf -/- knockout P1-P4 air exposure),  (3 groups  Nrf+/+ wild type P2-P4 with 100 percent O2 (hyperoxia exposure) and 3 groupsNrf -/- knockout P2-P4 with 100 percent O2 (hyperoxia exposure)) Biological replicates: 3 per group

first: Hye-Youn

last: Cho


title: Stem cell factor programs the mast cell activation phenotype

city: Hamilton

first: Dan

last: Sturdevant

state: MT

address: 903 S 4th street

department: NIAID

institute: NIH

summary: Mast cells, activated by antigen via the high affinity receptor for IgE (FcεRI), release an array of pro-inflammatory mediators that contribute to allergic disorders such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation and survival, and, under acute conditions, enhances mast cell activation. However, extended SCF exposure in vivo conversely protects against fatal antigen-mediated anaphylaxis. In investigating this dichotomy, we identified a novel mode of regulation of the mast cell activation phenotype through SCF-mediated programming. We found that mouse bone marrow-derived mast cells chronically exposed to SCF displayed a marked attenuation of FcεRI-mediated degranulation and cytokine production. The hypo-responsive phenotype was not a consequence of altered signals regulating calcium flux or protein kinase C, but of ineffective cytoskeletal reorganization, with evidence implicating a down-regulation of expression of the Src kinase Hck. Collectively, these findings demonstrate a major role for SCF in the homeostatic control of mast cell activation with potential relevance to mast cell-driven disease and the development of novel approaches for the treatment of allergic disorders.

overall_design: Mouse bone marrow-derived mast cells were treated with IL3 or IL3+SCF. Six replicates each.

first: Tomonobu

last: Ito

first: Daniel

last: Smrž

first: Mi-Yeon

last: Jung

first: Šárka

last: Smržová

first: Geethani

last: Bandara

first: Avanti

last: Desai

first: Hye

middle: S

last: Kuehn

first: Michael

last: Beaven

first: Dean

middle: D

last: Metcalfe

first: Alasdair

last: Gilfillan


title: Chronic dietary intake of quercetin alleviates hepatic fat accumulation associated with consumption of a Western-style diet in C57/BL6J mice

city: Tsukuba

first: Masuko

last: Kobori

state: Ibaraki

address: 2-1-13 Kannondai

institute: Food Research Institute, National Agriculture and Food Research Organization

summary:
To determine the effect of consumption of a quercetin-rich diet on obesity and dysregulated hepatic gene expression, C56BL/6J mice were fed for 20 weeks on control or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin. Chronic dietary intake of quercetin reduced body weight gain and visceral and liver fat accumulation, and improved hyperglyceamia, hyperinsulinaemia, dyslipidaemia in mice fed a Western-style diet.
Feeding a Western-style diet altered expression of genes related to inflammatory responses, lipid metabolism and oxidative phosphorylation in C57BL/6J mice after 20 weeks. The results from exhaustive gene expression analysis showed that quercetin minimally influenced hepatic gene expression in mice fed the Western diet. The gene screening results (GSEA) were consistent with the notion that it did improve mitochondrial function to some extent. Quantitative RT-PCR analysis indicated that quercetin did influence important regulators of fat accumulation and metabolic disorders. Our results suggest that quercetin reduces fat accumulation presumably through decreasing oxidative stress and increasing PPARα expression, and the following improvement of gene expression related to steatosis in the liver.

overall_design: C56BL/6J mice were fed for 20 weeks on AIN93G (con) or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin for 20 weeks.


title: Genetic modification of STAT5 levels reveals dose-dependent and isoform-specific requirement for cell lineage progression and differentiation.

city: Bethesda

first: WeiPing

last: Chen

state: MD

address: Bldg 8, Room 1A11, NIDDK/NIH

department: GCL

institute: NIDDK/NIH

summary: Two highly conserved transcription factors STAT5A and STAT5B play an identical role in the intracellular signaling pathway upon cytokine stimulation, while gene deletion experiments have revealed separable and overlapping functions of STAT5.  This questions whether the phenotypic differences in the organ development observed in the individual knockout mice result from isoform-specific functions or quantitative differences in the expression levels of each STAT5 isoform among tissues.  To elucidate the redundancy and isoform-specificity of STAT5 for development at molecular levels, mice carrying only a single allele of either Stat5a or Stat5b were generated.  Both of these mice overcame the lethal anemia observed in Stat5ab-null mice, indicating that development of erythroid cell lineage was totally dependent on the dosage of STAT5.  The blocked progression of B cell lineage at the pre-pro B cell stage in Stat5ab-/- mice was rescued in the presence of a single allele of either Stat5a or Stat5b, while the number of total B220+ cells in bone marrow was smaller in Stat5abnull/Stat5b- mice than Stat5abnull/Stat5a- mice.  The paucity of alveolar progenitor cells in the Stat5ab-null mammary epithelium was rescued by a single allele of either Stat5a but not Stat5b, suggesting cell-type dependent isoform-specific function. Genome-wide gene expression analyses revealed that different steps of cell lineage progression require different gene sets which expression requires the different isoform of STAT5 in a dose-dependent manner in the mammary epithelium.  Taken together, this study demonstrates that dose-dependent isoform specificity of STAT5A and STAT5B controls progression and differentiation of each cell lineage.

overall_design: Six days after observation of a plug, mammary tissues from three of each Stat5a-/- mice, Stat5ab+/null mice, Stat5abnull/Stat5b- and Stat5abnull/Stat5a- mice were collected, frozen in liquid nitrogen, and stored at -70 °C

first: Daisuke

last: Yamaji

first: Greg

last: Riedlinger

first: Alejandro

last: Villarino

first: Bingmei

last: Zhu

first: Weiping

first: Susanne

last: Pechhold

first: John

last: O'Shea

first: Lothar

last: Hennighausen

first: Gertraud

middle: W

last: Robinson


title: mRNA and microRNA expression profiles in a murine model of hyperoxia-induced bronchopulmonary

first: Jie

last: Dong

state: MN

address: 200 1st SW

department: Thoracic Surgery

institute: Mayo Clinic

type:
Expression profiling by array
Expression profiling by RT-PCR

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: mRNA expression profile in a murine model of hyperoxia-induced bronchopulmonary dysplasia

summary: We performed miRNA and mRNA profiling at postnatal day 14 and day 29 to compare hyperoxia-induced bronchopulmonary dysplasia  and wild type. We built potential miRNA-mRNA interaction networks specific to brochopulmonary dysplasia.

overall_design: Replicated time course of mouse lung development at 2 time points (P14, P29). Three replicates per time point for bronchopulmonary dysplasia induced by hyperoxia mouse lung, and two replicates per time point for wild type mouse lung. This dataset represents the mRNA expression profiling component of the study.

first: Dennis

last: Wigle


title: Expression profiling of the murine neural crest precursor cell line, JoMa1

status: Public on Apr 30 2012

city: Essen

first: Alexander

last: Schramm

address: Hufelandstr. 55

department: Childrens Hospital

country: Germany

institute: University Hospital Essen

summary: JoMa1 cells are pluripotent precursor cells, derived from the neural crest of mice transgenic for tamoxifen-inducible c-Myc. Following transfection with a cDNA encoding for MYCN, cells become immortlized even in the absence of tamoxifen.

overall_design: The expression profile of JoMa1 cells was compared to cell lines derived from tumors induced by JoMa1 transfected with MYCN.

first: Johannes

middle: H

last: Schulte


title: Dendritic cell and monocyte progenitors

status: Public on Apr 26 2012

first: Matthew

last: Meredith

state: New York

address: 1230 York Ave

institute: The Rockefeller University

summary: To compare the gene expression profiles of Macrophage & Dendritic cell Progenitors (MDPs), Common Dendritic cell Progenitors (CDPs), committed dendritic cell precursors (pre-DCs), and Ly6Chi monocytes from mouse bone marrow

overall_design: Four samples (MDPs, CDPs, pre-DCs, and monocytes) were collected in triplicate

first: Kang

last: Liu


title: Kras is required for pancreatic tumor maintenance through regulation of hexosamine biosynthesis and the non-oxidative pentose phosphate pathway

city: Houston

first: Sujun

last: Hua

state: Tx

address: 1901 East Rd

institute: MD Anderson Cancer Center

summary: The maintenance of advanced malignancies relies on continued activity of driver oncogenes, although their rate-limiting role is highly context-dependent with respect to tumor types and associated genetic alterations.  Oncogenic Kras mutation is the signature event in human pancreatic ductal adenocarcinoma (PDAC), serving a critical role in tumor initiation.  Here, an inducible KrasG12D-driven p53 mutant PDAC mouse model establishes that advanced PDAC remains strictly dependent on continued KrasG12D expression and that KrasG12D serves a vital role in the control of tumor metabolism, through stimulation of glucose uptake and channeling of glucose intermediates through the hexosamine biosynthesis pathway (HBP) and the pentose phosphate pathway (PPP). Notably, these studies reveal that oncogenic Kras regulates ribose biogenesis. Unlike canonical models of PPP-mediated ribose biogenesis, we demonstrate that oncogenic Kras drives intermediates from enhanced glycolytic flux into the non-oxidative arm of the PPP, thereby decoupling ribose biogenesis from NADPNADPH-mediated redox control. Together, this work provides in vivo mechanistic insights into how oncogenic Kras promotes metabolic reprogramming in native tumors and illuminates potential metabolic targets that can be exploited for therapeutic benefit in Kras-driven PDAC.

overall_design: Primary pancreatic tumor lines were established from p48Cre tetO_LKrasG12D ROSA_rtTAL+ p53L+ mice. Five independent tumor lines (iKras1-5) were used for pancreatic injection into nude mice to generate orthotopic tumors. The mice were kept on doxycycline for 2 weeks until obvious tumor formation. Half of the animals were pulled off doxycycline for 24 hours. Tumors with over 75% cellularity were collected for total RNA prepartion. For in vitro expression profiles, the same five tumor lines were cultured in the presence or absence of doxycycline for 24 hours and total cellular RNA was prepared. For control samples, two independent tumor lines from LSL-KrasG12D p53L+ tumors were cultured in the presence or absence of doxycycline for 24 hours and total cellular RNA was prepared.

first: Haoqiang

last: Ying

first: Ron

last: DePinho


title: Testosterone- and estrogen-induced genes in urogenital sinus mesenchyme

status: Public on Apr 27 2012

city: Madison

first: William

last: Ricke

state: Wisconsin

address: 1111 Highland Ave

department: Urology

institute: University of Wisconsin

summary: The goal of this experiment was to determine if testosterone (T) and estradiol-17 beta (E2) induced gene expression in mouse urogenital sinus mesenchymal (UGM) cells. When UGM grown in culture was treated with T+E2, numerous genes were increased and decreased compared to untreated controls. Quantitative RT-PCR was used to verify results of a subset of genes.

overall_design: UGM cells were untreated or treated with T+E2 for 72hrs. One mouse gene expression array was used for each group.


title: mRNA expression data from AG-haESC, E14 and MEF

city: Shanghai

first: Linyu

last: Shi

address: 320 Yueyang Road

country: China

institute: Institute of Biochemistry and Cell Biology,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences

summary:
Haploid cells are amenable for genetic analysis because they contain only one set of chromosomes.Here,we report the derivation of haESCs from androgenetic blastocysts. These cells, which we designated AG-haESCs, express classical ESC markers, are pluripotent, and contribute to various tissues including the germline upon injection into diploid blastocysts.
We used microarrays to compare the gene expression levels among androgenetic haploid embryonic stem cell lines(AG-haESC) E14 and male mouse embryonic fibroblasts (MEFs) and identified that most paternally imprinted genes were down-regulated and  the maternally imprinted genes were  up-regulated.

overall_design: To avoid the influence of diploidized cells on the expression profile, we collected samples from FACS of cells at G1/G0 stage by staining Hochest 33342. We used E14,which was a male embryonic stem cell lines, and MEFs isloated from male individuals as control. Gene expression profiles of all the cell lines were analysed on an Affymetrix GeneChip 430 2.0 array.

first: Jinsong

last: Li

first: Guoliang

last: Xu


title: Mouse Androgenetic Haploid Embryonic Stem Cells Support Targeted Gene Transmission to Progeny

type: Genome variation profiling by genome tiling array


title: Endothelial cell-enriched genes expression in mouse embryo

status: Public on Apr 23 2012

city: Ibaraki

first: Ken

last: Matsumoto

address: 1-1-1 Tennodai Tsukuba

institute: University of Tsukuba

summary:
The early blood vessels of the embryo and yolk sac in mammals develop by aggregation of de novo forming angioblasts into a primitive vascular plexus, which then undergoes a complex remodeling process. Angiogenesis is also important for disease progression in the adult. However, the precise molecular mechanism of vascular development remains unclear.
It is therefore of great interest to determine which genes are specifically expressed in developing endothelial cells.Here, we utilized Flk1-deficient mouse embryos, which lack endothelial cells, to perform a genome-wide survey for genes related to vascular development.

overall_design: Wild type (WT), Flk1+/GFP and Flk1 KO embryos proper (fetuses) were dissected out at 8.5 dpc. Total RNAs from these embryos were prepared using RNeasy kit. Gene expression analysis was performed by GeneSpring software.

first: Masatsugu

last: Ema


title: Disturbed Hepatic Carbohydrate Management During High Metabolic Demand in Medium-Chain Acyl-CoA Dehydrogenase (MCAD)-deficient Mice

city: Groningen

first: vincent

last: bloks

department: Pediatrics

country: Netherlands

institute: UMCG

summary: Medium-chain acyl-coenzyme A (CoA) dehydrogenase (MCAD) catalyzes crucial steps in mitochondrial   fatty acid oxidation, a process that is of key relevance for maintenance of energy homeostasis, especially during high metabolic demand. To gain insight into the metabolic consequences   of MCAD deficiency under these conditions, we compared hepatic carbohydrate metabolism in vivo in wild-type and MCAD-/- mice during fasting and during a lipopolysaccharide   (LPS)-induced acute phase response (APR). MCAD-/- mice did not become more hypoglycemic on fasting or during the APR than wild-type mice did. Nevertheless, microarray   analyses revealed increased hepatic peroxisome proliferator-activated receptor gamma coactivator-1a (Pgc-1a) and decreased peroxisome proliferator-activated receptor alpha (Ppar a) and   pyruvate dehydrogenase kinase 4 (Pdk4) expression in MCAD-/- mice in both conditions,suggesting altered control of hepatic glucose metabolism. Quantitative flux measurements revealed   that the de novo synthesis of glucose-6-phosphate (G6P) was not affected on fasting in MCAD-/- mice. During the APR, however, this flux was significantly decreased (-20%) in   MCAD-/- mice compared with wild-type mice. Remarkably, newly formed G6P was preferentially directed toward glycogen in MCAD-/- mice under both conditions. Together with diminished   de novo synthesis of G6P, this led to a decreased hepatic glucose output during the APR in MCAD-/- mice; de novo synthesis of G6P and hepatic glucose output were maintained in   wild-type mice under both conditions. APR-associated hypoglycemia, which was observed in wild-type mice as well as MCAD-/- mice, was mainly due to enhanced peripheral glucose   uptake. Conclusion: Our data demonstrate that MCAD deficiency in mice leads to specific changes in hepatic carbohydrate management on exposure to metabolic stress. This deficiency,   however, does not lead to reduced de novo synthesis of G6P during fasting alone, which may be due to the existence of compensatory mechanisms or limited rate control of MCAD in murine   mitochondrial fatty acid oxidation.

overall_design: Total RNA obtained from Liver ( 20 samples) , where comparing 4 groups, consisting out of 5 biological replicates, all groups where fasted for 12 hrs, and half of them where injected with LPS ( 100ug/20gr BW) or vehicle

first: H

last: Herrema

first: T

last: Derks

last: van Dijk

first: V

last: Bloks

first: A

last: Gerding

first: R

last: Havinga

first: U

last: Tietge

first: M

last: Muller

first: G

middle: P

last: Smit

first: F

last: Kuipers

first: DJ

last: Reijngoud


title: Strome SDQ2330_LIN15B_N2_LTEMB

city: Toronto

first: DCC

last: modENCODE

state: Ontario

address: MaRS Centre, South Tower, 101 College Street, Suite 800

country: Canada

institute: Ontario Institute for Cancer Research

type: Genome binding/occupancy profiling by genome tiling array

summary:
modENCODE_submission_3439
This submission comes from a modENCODE project of Jason Lieb. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The focus of our analysis will be elements that specify nucleosome positioning and occupancy, control domains of gene expression, induce repression of the X chromosome, guide mitotic segregation and genome duplication, govern homolog pairing and recombination during meiosis, and organize chromosome positioning within the nucleus. 126 strategically selected targets include key histone modifications, histone variants, RNA polymerase II isoforms, dosage-compensation proteins, centromere components, homolog-pairing facilitators, recombination markers, and nuclear-envelope constituents. We will integrate information generated with existing knowledge on the biology of the targets, perform ChIP-chip analysis on mutant and RNAi extracts lacking selected target proteins, use extrachromosomal arrays to assess the ability of candidate identified sequence motifs to recruit targets in vivo, identify tissue-specific patterns of selected targets, and create integrated, quantitative models of transcription and whole-chromosome functions.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: N2; Developmental Stage: Late Embryos; Genotype: wild type; Sex: Hermaphrodite;  NUMBER OF REPLICATES: 2;  EXPERIMENTAL FACTORS: Developmental Stage Late Embryos; temp (temperature) 20 degree celsius; Antibody SDQ2330-LIN15B (target is LIN-15B); Strain N2

first: Jacob

last: Garrigues

first: Susan

last: Strome


title: Gene expression data from postnatal day 7 subventricular zone (SVZ), IV ventricle and cerebellar white matter-derived neural stem cells (NSCs) and of cancer stem cells (CSCs) from Ptch het p53 wt and Ptch het p53 het mouse medulloblastomas

status: Public on Apr 17 2012

city: Milano

first: Rossella

last: Galli

state: MI

address: via Olgettina 58

department: Regenerative Medicine, Stem Cells and Gene Therapy

country: Italy

institute: San Raffaele Scientific Institute

summary: We exploited microarrays to detail the global program of gene expression underlying normal stem cells and cancer stem cells in the cerebellum and in medulloblastomas (MBs).

overall_design: To identify novel molecular mediators involved in medulloblastomagenesis, we compared the distinct postnatal hindbrain-derived NSC populations, which are potentially tumor-initiating, with murine single Ptch and compound Ptch/p53-mutant MB cancer stem cells (CSCs), the latter faithfully phenocopying the different variants of human MB in vivo. Transcriptome analysis of both hindbrain NSCs and MB CSCs resulted in the generation of well-defined gene signatures, each reminiscent of a specific human MB molecular subclass.

first: Mauro

last: Pala


title: All exon array expression data in normal colon and primary colon cancer lines [expression]

status: Public on Apr 16 2012

city: Cleveland Heights

first: Peter

last: Scacheri

state: OH

address: 10900 Euclid Ave; BRB 647

institute: Case Western Reserve University

summary:
Cancer is characterized by gene expression aberrations. Studies have largely focused on coding sequences and promoters, despite the fact that distal regulatory elements play a central role in controlling transcription patterns.  Here we utilize the histone mark H3K4me1 to analyze gain and loss of enhancer activity genome wide in primary colon cancer lines relative to normal colon crypts. We identified thousands of variant enhancer loci (VELs) that comprise a signature that is robustly predictive of the in vivo colon cancer transcriptome.  Furthermore, VELs are enriched in haplotype blocks containing colon cancer genetic risk variants, implicating these genomic regions in colon cancer pathogenesis.  We propose that reproducible changes in the epigenome at enhancer elements drive a unique transcriptional program to promote colon carcinogenesis.
We used gene expression profiles to assess correlations between the colon cancer epigenome and transcriptional activity.

overall_design: RNA from normal colon epithelial crypt controls and primary colon cancer cell lines was hybridized to Affymetrix All Exon Human ST 1.0 microarrays.

first: Sanford

last: Markowitz

first: Lois

last: Myerhoff

first: Alina

last: Saiakhova

first: Batool

last: Akhtar-Zaidi


title: Critical Role of STAT5 Transcription Factor Tetramerization for Cytokine Responses and Normal Immune Function (RNA)

status: Public on Apr 25 2012

first: Peng

last: Li

address: 9000 Rockville Pike

department: NHLBI

summary: Cytokine-activated STAT proteins dimerize and bind to high-affinity motifs, and N-terminal domain-mediated oligomerization of dimers allows tetramer formation and binding to low-affinity tandem motifs, but the functions of dimers versus tetramers are unknown. We generated Stat5a and Stat5b double knock-in (DKI) N-domain mutant mice that form dimers but not tetramers, identified cytokine-regulated genes whose expression required STAT5 tetramers, and defined consensus motifs for dimers versus tetramers. Whereas Stat5- deficient mice exhibited perinatal lethality, DKI mice were viable, indicating that STAT5 dimers were sufficient for survival. Nevertheless, STAT5 DKI mice had fewer CD4+CD25+ T cells, NK cells, and CD8+ T cells, with impaired cytokine-induced proliferation and homeostatic proliferation of CD8+ T cells. DKI CD8+ T cell proliferation following viral infection was diminished and DKI Treg cells did not efficiently control colitis. Thus, tetramerization of STAT5 is dispensable for survival but is critical for cytokine responses and normal immune function.

overall_design: T cells were extracted from spleen of wt and STAT5 double knocked in mice, and treated with IL-2.  The cells were collected from 0h (without treatment), 2h, 6h and 17h, and chipped on Affy mouse 430 2.0 arrays.

first: Jian-Xin

last: Lin

first: Delong

last: Liu

first: Hyun

last: T Jin

first: Jianping

last: He

first: Mohammedr

last: Rasheed

first: Yrina

last: Rochman

first: Lu

last: Wang

first: Kairong

last: Cui

first: Chengyu

first: Brian

last: Kelsall

first: Rafi

last: Ahmed

first: Warren

last: Leonard


title: Metastasis and Survival of Breast Cancer Stem Cells Mediated by Cytoskeleton Remodeling and PI3K/mTOR Signaling transcription factors

status: Public on Apr 14 2012

first: WeiPing

last: Chen

summary: Cancer metastasis is a fetal problem that claims life of over 90% of cancer patients. It is hypothesized that cancer stem cells (CSCs) mediate cancer metastasis and such cells are often resistant to chemotherapy. Studying BRCA1 associated cancers, we found that CSCs form fillopodia and protrusions enriching for active forms of ezrin/radixin/moesin proteins and they have a much higher potential to metastasize than non-CSCs. Microarray analysis indicated that many pathways related to cell adhesion, extracellular matrix and cytoskeleton were differentially regulated in CSCs. Although inhibition of cytoskeleton remodeling by cisplatin treatment retarded CSC motility and cancer metastasis, drug resistant cancers eventually emerge containing markedly increased number of CSCs. This event is at least partially attributed to the activation of PI3K/mTOR signaling, and can be significantly inhibited by the treatment of rapamycin. These results provide strong evidence that cytoskeletal rearrangement and PI3K/mTOR signaling play a distinct role in mediating CSC mobility and viability, and blocking of both pathways in CSCs synergistically inhibits primary and metastatic cancer growth in BRCA1 associated tumors.

overall_design: The sorted subpopulations based upon CD24, CD29 expression were used in the microarray analysis that was performed with 3 independent biologic sample sets.

first: Athanassios

last: Vassilopoulos

first: Cuiying

last: Xiao

first: Weiping

first: Cristine

last: Chisholm

first: Carole

last: Bewley

first: Chu-Xia

last: Deng


title: Fz2-Fz7 double knock-out E8.5 mouse

status: Public on Apr 13 2012

city: Baltimore

first: Huimin

last: Yu

address: 725 N Wolfe Street, PCTB 805

department: Molecular Biology and Genetics

institute: Johns Hopkins School of Medicine

summary: Fz2Fz7 double knock out mouse microarray (E8.5)

overall_design: Fz2-Fz7 double KO vs. Fz7 KO


title: Olig2 defines subpopulations of retinal progenitor cells

city: Boston

first: jeffrey

last: trimarchi

address: 77 Avenue Louis Pasteur

department: Genetics

institute: Harvard Medical School

summary: Previous lineage analyses have shown that retinal progenitor cells (RPCs) are multipotent throughout development, and expression profiling studies have shown a great deal of molecular heterogeneity among RPCs. To determine if the molecular heterogeneity predicts that an RPC will produce particular types of progeny, clonal lineage analysis was used to investigate the progeny of a subset of RPCs, those that express the basic helix-loop-helix (bHLH) transcription factor, Olig2. In contrast to the large and complex set of clones generated by viral marking of random embryonic RPCs, the embryonic Olig2+ RPCs underwent terminal divisions, producing small clones with primarily two of the five cell types being made by the pool of RPCs at that time. The embryonically produced cell types made by Olig2+ RPCs were cone photoreceptors and horizontal cell (HC) interneurons. Moreover, the embryonic Olig2+ RPC did not make the later Olig2+ RPC. The later, postnatal Olig2+ RPCs also made terminal divisions, which were biased towards production of rod photoreceptors and amacrine cell (AC) interneurons. These data indicate that the multipotent progenitor pool is made up of distinctive types of RPCs, which have biases towards producing subsets of retinal neurons in a terminal division, with the types of neurons produced varying over time. This strategy is similar to that of the developing Drosophila melanogaster ventral nerve cord, with the Olig2+ cells behaving as ganglion mother cells.

overall_design: Single retinal cells were isolated in tubes containing lysis buffer, their mRNAs were reverse transcribed, and the resulting cDNAs were PCR amplified for 35 cycles. Labeled cDNA samples were hybridized to Affymetrix 430 2.0 microarrays and the data was normalized using MAS5.0 software. These cells were examined for the expression of Olig2 or other bHLH factors.

first: Jeff

last: Trimarchi

first: Connie

last: Cepko


title: Long-term pioglitazone improves learning and attenuates pathological markers in a mouse model of AD

city: Lexington

first: Eric

last: Blalock

state: KY

address: 800 Rose St.

department: Molecular and Biomedical Pharmacology

institute: University of Kentucky

summary:
Thiazolidinediones (TZDs) are agonists at peroxisome proliferator-activated gamma-type (PPAR-y) receptors and are used clinically for the treatment of type 2 diabetes where they have been shown to reestablish insulin sensitivity, improve lipids profile, and reduce inflammation. Recent work also suggests that TZDs may be beneficial in Alzheimer's disease (AD), ameliorating cognitive decline early in the disease process. However, there have been only a few studies identifying mechanisms through which cognitive benefits may be exerted. Starting at 10 months of age, the triple transgenic mouse model of AD (3xTg-AD) with accelerated amyloid-B (AB) deposition and tau pathology was treated with the TZD pioglitazone (PIO- Actos) at 18 mg/Kg body weight/day. After four months, PIO-treated animals showed multiple beneficial effects, including improved learning on the active avoidance task, reduced serum cholesterol, decreased hippocampal AB deposits, and enhanced short- and long-term plasticity. Baseline electrophysiological membrane properties and blood glucose levels were unchanged by PIO treatment. Gene microarray analyses of hippocampal tissue identified predicted transcriptional responses following TZD treatment as well as potentially novel targets of TZDs, including facilitation of estrogenic processes, and decreases in glutamatergic and ketone metabolic/ cholesterol dependent processes. Taken together, these results confirm prior animal studies showing that TZDs can ameliorate cognitive deficits associated with AD-related pathology, but also extend these findings by pointing to novel molecular targets in the brain.
Keywords : Hippocampus; LTP; Microarray analysis; Avoidance learning; Aging; PPAR; Synaptic hyperpolarization; T2DM

overall_design: We used the 3xTg-AD mouse model of Alzheimer's disease and monitored the effects of pioglitazone (PIO-Actos a TZD) on behavioral, electrophysiological, and molecular variables. Emphasis was placed on identifying hippocampal PIO-sensitive genes that were also associated with learning and memory processes. Starting at 10 months of age, female mice were treated for approximately 14 weeks with either a control diet or a PIO-containing diet. PIO was incorporated into the diet to yield a final dose of approximately 18 mg/kg body weight/day.

first: James

last: Searcy

first: Jeremiah

last: Phelps

first: Tristano

last: Pancani

first: Inga

last: Kadish

first: Jelena

last: Popovic

first: Katie

last: Anderson

first: Tina

last: Beckett

first: Michael

last: Murphy

first: Kuey-Chu

first: Nada

last: Porter

first: Philip

last: Landfield

first: Olivier

last: Thibault


title: Gene expression data from livers of Yap+/+ and Yap+/- mice at postnatal day 30

status: Public on Apr 05 2012

city: Kansas City

first: Udayan

last: Apte

state: KS

address: 3901 Rainbow Blvd, MS1018

department: Pharmacology

institute: University of Kansas Medical Center

summary: Liver undergoes both size increase and differentiation during postnatal period, which in mice is approximately first 30 days. The mechanisms of simultaneous postnatal liver cell proliferation and maturation are not clear. In these experiments, role of yes associated protein (Yap), the downstream effector of Hippo Kinase signaling pathway was investigated.

overall_design: Total RNA isolated from livers of Yap+/+ and Yap+/- mice at Postnatal day 30. Pooled livers from 5 mice per genotype were used.


title: Genome-wide profiling of altered gene expression in the neocortex of Alzheimer's disease (gene level)

city: Singapore

first: Michelle

middle: GK

last: Tan

address: 20 College Road

department: Clinical Translational Research

country: Singapore

institute: Singapore General Hospital

summary: We investigated genome-wide gene alterations in the temporal cortex of a well-characterized cohort of Alzheimer’s disease (AD) patients using Affymetrix exon arrays.

overall_design:
The AD patients and controls are subjects originally recruited into OPTIMA (Oxford Project to Investigate Memory and Ageing). Subjects underwent annual clinical and neuropsychological assessments, including the Cambridge Cognitive Examination (CAMCOG). Among subjects who died with autopsy consent given by next of kin, 1 cm3 blocks of grey matter from BA22 were dissected from fresh frozen brains of AD subjects. Tissues from elderly controls, followed longitudinally in life and with CAMCOG scores >80 at the last assessment before death, were collected. Affymetrix exon array was carried out in 8 control and 8 AD samples. The samples processed in each hybridization run were matched for AD vs. control, sex and postmortem interval (PMI) as far as possible.

This submission includes the gene-level analysis.

first: Mitchell

middle: K

last: Lai


title: Gene expression profiling of Wwox targeted ablation in mouse mammary epithelial cells

status: Public on Apr 15 2012

city: Smithville

first: C. Marcelo

last: Aldaz

address: POB 389

department: Molecular Carcinogenesis

institute: The University of TX M.D. Anderson Cancer Center

summary:
The WWOX gene has been implicated in human cancers, including breast cancer.The development and tumorigenesis between human and mouse mammary glands (MGs) share similar molecular details and signal transduction pathways. We established mouse line that specifically knockout the expression of WWOX gene in the MG epithelial cells (MECs) by crossing BK5-cre mice with our WWOX flox stain. In order to study the gene expression profile in the subpopulation MECs, we isolated the organoids from the 4th MGs of both BK5-cre +; WWOX flox/flox (KO) mice and their WT counterparts (BK5-cre -; WWOX flox/flox), 3 mice each genotype. The total RNA from the mouse MG organoids was extracted and purified by TRIzol/RNeasy Kit and their integrity was checked on Agilent RNA 6000 Nanochip.
The goal is to identify the significant perturbation in tumorigenic pathways in these cells induced by WWOX ablation.

overall_design: Mammary gland epithelial organoids samples and gene expression profiles were deribed from three WWOX-KO mice (BK5-cre +; WWOX flox/flox) and from three WWOX-WT mice (BK5-cre -; WWOX flox/flox)

first: Brent

last: Ferguson

first: Claudio

middle: M


title: Microarray analyses for wild type and Mof knockout murine ES cells.

status: Public on Apr 12 2012

city: Ann Arbor

first: Yali

last: Dou

address: Rm 5215A, MS I, 1301 Catherine Rd,

department: Department of Pathology, Department of Biological Chemistry

institute: University of Michigan

summary: We report the application of Affy based microarray technology for profiling of gene expression in mouse embryonic stem cells with or without histone acetytransferase MOF. We find that Mof regulates a wide range of genes in mouse ESCs including those important for ESC pluripotency and ESC differentiation. Mof deletion leads to similar number of genes that are up or down regulated. This study provides a framework for understanding the function of Mof in regulating ESC core transcription network.

overall_design: Compare gene expression difference in two cell lines

first: Xiangzhi

last: Li

first: Ruchi

last: Pandey

first: Zhaohui

last: Qin

first: Li


title: Influenza virus A infected monocytes

status: Public on Apr 04 2012

city: Bethesda

first: Timothy

last: Myers

address: 50 South Drive, Room 5509

department: Research Technologies Branch

institute: National Institute of Allergy and Infectious Diseases

summary: Gene expression profiles 6 hours post-influenza A virus infection in human monocytes at multiplicities of infection of 10 versus uninfected monocytes

overall_design: total six samples - comparing uninfected and infected samples from three individual subjects

first: W

last: Hou

first: J

first: X

last: Lu

first: C

last: Brooke

first: D

last: Roy

first: R

last: Modlin

last: Bennink

last: Yewdell


title: Importance of histone demethylation in adipogenic differentiation and function

city: Kumamoto

first: Mitsuyoshi

last: Nakao

address: 2-2-1 Honjo

institute: Kumamoto University

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Differentiating 3T3-L1 adipocytes, introduced with siRNA against phf21a gene

summary:
Adipogenic differentiation and metabolic adaptation are initiated through transcriptional and epigenetic reprogramming. In particular, dynamic changes in histone modifications may play central roles in the rearrangement of gene expression patterns. BHC80 protein, encoded by phf21a gene, is a part of LSD1 histone demethylase complex and is essential for the demethylation activity.
To address the importance of histone demethylation in adipogenic differentiation and function, we performed cDNA microarray in BHC80-deficient 3T3-L1 cells

overall_design: 3T3-L1 preadipocytes were transfected with either BHC80-specific siRNA or control siRNA (siGL3). 24 hours later, cells were subjected to adipogenic induction. 24 hours later, cells were harvested for total RNA extraction.

first: Shinjiro

last: Hino


title: Differentiating 3T3-L1 adipocytes, introduced with siRNA against aof2 and rfk genes, or treated with tranylcypromine

summary:
Adipogenic differentiation and metabolic adaptation are initiated through transcriptional and epigenetic reprogramming. In particular, dynamic changes in histone modifications may play central roles in the rearrangement of gene expression patterns. LSD1 (KDM1) protein, encoded by aof2 gene, is a histone demethylase, which is involved in transcriptional regulation. Since the enzymatic activity of LSD1 is FAD (flavin adenine dinucleotide)-dependent, its effects on gene expression may be influenced by FAD availability.
To address the importance of histone demethylation in adipogenic differentiation and function, we performed cDNA microarray in LSD1-deficient 3T3-L1 cells as well as in the cells treated with LSD1 inhibitor tranylcypromine (TC). FAD-synthesizing enyme, riboflavin kinase (RFK) -deficient cells were also subjected to the microarray analysis.

overall_design: 3T3-L1 preadipocytes were transfected with  aof2- or rfk- specific siRNA or control siRNA (siGL3) . 24 hours later, cells were subjected to adipogenic induction. 24 hours later, cells were harvested for total RNA extraction. For the TC treatment, TC was added to the adipogenic induction medium.


title: Expression and MeDIP microarray data from IL13-induced allergic airway inflammation of mice lungs

status: Public on Apr 07 2012

city: Los Angeles

first: Aik

middle: T

last: Ooi

address: 650 Charles E Young Dr S, Factor 9-240

institute: UCLA

type: Methylation profiling by genome tiling array

platform_organism:
Mus musculus
synthetic construct


title: Expression data from a Tbx1 gene allelic series

city: Naples

first: Luna Simona

last: Pane

state: Italy

address: via Pietro Castellino, 111

institute: TIGEM

summary: This study was aimed at identifying Tbx1 dosage-dependent genes in vivo, so we performed a transcriptome analysis of Tbx1 mutants with nine different genotypes corresponding to different Tbx1 mRNA dosages.

overall_design:
RNA isolated from whole E9.5 embryos with 9 different genotypes was hibridized to Affymetrix GeneChip Mouse Genome 430 2.0 arrays. For each genotype, we used two embryos (biological replicates), each hybridized to one array, thus we analyzed a total of 18 arrays.
Tbx1 gene dosage

first: Luna

first: Zhen

last: Zang

first: Antonio

last: Baldini


title: Gene expression profile in Yaf2 KD and/or RYBP KO ES cells.

city: Yokohama

first: Takaho

middle: A.

last: Endo

state: Kanagawa

address: 1-7-22 Suehiro, Tsurumi

department: IMS

institute: RIKEN

summary: Gene expression change by Yaf2 KD in wild type or RYBP KO ES cells.

overall_design: Total RNAs were extracted from the respective ES cells, and were subjected to microarray analysis using Affymetrix GeneChip Mouse Genome 430A 2.0 arrays

first: Kaori

last: Hisada

middle: A

first: Miguel

last: Vidal


title: Expression data from wild-type and Rybp-deficient ES cells

summary: We used microarrays to investigate a global change in gene expression by conditional depletion of Rybp in mouse ES cells.

overall_design: Total RNAs were extracted from wild-type and Rybp-deficient ES cells, and were subjected to microarray analysis using Affymetrix GeneChip Mouse Genome 430A 2.0 arrays


title: Expression profiling of murine neuroblastoma in transgenic mice

status: Public on Apr 01 2012

city: Essen

first: Alexander

last: Schramm

address: Hufelandstr. 55

institute: University Hospital Essen

summary: Neuroblastoma is an embryonal tumor arising from the neural crest. It can be mimicked in mice by neural crest-specific overepxression of oncogenes such as MYCN or mutated ALK.

overall_design: Expression profiling of murine neuroblastoma driven by MYCN were compared to those driven by mutated ALK or both oncogenes. Mouse normal adrenal tissue served as a control.

first: Johannes

last: Schulte


title: Identification of prognostic gene signatures in AML

city: chicago

first: chunjiang

last: he

state: il

address: 900 east 57th st

institute: university of chicago

summary:
Increased expression levels of miR-181 family members have been shown to be associated with favorable outcome in patients with cytogenetically normal acute myeloid leukemia. Here we show that increased expression of miR-181a and miR-181b is also significantly (P < .05; Cox regression) associated with favorable overall survival in cytogenetically abnormal AML (CA-AML) patients. We further show that up-regulation of a gene signature composed of 4 potential miR-181 targets (including HOXA7, HOXA9, HOXA11, and PBX3), associated with down-regulation of miR-181 family members, is an independent predictor of adverse overall survival on multivariable testing in analysis of 183 CA-AML patients. The independent prognostic impact of this 4-homeobox-gene signature was confirmed in a validation set of 271 CA-AML patients. Furthermore, our in vitro and in vivo studies indicated that ectopic expression of miR-181b significantly promoted apoptosis and inhibited viability/proliferation of leukemic cells and delayed leukemogenesis; such effects could be reversed by forced expression of PBX3. Thus, the up-regulation of the 4 homeobox genes resulting from the down-regulation of miR-181 family members probably contribute to the poor prognosis of patients with nonfavorable CA-AML. Restoring expression of miR-181b and/or targeting the HOXA/PBX3 pathways may provide new strategies to improve survival substantially.

In addition, this data set has also been used to identify a common prognostic gene signature in human AML (Li Z. et al., unpublished).

overall_design: 93 human AML samples bearing various cytogenetic and molecular abnormalities are used to identify miR-181 target genes and a common prognostic gene signature.

first: Zejuan

last: Li

first: Hao

last: Huang

first: Ping

last: Chen

first: Chunjiang

last: He

first: Xi

last: Jiang

first: Yuanyuan

first: Michael

last: Radmacher

first: Kati

last: Maharry

first: Abdel

last: Elkahloun

first: Xinan

last: Yang

first: Stephen

last: Arnovitz

first: Ruud

last: Delwel

first: Konstanze

last: Dohner

first: Zhiyu

last: Zhang

first: Chen

last: Shen

first: Mary

last: Neilly

first: Yanming

first: Richard

last: Larson

first: Michelle

last: Le Beau

last: Caligiuri

first: Lars

last: Bullinger

first: Peter

last: Valk

first: Bob

last: Lowenberg

first: Paul

last: Liu

first: Guido

last: Marcucci

first: Janet

last: Rowley

first: Clara

last: Bloomfield

first: Jianjun


title: Expression data from E12.5 embryonic kidneys isolated from wild-type and Ret-deficient mice

city: La Jolla

first: Sanjay

middle: K.

last: Nigam

state: CA

address: 9500 Gilman Drive

institute: University of California San Diego

summary: To better understand the signaling and transcriptional events involved in the GDNF-independent emergence of the ureteric bud from the Wolffian duct, microarray expression analysis was performed on embryonic kidneys from wild-type and Ret-deficient mice.  Microarray data was used to identify genes and gene networks involved in the GDNF-independent outgrowth of the ureteric bud.

overall_design: Whole embryonic kidneys from E12.5 Ret mutant and wild-type mice were isolated.  Isolated kidneys were lysed and RNA was extracted with the Qiagen RNEasy Micro kit.  The RNA was amplified using the NuGEn Ovation kit and hybridized to the Affymetrix GeneChip Mouse Whole Genome 430 2.0 microarray.  Three biological replicates for Ret-knockout and wild-type kidneys were performed.

first: Y

last: Choi

first: J

last: Tee

first: A

last: Dnyanmote

first: M

last: DeCambre

first: C

last: Ito

first: K

last: Bush

first: S


title: Identification of a common prognostic gene signature and its association with miR-181 regulation in human acute myeloid leukemia

first: chunjiang

last: he


title: Progression of ductal carcinoma in situ to invasive breast cancer

city: PHILADELPHIA

first: Adam

last: Ertel

state: PA

address: 233 S 10TH ST

department: Cancer Biology

institute: Thomas Jefferson University

summary: Ductal carcinoma in situ (DCIS) is a precursor lesion that can give rise to invasive breast cancer (IBC).    It has been proposed that both the nature of the lesion and the tumor microenvironment play key roles in progression to IBC.  Here, laser capture microdissected tissue samples from epithelium and stroma in normal breast, pure DCIS, and pure IBC were employed to define key gene expression profiles associated with disease progression.

overall_design: Tumor and matching stroma were profiled for 9 DCIS patients, 10 IBC patients, and 3 normal breast.  Differential gene expression was evaluated for paired normal stroma versus normal epitelium samples, paired DCIS stroma versus DCIS epitelium samples, paired IBC stroma versus IBC epitelium, IBC stroma versus DCIS stroma, and IBC epithelium versus DCIS epithelium.

first: Erik

last: Knudsen

first: Elai

last: Davicioni

first: Jessica

last: Kline

first: Gordon

middle: F

last: Schwartz

first: Agnieszka

last: Witkiewicz


title: Evaluation of microRNA expression profiles and their associations with risk alleles in lymphoblastoid cell lines of familial ovarian cancer

city: buffalo

first: Dan

last: Wang

state: NY

address: Elm & Carlton Streets

institute: RPCI

summary: We evaluated the genome-wide microRNA expression profiles in lymphoblastoid cell lines of familial ovarian cancer patients and controls

overall_design: We used microarray to perform microRNA profiling in lymphoblastoid cell lines from 74 women with familial ovarian cancer patients and 47 controls.

first: Jie

last: Shen

first: Steven

last: Gregory

first: Leonard

last: Medico

first: Qiang

last: Hu

first: Kunle

last: Odunsi

first: Shashikant

middle: B

last: Lele

first: Christine

last: Ambrosone

first: Song

last: Liu

first: Hua

last: Zhao


title: Dicer knockout mouse subcutaneous preadipocytes

status: Public on Mar 31 2012

first: Marcelo

last: Mori

state: MA

address: 1 Joslin Place

institute: Joslin Diabetes Center

summary:
Dicer is required for miRNA processing and RNA interference. Here we knocked out Dicer in SV40 T antigen immortalized subcutaneous preadipocytes isolated from Dicer flox mice by transducing these cells with adenoviruses harboring Cre recombinase. Control cells were transduced with adenovirus harboring GFP.
We used microarrays to detail the gene expression profile of Dicer knockout preadipocytes.

overall_design: Four days after adenovirus infection, cells were harvested for RNA isolation and hybridization on Affymetrix microarrays. At this point, Dicer knockout was confirmed by several methods.

first: C

last: Kahn


title: Expression data from directly induced neural stem cells

city: Kobe

first: Kenji

last: Yoshida

address: 2-2-2, Minatojima Minamimachim Chuo-ku

department: Regenerative & Cellular Medicine

institute: Sumitomo Dainippon Pharma Co.,Ltd.

summary: Induced pluripotent stem (iPS) cells give rise to neural stem cells, which are applicable for therapeutic transplantation in treatment of neural diseases. However, generation of neural stem cells from iPS cells requires a careful selection of safe iPS clones. We sought to determine whether direct induction of neural stem cells from partially reprogrammed somatic cells is able to generate safer cells rapidly. We have successfully established direct induction system from fibroblast to neural stem cells. To characterize these directly induced neural stem cells, Gene expression profiles were compared with iPS cell or ES cell-derived neurosphere. We used affymetrix microarrays to compare the global gene expression of neurospheres prepared several method.

overall_design:
RNA extracted from neurospheres was hybridized to Affymetrix microarrays.
The mouse strain used in this study except ES/iPS cells was C57BL/6.

first: Takeshi

last: Matsui

first: Wado

last: Akamatsu


title: Expression data from caudal artery of Notch3WT and Notch3KO mice

city: Paris

first: Anne

last: Joutel

address: 10 avenue de Verdun

country: France

institute: INSERM

summary:
Notch3 is a transmembrane receptor which is critically important for the structure and myogenic response of distal arteries, particularly cerebral arteries. After activation of the receptor, the intracellular domain translocates in the nucleus to activate target genes transcription.
In order to identify Notch3 target genes, we used microarrays to compare gene expression from caudal arteries (Notch3+/+ vs Notch3-/-) and selected down-regulated genes in Notch3-/- arteries.

overall_design: Caudal arteries were dissected from 1 month old Notch3+/+ and Notch3-/- mice. RNA was prepared with arteries pooled from three (AJ_N3WT_3, AJ_N3WT_4) or four (AJ_N3WT_1, AJ_N3KO_1, AJ_N3KO_2, AJ_N3KO_4) mice and hybridized on Mouse MOE430.2 Affymetrix chips. For each group (Notch3+/+ and Notch3-/-), three biological replicates were performed.

first: Charles

last: Fouillade


title: Mouse oral tumors induced by activation of Ras and p53 mutations

city: Houston

first: Carlos

last: Caulin

state: TX

address: 1515 Holcombe Blvd

institute: MD Anderson Cancer Center

summary:
The p53 gain of function p53R172H promotes accelerated tumor growth and progression to carcinoma.  To identify gene expression changes associated with the oncogenic function of mutant p53 we compared the expression profiles of oral tumors induced by activation of oncogenic K-ras and p53 gain- or loss-of-function mutations
Oral tumors were induced by activation of endogenous oncogenic K-rasG12D and p53  loss- or gain-of-function mutations (p53R172H)

overall_design: Oral tumors from mice carrying the p53R172H mutation or deletion of p53 were collected for gene expression analysis


title: Expression regulation by RYBP in mouse embryonic stem cells

first: Takaho

last: Endo

type: Genome binding/occupancy profiling by array

summary:
Polycomb repressive complexes (PRCs) are important chromatin regulators of ES cell function. RYBP binds Polycomb H2A monoubiquitin ligases Ring1A and Ring1B, and has been suggested to participate in localizing Polycomb complexes to their targets. Moreover, constitutive inactivation of RYBP precludes ES cell formation. Here we have used ES cells conditionally deficient in RYBP to investigate RYBP function. Chromosome immunoprecipitation on a chip (ChIP-chip) of RYBP and microarray experiments were performed using wild type and knocked-out ES cells.

This SuperSeries is composed of the SubSeries listed below.

overall_design: Gene expression profiling of WT, conditionally deficient in RYBP with or without Yaf2 RNAi, and ChIP-chip of RYBP on promoters of WT, Dnmt1-KO or Eed-KO ES cells.

first: Kaori

last: Hisada

first: Mitsuhiro

last: Endoh

first: Miguel

last: Vidal


title: Expression profiling of aging liver in low-fat diet mice

status: Public on Mar 28 2012

city: Beijing

first: Bing

last: Zhou

address: Datun Road

department: Center for Molecular Systems Biology

institute: Institute of Genetics and Developmental Biology, Chinese Academy of Sciences

summary: Dietary interventions are effective ways to extend or shorten lifespan. By examining midlife hepatic gene expressions in mice under different dietary conditions, which resulted in different lifespans and aging-related phenotypes, we were able to identify genes and pathways that modulate the aging process. To determine how our dietary intervention-based transcriptomic approach for predicting aging-regulatory genes compares to more traditional approach of using age-dependent transcriptional changes, we examined the hepatic gene expression changes in LF-fed mice during aging at 4, 8, 13 and 21 months.

overall_design:
Male C57BL/6J mice at 4 weeks of age were purchased from Shanghai Animal Co, Ltd. Mice were maintained under a 12-hour dark/light cycle (lights on at 6:30 am) at a temperature of 22 ± 3 °C in accredited animal facilities. Prior to the start of experiment, mice were maintained on a low-fat diet (Research Diets Inc., New Brunswick, NJ) for one week.
Liver RNAs extracted from six male C57BL/6J mice of the same age were pooled at each age point to obtain an average microarray profile at 4, 8, 13 and 21 months.

first: Liu

last: Yang

first: Shoufeng

last: Li

first: Jialiang

last: Huang

first: Haiyang

last: Chen

first: Lei

last: Hou

first: Jinbo

last: Wang

first: Christopher

last: Green

first: Zhen

last: Yan

first: Xun

first: Matt

last: Kaeberlein

first: Li

last: Zhu

first: Huasheng

last: Xiao

first: Yong

first: Jing-Dong

middle: J

last: Han


title: Target genes of thyroid hormone in cerebellum neurons

status: Public on Mar 30 2012

city: Oullins

first: Fabrice

last: Chatonnet

address: 165 Chemin du Grand Revoyet

summary:
Cerebellar post-natal development is particularly sensitive to thyroid hormone and low levels of thyroid hormone (hypothyroidism) result in permanent defects in cerebellar architecture and function. All cell types of the cerebellum are affected, but the main sign of hypothyroidism in mice is the persistence of the external granular layer, composed of mitotic neuronal precursors at P21.
To make the genetic link between thyroid hormone and cerebellar development, we sought to identify new thyroid hormone target genes, in particular in granule cells which represent the vast majority of cerebellar cells.

overall_design: Primary cultures of cerebellar neurons were made by dissociation of cerebella from newborn wild-type mice. These cells were plated 48 hours in serum-free medium to avoid invasion of the culture by glial cells. In order to include a kinetic and a maximum number of target genes, several cultures were either treated or left untreated as controls for 6 hours (T1), 16 hours (T2), 24 hours (T3) or 48 hours (T4) and results were pairwise compared for each time point.

first: Frédéric

last: Flamant

first: Maria

last: Bondesson


title: Expression data from endothelial SP and MP cells

status: Public on Mar 29 2012

city: Suita

first: Hisamichi

last: Naito

state: Osaka

address: Yamada-oka 3-1

department: Signal Transduction

institute: The Research Institute for Microbial Diseases

summary:
We identified an endothelial progenitor/stem like population in the endothelial fraction of preexsiting blood vessels.
And we used microarray to see the difference of gene expression profiles between these two populations.

overall_design: Hindlimb muscle of wild type C57BL/6 were digested to single cells and stained with anti-CD31 antibody, anti- CD45 antibody, Propidium iodide and hoechst 33342. CD31+CD45- side population cells and CD31+CD45- main population cells were sorted by flow cytometry for RNA extraction and hybridized on Affimetrix microarrays.

first: Nobuyuki

last: Takakura


title: Genetic and epigenetic determinants of neurogenesis and myogenesis [expression profiling]

status: Public on Mar 26 2012

city: Seattle

first: Stephen

last: Tapscott

state: WASHINGTON

address: 1100 Fairview N. Ave

department: Human Biology

institute: Fred Hutch Cancer Research Center

summary: The regulatory networks of differentiation programs have been partly characterized; however, the molecular mechanisms of lineage-specific gene regulation by highly similar transcription factors remain largely unknown. Here we compare the genome-wide binding and transcription profiles of NEUROD2-mediated neurogenesis with MYOD-mediated myogenesis. We demonstrate that NEUROD2 and MYOD bind a shared CAGCTG E-box motif and E-box motifs specific for each factor: CAGGTG for MYOD and CAGATG for NEUROD2. Binding at factor-specific motifs is associated with gene transcription, whereas binding at shared sites is associated with regional epigenetic modifications but not as strongly associated with gene transcription. Binding is largely constrained to E-boxes pre-set in an accessible chromatin context that determines the set of target genes activated in each cell type. These findings demonstrate that the differentiation program is genetically determined by E-box sequence whereas cell lineage epigenetically determines the availability of E-boxes for each differentiation program.

overall_design: Total RNA samples were collected in triplicate from undifferentiated and differentiated P19 cells and MEFs, and labeled cDNA was made per Affymetrix protocol

first: Abraham

last: Fong

first: Zizhen

last: Yao

first: Jun

last: Zhong

first: Yi

last: Cao

first: Walter

middle: L

last: Ruzzo

first: Robert

middle: C

last: Gentleman


title: Expression data from mouse skin

status: Public on Mar 22 2012

first: Michio

last: Shibata

address: 2-12-1 Fukuura, Kanazawa-ku

institute: Shiseido Research Center

summary:
Winged bean (WB), Psophocarpus tetragonolobus, is a tropical legume, the potential of which is not yet been understood. We found that a 5 week-oral administration of WB seed extract inhibited wrinkle formation induced by repeated tape stripping (TS), which is a model of lichenification in human chronic eczematous dermatitis.
To elucidate mechanism of the effect of WB on this model, we applied microarray analysis.

overall_design: Skin barrier was disrupted by repeated application and removal (tape stripping; TS) of cellophane tape on the dorsal skin of the left side. This procedure was started after 1 week-administration of winged bean (WB) extract, and was conducted 3 times per week for 4 weeks. Dorsal skin samples from three experimental groups were used for microarray experiment. These groups were the non-TS (NT), TS, and TS with oral administration of WB extract (TS/WB). The DNA microarray experiment was performed using Affymetrix Mouse Genome 430 2.0 Array.

first: Yumiko

last: Ishimatsu-Tsuji

first: Mihoshi

last: Yokoo

first: Yuji

last: Nakai

first: Keiko

last: Abe

last: Muta-Takada


title: Expression profiling of the effect of high-fat diet, low-fat diet, CR and exercise on mice liver

first: Bing

last: Zhou

summary: Dietary interventions are effective ways to extend or shorten lifespan. By examining midlife hepatic gene expressions in mice under different dietary conditions, which resulted in different lifespans and aging-related phenotypes, we were able to identify genes and pathways that modulate the aging process. We found that pathways transcriptionally correlated with diet-modulated lifespan and physiological changes were enriched for lifespan-modifying genes.

overall_design:
Male C57BL/6J mice at 4 weeks of age were purchased from Shanghai Animal Co, Ltd. Mice were maintained under a 12-hour dark/light cycle (lights on at 6:30 am) at a temperature of 22 ± 3 °C in accredited animal facilities. Prior to the start of experiment, mice were maintained on a low-fat diet (Research Diets Inc., New Brunswick, NJ) for one week.
At the age of 5 weeks, animals were randomly assigned to one of the 6 intervention groups (n = 30 for each group): feeding of a low-fat diet (10% fat, D12450B, Research Diets) ad libitum (LF) or with 30% calorie restriction (LF+CR) or with voluntary running exercise (LF+Ex), feeding of a high-fat diet (60% fat, D12492, Research Diets) ad libitum (HF) or with 30% calorie restriction (HF+CR) or with voluntary running exercise (HF+Ex). All mice were housed individually during the study. The daily consumption of food in LF and HF groups was recorded over a week and averaged to determine the amount of food for the following week for the LF+CR and HF+CR groups, respectively. After 1 week acclimation in cage with the locked running wheels, mice in the LF+Ex and HF+Ex groups were allowed free access to a running wheel, and the running distance and time were recorded automatically by the equipment. The hepatic transcriptional level for 3 mice from each intervention group at 62 weeks of age was analyzed using Affymetrix Mouse Genome 430 2.0 Arrays.

first: Liu

last: Yang

first: Shoufeng

last: Li

first: Jialiang

last: Huang

first: Haiyang

last: Chen

first: Lei

last: Hou

first: Jinbo

last: Wang

first: Christopher

last: Green

first: Zhen

last: Yan

first: Xun

first: Matt

last: Kaeberlein

first: Li

last: Zhu

first: Huasheng

last: Xiao

first: Yong

last: Liu

first: Jing-Dong

last: Han


title: MiRNA-127 Inhibits IgG Immune Complex-induced Lung Inflammation by Targeting IgG Fcγ Receptor I

first: ting

last: Xie

address: 127 San Vicente Blvd

department: Pulmonary

institute: Cedars-Sinai Medical Center

summary: The molecular mechanisms of acute lung injury are incompletely understood. MicroRNAs (miRNAs) are crucial biological regulators that act by suppressing their target genes and are involved in a variety of pathophysiologic processes. MiR-127 appeared to be down-regulated during lung injury. We set out to investigate the role of miR-127 in lung injury and inflammation. Expression of miR-127 significantly reduced cytokine release by macrophages. Looking into the mechanisms of the regulation of inflammation by miR-127, we found that IgG Fcγ Receptor I (FcγRI/CD64) was a target of miR-127, as evidenced by reduced CD64 protein expression in macrophages over-expressing miR-127. Furthermore, miR-127 significantly reduced the luciferase activity with a reporter construct containing the native 3’-UTR of CD64. Importantly, we demonstrated that miR-127 attenuated lung inflammation in an IgG immune complex (IgG IC) model in vivo. Collectively, these data show that miR-127 targets macrophage CD64 expression and promotes the reduction of lung inflammation. Understanding how miRNAs regulate lung inflammation may represent an attractive way to control inflammation induced by infectious or non-infectious lung injury.

overall_design: MH.S-miR127 and MH.S-Sico cells were cultured for RNA extraction.Total RNA were assessed for quality with Agilent 2100 Bioanalyzer G2939A (Agilent Technologies,Santa Clara, CA)) and Nanodrop 8000 spectrophotometer (Thermo Scientific/Nanodrop, Wilmington, DE). Hybridization targets were prepared with MessageAmp™ Premier RNA Amplification Kit (Applied Biosystems/Ambion, Austin, TX) from total RNA, hybridized to GeneChip® Mouse Genome 430 2.0 arrays in Affymetrix  GeneChip® hybridization oven 645, washed in Affymetrix GeneChip®  Fluidics Station 450 and scanned with Affymetrix GeneChip® Scanner 7G according to standard Affymetrix GeneChip® Hybridization, Wash, and Stain protocols. (Affymetrix, Santa Clara,CA).

first: Ting

first: Dianhua

last: Jiang


title: MicroRNA profiling and prediction of recurrence/relapse-free survival in stage I lung cancer

status: Public on Mar 27 2012

city: Milwaukee

first: Yan

last: Lu

address: 8701 Watertown Plank Rd

institute: Medical College of Wisconsin

summary:
Despite surgical treatment of stage I non-small cell lung cancer (NSCLC), one third of patients will eventually have a recurrence. Robust prognostic markers are required to better manage therapy options. MicroRNAs play important roles in human cancers. The purpose of this study is to identify miRNA expression profiles that would better predict prognosis. Small RNAs extracted from formalin-fixed and paraffin-embedded (FFPE) tumor tissues of 357 stage I NSCLC patients were profiled on the human MicroRNA expression profiling V2 panel (Illumina). The expression differences between cancer subtypes were compared by t tests.  The association of miRNA expression profile with recurrence free survival (RFS) was assessed using partial Cox regression models.
Two miRNA signatures that are highly predictive of RFS were identified. The first contained 32 miRNAs derived from 357 stage I NSCLC patients independent of cancer subtype; while the second containing 27 miRNAs was adenocarcinoma specific. Both of them were validated using FFPE and/or fresh frozen tissues in independent data set with 170 stage I patients. This has important prognostic or therapeutic implications for the management of patients.  The identified miRNAs hold great potential as targets for histology-specific treatment or prevention and treatment of recurrent disease.

first: Ramaswamy

last: Govindan

first: Ming

last: You


title: Genes regulated by Sox9

status: Public on Mar 23 2012

first: Toni-Ann

last: Mistretta

address: 1 Baylor Plaza, BCM 315

department: Pathology

institute: Baylor College of Medicine

summary: We compared gene expression profile of jejunum crypt samples of Sox9 deficient mice and wild type control mice in order to identify the genes that are regulated by SOX9 in the small intestinal crypt epithelial cells.

overall_design: The intestinal epithelial cells were collected from crypts of jejunum of three 3-mo-old Sox9 mutant mice and three littermate controls.

first: Yuko

last: Mori-Akiyama

first: Chi-I

last: Chiang


title: Expression data from BCL11A-null and wild-type bone marrow erythroid pregenitors

city: Memphis

first: Jian

last: Xu

state: Tennessee

address: 262 Danny Thomas Place, MS 345

institute: St. Jude Children's Research Hospital

summary:
BCL11A is a critical mediator of hemoglobin switching and gamma-globin silencing. In this study, we showed the BCL11A is required in vivo for developmental silencing of gamma-globin genes in adult animals.
We used microarray to determine the changes in gene expression profile after loss of BCL11A in adult erythroid cells

overall_design: CD71+Ter119+ erythroid progenitor cells were FACS-sorted from bone marrows of 6-week old control (Bcl11a +/+) and BCL11A knockout (Bcl11a fl/fl EpoR-Cre+) mice.

first: Stuart

last: Orkin


title: Expression data from mouse lungs exposed in-utero and/or as an adult to second-hand smoke (SHS)

city: New York

first: Rui

address: 630 West 168th Street

department: Anesthesiology

institute: Columbia University

summary: Second-hand smoke (SHS) exposure during pregnancy has adverse effects on offspring. We used microarrays to characterize the gene expression changes caused by in-utero exposure and adult exposure to SHS in adult mouse lungs.

overall_design: Left lungs from Balb/c male mice were collected at 15 weeks of age for RNA extraction and hybridization on Affymetrix mouse 430 2.0 microarrays. Based on their smoke exposure status, there are 4 groups of mice, each exposed in-utero to filtered-air or SHS and as an adult to filtered-air or SHS. We extracted RNA from 4 animals from each group for microarray analysis (N = 16 samples).

first: Arthur

last: Penn

first: Zakia

last: Perveen

first: Paula

last: Polk


title: Mechanisms of terminal erythroid differentiation defect in EKLF-deficient mice

status: Public on Mar 20 2012

city: Durham

first: Holly

middle: Kloos

last: Dressman

state: NC

address: 101 Science Drive

department: Institute for Genome Sciences and Policy

institute: Duke University Medical Center

summary: EKLF is a Krüppel-like transcription factor identified as a transcriptional activator and chromatin modifier in erythroid cells. EKLF-deficient (Eklf -/-) mice die at day 14.5 of gestation from severe anemia. In this study, we demonstrate that early progenitor cells fail to undergo terminal erythroid differention in Eklf -/- embryos. To discover potential EKLF target genes responsible for the failure of erythropoiesis, transcriptional profiling was performed with RNA from wild type and Eklf -/- early erythroid progenitor cells. These analyses identified significant perturbation of a network of genes involved in cell cycle regulation, with the critical regulator of the cell cycle, E2f2, at a hub. E2f2 mRNA and protein levels were markedly decreased in Eklf -/- early erythroid progenitor cells, which showed a delay in the G1-to-S-phase transition. Chromatin immunoprecipitation analysis demonstrated EKLF occupancy at the proximal E2f2 promoter in vivo. Consistent with the role of EKLF as a chromatin modifier, EKLF binding-sites in the E2f2 promoter were located in a region of EKLF-dependent DNase I sensitivity in early erythroid progenitor cells. We propose a model in which EKLF-dependent activation and modification of the E2f2 locus is required for cell cycle progression preceding terminal erythroid differentiation.

overall_design: RNA was isolated from flow-sorted early erythroid progenitors in 13.5 day old fetal livers from EKLF knock out mice (n=3 fetal livers) and wild-type control mice (n=3 fetal livers) for gene expression analysis

first: A

last: Pilon

first: M

middle: O

last: Arcasoy

first: H

first: S

middle: E

last: Vayda

first: Y

last: Maksimova

first: J

middle: I

last: Sangerman

first: P

middle: G

last: Gallagher

first: D

last: Bodine


title: Adipose tissue in the presence or absence of kinin B1 receptors

city: Boston

first: Marcelo

last: Mori

summary:
We studied adipose tissue from wild type mice, kinin B1 receptor knockout mice (B1KO), and B1KO mice with rescued expression of kinin B1 receptor selectively in fat.
We used microarrays to detail the gene expression profile of the epididymal fat of these mice.

overall_design: Three-month-old mice were killed and tissue was collected for RNA processing and microarray analysis.

first: Joao

last: Pesquero


title: DNA methylation and gene expression in lung adenocarcinoma

status: Public on Mar 21 2012

city: Los Angeles

first: Ite

last: Laird-Offringa

address: 1441 Eastlake Avenue, Suite 6420

department: Biochemistry

institute: University of Southern California

type:
Methylation profiling by array
Expression profiling by array

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Gene expression analysis of lung adenocarcinoma and matched adjacent non-tumor lung tissue

summary:
Gene expression profiling of 60 lung adenocarcinoma tumors and their matched histologically normal adjacent lung tissue samples were analyzed using Illumina HumanWG-6 v3.0 expression beadchip. We integrated these data with DNA methylation profiles of the same samples to identify potential DNA methylation regulated genes.
Lung cancer is the leading cause of cancer death worldwide and adenocarcinoma is its most common histological subtype. Clinical and molecular evidence indicates that lung adenocarcinoma is a heterogeneous disease, which has important implications for treatment. Here we performed genome-scale DNA methylation profiling using the Illumina Infinium HumanMethylation27 platform on 59 matched lung adenocarcinoma/non-tumor lung samples, with genome-scale verification on an independent set of tissues. We identified 766 genes showing altered DNA methylation between tumors and non-tumor lung.  By integrating DNA methylation and mRNA expression data, we identified 164 hypermethylated genes showing concurrent downregulation, and 57 hypomethylated genes showing increased expression. Integrated pathways analysis indicates that these genes are involved in cell differentiation, epithelial to mesenchymal transition, RAS and WNT signaling pathways and cell cycle regulation, among others. Comparison of DNA methylation profiles between lung adenocarcinomas of current and never-smokers showed modest differences, identifying only LGALS4 as significantly hypermethylated and downregulated in smokers. LGALS4, encoding a galactoside-binding protein involved in cell-cell and cell-matrix interactions, was recently shown to be a tumor-suppressor in colorectal cancer. Unsupervised analysis of the DNA methylation data identified two tumor subgroups, one of which showed increased DNA methylation and was significantly associated with KRAS mutation and to a lesser extent, with smoking. Our analysis lays the groundwork for further molecular studies of lung adenocarcinoma by providing new candidate DNA methylation biomarkers for early detection, identifying novel molecular alterations potentially involved in lung adenocarcinoma development/progression, and describing an epigenetic subgroup of lung adenocarcinoma associated with KRAS mutation.

overall_design: 58 lung adenocarcinoma and 58 adjacent non-tumor lung fresh frozen tissues were macrodissected, and total RNA was isolated to be analyzed using the Illumina HumanWG-6 v3.0 expression beadchip.

first: Suhaida

last: Selamat

first: Adi

last: Gazdar


title: Effects of knockdown of Jmjd6 on human umbilical vein endothelial cells - gene and exon expression

status: Public on May 04 2012

city: Frankfurt

first: niels

last: boeckel

address: Theodor-Stern-Kai 7

department: Institut for Cardiovascular Regenration

institute: University Frankfurt

summary:
Human umbilical vein endothelial cells (HUVECs) were incubated for 48 h after transfection of scrambled siRNA or siRNA targeting Jmjd6 .
Changes in transcript and exon levels were analyzed.

overall_design: 6 samples; 2 conditions: Scrambled siRNA vs. siJmjd6 ; 3 replicates per condition

middle: N

last: Boeckel

first: V

last: Guarani

last: Koyanagi

first: T

last: Roexe

last: Lengeling

first: R

last: Schermuly

last: Gellert

last: Braun

last: Zeiher

last: Dimmeler


title: Dendritic cell maturation by proinflammatory TNF or pathogenic Trypanosoma brucei antigens instruct similar T helper-2 cell responses in murine models of autoimmunity and asthma

status: Public on Mar 19 2012

city: Wuerzburg

first: Susanne

middle: Elma

last: Kneitz

address: Biozentrum, Am Hubland

department: Physiologigcal Chemistry

institute: University of Wuerzburg

summary:
Background
Dendritic cells (DC) represent the major cell type leading to polarized T helper (Th) cell responses in vivo. The current data indicate that DC maturation under inflammatory conditions or by helminth infections induce only incomplete DC maturation bearing a partially tolerogenic potential. Such semi-mature DC promoted a Th2 profile with increasing proportions of regulatory IL-10 producing T cells (Tr-1) upon restimulation.

Methodology/Principal Findings
Here we asked whether the instruction of DC by the proinflammatory cytokine TNF is qualitatively different from maturation by two types of variant surface glycoproteins (VSGs) of Trypanosoma brucei. We tested differentially matured murine bone marrow (BM)-derived DC for changes in surface markers or cytokines, by microarray analyses, for their induction of Th2 responses and their capacity to influence the disease models asthma for Th2 immunity and experimental autoimmune encephalomyelitis (EAE) for a Th1/Th17 response.

Conclusions/Significance
Together, our data suggest that the partial maturation signatures induced by TNF and VSG antigens are highly similar and result in comparable Th2/Tr1 profiles, effects on asthma and EAE. This is remarkable since the responses resulting from endogenous inflammatory TNF-receptor signals or exogenous pathogenic MyD88 ligands are comparable.

overall_design: total samples analysed are 5

first: Katrien

last: Pletinckx

first: Benoit

last: Stijlemans

first: Vladimir

last: Pavlovic

first: Regina

last: Laube

first: Carolin

last: Brandl

first: Alain

last: Beschin

first: Patrick

last: De Baetselier

last: Lutz


title: Expression Profiling of Early Myogenesis - Affymetrix Dataset

city: Montreal

first: Saravanan

last: Sundararajan

state: Quebec

address: 740, Dr Penfield Ave

department: Human Genetics

institute: McGill University

summary:
Analysis of Early Myogenesis Reveals an Extensive Set of Transcriptional Regulators Whose Knock-down Can Inhibit Differentiation
Myogenesis is a tightly controlled process involving the transcriptional activation and repression of thousands of genes. Although many components of the transcriptional network are known for the later phases of myogenesis, relatively little work has described the transcriptional landscape within the first 24 hours, when myoblasts commit to differentiate. Through dense temporal sampling of differentiating C2C12 myoblasts, we identify 266 transcriptional regulators (TRs) whose expression is altered within the first 12 hours of myogenesis. A high-content shRNA screen of 76 TRs involving 427 stable lines identified 48 genes whose knockdown significantly inhibits differentiation of C2C12 myoblasts. These include known regulators of myogenesis (Myod1, Myog and Myf5), as well as 26 regulators not previously associated with the process. Of the TRs differentially expressed within the first 24 hours, two-thirds inhibited differentiation when knocked down. Surprisingly, a similar proportion (67%) of shRNAs targeting TRs whose expression did not change during differentiation also inhibited myogenesis, suggesting that both stably and differentially expressed TRs are essential for this complex differentiation program. This implies that microarray-based approaches that concentrate functional validation studies on differentially-expressed genes will fail to identify many genes that are critically implicated in complex biological processes.

overall_design: C2C12 myoblasts were differentiated into myotubes and sampled at various timepoints for gene expression measurement on MOE-430v2 chips.  Cells grown in separate plates were harvested at 14 different timepoints: t_-24h, t_0h, t_0.5h, t_1h, t_1.5h, t_2h, t_3h, t_6h, t_9h, t_12h, t_24h, t_48h, t_96h, t_144h.  Cells were also pre-treated with 50uM cycloheximide 1 hour prior to inducing differentiation and harvested at two timepoints: t_chx_1h, t_chx_3h.  All harvests were performed in triplicate using growths from successive passages.

first: Rob

last: Sladek

first: Thomas

last: Hudson


title: Expression Profiling of Early Myogenesis


title: Expression data from tail skin in young (5 months) and old (30 months) CB6F1 mice

status: Public on Mar 15 2012

first: William

middle: R

last: Swindell

address: 77 Avenue Louis Pasteur

department: Genetics

institute: Harvard University

summary:
Background: Skin aging is associated with intrinsic processes that compromise structure of the extracellular matrix while promoting loss of functional and regenerative capacity. These processes are accompanied by a large-scale shift in gene expression, but underlying mechanisms are not understood and conservation of these mechanisms between humans and mice is uncertain.   Results: We used genome-wide expression profiling to investigate the aging skin transcriptome. In humans, age-related shifts in gene expression were sex-specific. In females, aging increased expression of transcripts associated with T-cells, B-cells and dendritic cells, and decreased expression of genes in regions with elevated Zeb1, AP-2 and YY1 motif density. In males, however, these effects were contrasting or absent. When age-associated gene expression patterns in human skin were compared to those in tail skin from CB6F1 mice, overall human-mouse correspondence was weak. Moreover, inflammatory gene expression patterns were not induced with aging of mouse tail skin, and well-known aging biomarkers were in fact decreased (e.g., Clec7a, Lyz1 and Lyz2). These unexpected patterns and weak human-mouse correspondence may be due to decreased abundance of antigen presenting cells in mouse tail skin with age.  Conclusions: Aging is generally associated with a pro-inflammatory state, but we have identified an exception to this pattern with aging of CB6F1 mouse tail skin. Aging therefore does not uniformly heighten inflammatory status across all mouse tissues. Furthermore, we identified both intercellular and intracellular mechanisms of transcriptome aging, including those that are sex- and species-specific.
We used Affymetrix microarrays to evaluate genome-wide expression in tail skin from young (5 month) and old (30 month) CB6F1 mice (males and females).

overall_design: Genome-wide expression was evaluated in tail skin from young (5 months) and old (30 months) CB6F1 mice of both sexes. Samples were collected simultaneously but RNA samples were processed in two separate batches.

first: Andrew

last: Johnston

first: Johann

last: Gudjonsson


title: Identification of a new pathway for Th1 cell development induced by cooperative stimulation with IL-4 and TGFbeta [Affymetrix]

status: Public on Mar 17 2012

city: Kisarazu

first: Soichi

last: Tofukuji

address: 2-6-7 Kazusa-kamatari

department: Human Genome Research

institute: Kazusa DNA Research Institute

summary: IL-4 plays an important role in the induction of Th2 and Th9 cells as well as in the inhibition of Th1 cell generation.  We herein show that a combination of IL-4 and TGFbeta augment the development of Th1 cells that express CD103 (CD103+ Th1 cells) if IFNgamma is present.  The T-box containing transcription factor, eomesodermin (Eomes) is preferentially expressed in CD103+ Th1 cells, and is involved in IFNgamma production.  The induction of T-bet during early T cell activation is essential for the formation of the active chromatin at both the Eomes and IFNgamma gene loci.  TGFbeta is required for the induction of Eomes and CD103, as well as the inhibition of Th2 cytokine expression.  In addition, IL-4 induces Eomes transcription through activation of the Stat6 signaling pathway.  IFNgamma-producing CD103+ Th1 cells are detected in the IEL of normal mice, and their numbers significantly decrease in Tbet- and Stat6-deficient mice.  These results represent the first molecular mechanism of IL-4/TGFbeta-dependent augmentation of Th1 cell generation, and raise the possibility that IL-4 and TGFbeta may simultaneously enhance the Th1 cell-mediated immune responses under certain cytokine conditions.

overall_design: CD103+ Th1 and Th1 cells are profiled for mRNA expression

first: Makoto

last: Kuwahara

first: Junpei

last: Suzuki

first: Osamu

last: Ohara

first: Toshinori

last: Nakayama

first: Masakatsu

last: Yamashita


title: Analysis of the implication of the DBIRD complex (DBC1 and ZNF326/ZIRD) in gene expression and alternative splicing

city: Liegge

first: pierre

last: close

address: Avenue de l'hopital

department: GIGA-Institute

country: Belgium

institute: University of Liege

summary: Alternative mRNA splicing is the main reason vast mammalian proteomic complexity can be achieved with a limited number of genes. Splicing is physically and functionally coupled to transcription and the rate of transcript elongation has a profound effect on splicing. As the nascent pre-mRNA emerges from transcribing RNA polymerase II (RNAPII), it is assembled into a messenger ribonucleoprotein (mRNP) particle that represents its functional form, and the composition of which determines the fate of the mature transcript4. However, factors that connect the transcribing polymerase with the mRNP particle and help integrate transcript elongation with mRNA splicing remain obscure. Here, we characterized the interactome of chromatin-associated mRNP particles and thereby identified Deleted in Breast Cancer 1 (DBC1) and a protein we named ZIRD. These proteins are subunits of a novel protein complex, named DBIRD, which binds directly to RNAPII. DBIRD regulates alternative splicing of a large set of exons embedded in A/T-rich DNA, and is present at the affected exons. RNAi-mediated DBIRD depletion results in region-specific decreases in transcript elongation, particularly across areas encompassing affected exons. These data indicate that DBIRD complex acts at the interface between mRNP particles and RNAPII, integrating transcript elongation with regulation of alternative splicing.

overall_design: HEK 293 cells were transfected with CTR-, DBC1- and ZIRD (ZNF326)- specific stealth siRNAs. Total RNAs from three independent experiments were extracted after 48 hours. All conditions were analyzed in triplicate.

first: Pierre

last: Close

first: Phil

last: East

first: Jesper

middle: Q

last: Svejstrup