title: A new mouse model for mania shares genetic correlates with human bipolar disorder.

city: Bar Harbor

first: Michael

middle: C.

last: Saul

state: ME

address: 600 Main St

institute: The Jackson Laboratory

summary: Bipolar disorder (BPD) is a debilitating heritable psychiatric disorder.  Contemporary models for the manic pole of BPD have primarily utilized either single locus transgenics or treatment with psychostimulants.  Our lab recently characterized a mouse strain, termed Madison (MSN), which naturally displays a manic phenotype, exhibiting elevated locomotor activity, increased sexual behavior, and higher forced swimming relative to control strains.  Lithium chloride and olanzapine treatments attenuate this phenotype.  In this study, we replicated our locomotor activity experiment, showing that MSN mice display generationally-stable mania relative to their outbred ancestral strain, hsd:ICR (ICR).  We then performed a gene expression microarray experiment to compare hippocampus of MSN and ICR mice.  We found dysregulation of multiple transcripts whose human orthologs are associated with BPD and other psychiatric disorders including schizophrenia and ADHD, including: Epor, Smarca4, Cmklr1, Cat, Tac1, Npsr1, Fhit, and P2rx7.  RT-qPCR confirmed dysregulation for all of seven transcripts tested.  Using a network analysis, we found dysregulation of a gene system related to chromatin packaging, a result convergent with recent human findings on BPD.  Using a novel genomic enrichment algorithm, we found enrichment in genome regions homologous to human loci implicated in BPD in replicated linkage studies including homologs of human cytobands 1p36, 3p14, 3q29, 6p21-22, 12q24, 16q24, and 17q25.  Our findings suggest that MSN mice represent a polygenic model for the manic pole of BPD showing much of the genetic systems complexity of the corresponding human disorder.  Further, the high degree of convergence between our findings and the human literature on BPD brings up novel questions about evolution by analogy in mammalian genomes.

overall_design: In total, 12 total RNA samples were used for microarray analysis: 6 samples from Madison mice and 6 samples from ICR outbred mice.  All samples were biological replicates.

first: Griffin

middle: M

last: Gessay

first: Stephen

last: Gammie


title: Expression data from mouse embryonic neural stem cells

status: Public on May 09 2012

city: St. Louis

first: Da Yong

last: Lee

state: MO

address: 660 S. Euclid Avenue

department: Neurology

country: USA

institute: Washington University School of Medicine

summary:
Neural stem cells from different brain regions show differencies in gene expression patterns and physiological functions.
We used microarrays to find differential gene expression between the neuralstem cells from the subventricular zone of lateral ventricle and the subventricular zone of third ventricle.

overall_design: Cultured neural stem cells from embryonic day 17.5 mouse embryos were selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain embryonic neural stem cell cultures from three indipendent females.

first: Da

middle: Y

first: David

middle: H

last: Gutmann


title: Polycomb function during oogenesis is required for mouse early embryonic development (germinal vesicle oocytes)

status: Public on May 07 2012

city: Basel

first: Antoine

last: Peters

address: Maulbeerstrasse 66

country: Switzerland

institute: Friedrich Miescher Institute for Biomedical Research (FMI)

summary:
In mammals, totipotent pre-implantation embryos are formed by fusion of highly differentiated oocytes and spermatozoa. Acquisition of totipotency concurs with remodeling of chromatin states of parental genomes (“epigenetic reprogramming”), changes in maternally contributed transcriptome and proteome, and zygotic genome activation. Genomes of mature germ cells are more proficient in supporting embryonic development than those of somatic cells. It is currently unknown whether transgenerational inheritance of chromatin states present in mature gametes underlies the efficacy of early embryonic development after natural conception. Here, we show that Ring1 and Rnf2, two core components of the Polycomb Repressive Complex 1 (PRC1), serve redundant gene regulatory functions during oogenesis that are required to support embryonic development beyond the two-cell stage. Numerous developmental regulatory genes that are established Polycomb targets in various somatic cell types are de-repressed in Ring1/Rnf2 double mutant (dm) fully grown germinal vesicle (GV) oocytes. Translation of tested aberrant maternal transcripts is, however, delayed until after fertilization. Exchange of maternal pro-nuclei between control and Ring1/Rnf2 maternally dm early zygotes demonstrates an essential role for Ring1 and Rnf2 during oogenesis in defining cytoplasmic and nuclear maternal contributions that are both essential for proper initiation of embryonic development. A large number of genes up-regulated in Ring1/Rnf2 dm GV oocytes harbor PRC2-mediated histone H3 lysine 27 trimethylation (H3K27me3) in spermatozoa and in embryonic stem cells (ESCs), and are repressed during normal oogenesis and early embryogenesis. These data strongly support the model that Polycomb acts in the female and male germline to silence differentiation inducing genes and to program chromatin states, thereby sustaining developmental potential across generations.
Expression profiling of fully grown mouse GV oocytes was performed with the following genotypes: Ring1+/+Rnf2F/F (control), Ring1-/-Rnf2F/F (Ring1 mutant), Ring1+/+Rnf2F/FZp3-cre (Rnf2 mutant) and Ring1-/-Rnf2F/FZp3-cre (Ring1/Rnf2 double mutant).

overall_design: 12 samples were analyzed: 3 biological replicates of each of the 4 genotypes (Ring1+/+Rnf2F/F (control), Ring1-/-Rnf2F/F (Ring1 mutant), Ring1+/+Rnf2F/FZp3-cre (Rnf2 mutant) and Ring1-/-Rnf2F/FZp3-cre (Ring1/Rnf2 double mutant)). Each sample contains 50 GV oocytes.

first: Eszter

last: Posfai


title: Gene expression profile in MCF7 breast cancer cells after siRNA knock down of estrogen receptor alpha (ESR1)

city: Auckland

first: Anita

last: Muthukaruppan

address: 85 Park Road, Grafton

department: Obstetrics and Gynaecology

country: New Zealand

institute: The University of Auckland

summary: Affymetrix microarray data was generated from MCF7 breast cancer cells treated in vitro with siRNAs against estrogen receptor alpha (ESR1).

overall_design: Gene expresion of estrogen receptor alpha (ESR1) was knocked down in MCF7 breast cancer cells using siRNA. Then the gene expression profiles of these MCF7 cells, along with non-targetting control treated cells were analysed using Affymetrix Human Genome U133 Plus 2.0 microarrays.

first: Andrew

last: Shelling

first: Cris

last: Print


title: Polycomb function during oogenesis is required for mouse early embryonic development (2-cell embryos)

summary:
In mammals, totipotent pre-implantation embryos are formed by fusion of highly differentiated oocytes and spermatozoa. Acquisition of totipotency concurs with remodeling of chromatin states of parental genomes (“epigenetic reprogramming”), changes in maternally contributed transcriptome and proteome, and zygotic genome activation. Genomes of mature germ cells are more proficient in supporting embryonic development than those of somatic cells. It is currently unknown whether transgenerational inheritance of chromatin states present in mature gametes underlies the efficacy of early embryonic development after natural conception. Here, we show that Ring1 and Rnf2, two core components of the Polycomb Repressive Complex 1 (PRC1), serve redundant gene regulatory functions during oogenesis that are required to support embryonic development beyond the two-cell stage. Numerous developmental regulatory genes that are established Polycomb targets in various somatic cell types are de-repressed in Ring1/Rnf2 double mutant (dm) fully grown germinal vesicle (GV) oocytes. Translation of tested aberrant maternal transcripts is, however, delayed until after fertilization. Exchange of maternal pro-nuclei between control and Ring1/Rnf2 maternally dm early zygotes demonstrates an essential role for Ring1 and Rnf2 during oogenesis in defining cytoplasmic and nuclear maternal contributions that are both essential for proper initiation of embryonic development. A large number of genes up-regulated in Ring1/Rnf2 dm GV oocytes harbor PRC2-mediated histone H3 lysine 27 trimethylation (H3K27me3) in spermatozoa and in embryonic stem cells (ESCs), and are repressed during normal oogenesis and early embryogenesis. These data strongly support the model that Polycomb acts in the female and male germline to silence differentiation inducing genes and to program chromatin states, thereby sustaining developmental potential across generations.

Expression profiling of late 2-cell embryos was performed with the following genotypes: maternal Ring1-Rnf+ (control), maternal Ring1-Rnf2- (maternal Ring1/Rnf2 double mutant). These embryos were obtained by crossing Ring1-/-Rnf2F/F control females or Ring1-/-Rnf2F/F Zp3-cre expreimental females, respectively, to Ring1+/+Rnf2F/F control males. To distinguish between maternal transcripts present in the 2-cell embryo and newly (embryonicaly) transcribed transcripts, embryos from both genotypes were either not treated (expression profiling therefore shows all maternal and embryonic transcripts) or alpha-amanitin treated (alpha-amanitin inhibits de novo transcription, therefore expression profiling of treated embryos will only show maternal transcripts).

overall_design: 11 samples were analyzed: 3 biological replicates (except alpha-amanitin treated maternal Ring1/Rnf2 double mutant, where only 2 replicates were analyzed) of each genotype and treatment group were analyzed. Each sample contains 40 late 2-cell embryos.


title: PPARγ is a major driver of the accumulation and phenotype of adipose-tissue Treg cells

status: Public on May 04 2012

city: Boston

first: CBDM

last: Lab

state: MA

address: 77 Avenue Louis Pasteur

department: Microbiology and Immunobiology

institute: Harvard Medical School

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

overall_design: Refer to individual Series


title: Expression data from wildtype, MIST1-null, and induced MIST1 Mus musculus pancreata

city: West Lafayette

first: Daniel

last: DiRenzo

state: IN

address: 201 South University Street Rm. 213

department: Purdue Center for Cancer Research

institute: Purdue University

summary:
Although early developmental processes involve cell fate decisions that define the body axes and establish progenitor cell pools, development does not cease once cells are specified.  Instead, most cells undergo specific maturation events where changes in the cell transcriptome ensure that the proper gene products are expressed to carry out unique physiological functions. Pancreatic acinar cells mature post-natally to handle an extensive protein synthetic load, establsih organized apical-basal polarity for zymogen granule trafficking, and assemble gap-junctions to perimt efficient cell-cell communication. Despite significant progress in defining transcriptional networks that control initial acinar cell specification and differentiation decisions, little is know regarding the role of transcription factors in the specification and maintenance of maturation events. One candidate maturation effector is MIST1, a secretory cell-restricted transcription factor that has been implicated in controlling regulated exocytosis events in a number of cell types. Embryonic knock-out of MIST1 generates acinar cells that fail to establish an apical-basal organization, fail to properly localize zymogen granule and fail to communicate intra-cellularly, making the exocrine organ highly suceptible to pancreatic diseases.
In an effort to identify the gene expression differences responsible for MIST1 regulating mature acinar properties. We generated a tamoxifen-inducible mouse model where MIST1 expression could be activated in vivoand performed gene expression arrays on wildtype, MIST1-null, and induced MIST1 pancreatic RNA.

overall_design: RNA was isolated from pancreata of 8 week old mice using the Qiagen RNeasy Midi kit. Pancreta of wildtype, MIST1-null, and MIST1-null with a tamoxifen inducible MIST1-expressing transgene were harvested 36 hours post-tamoxifen administration. Therefore, this experiment provides information on steady-state gene expression differences between wildtype and MIST1-null mice as well as immediate gene expression changes induced by MIST1 expression.

middle: F

last: Konieczny


title: Expression data in human hepatocytes with HCV infection

status: Public on May 03 2012

city: Hiroshima

first: Masataka

last: Tsuge

address: 1-2-3, Kasumi, Minami-ku

country: Japan

institute: Hiroshima university

summary: Human hepatocyte chimeric mice were prepared and treated with hepatitis C virus (HCV) and/or interferon-alpha (IFN-α). To analyze the changes in gene expression, cDNA microarray analysis was performed with the collected human hepatocytes from the chimeric mouse livers. We consider that these results provide molecular insights into possible mechanisms used by HCV to evade innate immune responses, as well as novel therapeutic targets and a potential new indication for interferon therapy.

overall_design: A total of 15 human hepatocyte chimeric mice were prepared and divided into four experimental groups. Mice in group A were neither infected with HCV nor treated with IFN. Mice in group B were administered IFN-α 6 h before sacrifice but were not infected with HCV. The mice in groups C and D were both inoculated via the mouse tail vein with human serum containing HCV genotype 1b particles. At 8 weeks after inoculation, the mice in group D were administered IFN-α 6 h before sacrifice, but the mice in group C were not treated with IFN-α. The human hepatocytes in the mouse livers were collected after sacrifice and subjected to microarray analysis. After purification and reverse transcription of total RNA, cDNA was hybridized on Affymetrix GeneChip Human Gene U133 Plus 2.0 Arrays.

first: Kazuaki

last: Chayama


title: Expression data from monocytic cell lines (THP)

city: Kiel

first: Robert

last: Haesler

address: Schittenhelmstr. 12

department: IKMB / 1st Dept. of Medicine

country: Germany

institute: University Clinic of Schleswig Holstein

summary:
The experiment aims to identify transcriptional effects of Infliximab (an anti-TNF antibody) and CDP870 on human cell lines
Results were generated using 3 timepoints: 0h, 6h, and 24h with each stimuli.

overall_design: 3 biological replicates in each of the 5 groups: oh control; 6h IFX; 24h IFX; 6h CDP870; 24h CDP870

last: Häsler


title: A Chondrogenic Molecule that Repairs Cartilage by Transcriptional Regulation of CBF-beta

status: Public on May 02 2012

city: San Diego

first: John

middle: R

last: Walker

state: CA

address: 10675 John Jay Hopkins

institute: Genomics Institute of the Novartis Research Foundation

summary: Osteoarthritis (OA) is a degenerative joint disease that involves destruction of articular cartilage and eventually leads to disability. Mesenchymal stem cells (MSCs) reside in healthy and diseased cartilage, and through their chondrogenic potential may provide a strategy for cartilage repair. To this end, we performed an image-based, high throughput screen and identified the small molecule, kartogenin, that promotes selective MSC differentiation into chondrocytes (EC50=100nM), shows chondroprotective effects in vitro, and is efficacious in two OA animal models. Kartogenin binds filamin A and induces chondrogenesis by regulating the CBFbeta-RUNX1 transcriptional program. This work provides new insights into the control of chondrogenesis that may ultimately lead to an effective stem-cell based therapy for osteoarthritis.

overall_design: one compound, three doses, two time points, a vehicle control

first: Shoutian

last: Zhu

first: Matthew

middle: S

last: Tremblay

first: Joshua

middle: N

last: Payette

first: Jianing

last: Wang

first: Laure

middle: C

last: Bouchez

first: Shelly

last: Meeusen

first: Alana

last: Althage

first: Charles

last: Cho

first: Xu

last: Wu

first: Peter

middle: G

last: Schultz

first: Kristen

middle: A

last: Johnson


title: Gene expression profiles of myeloma cells treated with NAE inhibitor

first: Constantine

middle: S.

last: Mitsiades

address: 44 Binney Street

department: Medical Oncology

institute: Dana-Farber Cancer Institute

summary:
The transcriptional profile of the human multiple myeloma (MM) cell line MM.1S treated with MLN4924 vs control MM.1S cells was characterized by oligonucleotide microarray analysis, using the human U133 plus 2.0 Affymetrix GeneChip, according to previously described protocols for total RNA extraction and purification; cDNA synthesis; in vitro transcription reaction for production of biotin-labeled cRNA; hybridization of cRNA with U133plus2.0 Affymetrix gene chips; and scanning of image output files. Scanned image output files were analyzed using DNA-Chip Analyzer (dChip) (www.dchip.org), including conversion to DCP files, normalization and modeling. The gene expression profile of MM.1S cells for each time point of MLN4924 treatment was compared to the profile of control MM.1S cells.
The NEDD8 activating enzyme (NAE) is upstream of the 20S proteasome in the ubiquitin/proteasome pathway and catalyzes the first step in the neddylation pathway. NEDD8 modification of cullins is required for ubiquitination of cullin-ring ligases (CRLs), which regulate degradation of a distinct subset of proteins. The more targeted impact of NAE on protein degradation prompted us to study MLN4924, an investigational NAE inhibitor, in preclinical multiple myeloma (MM) models. In vitro treatment with MLN4924 led to dose-dependent decrease of viability in a panel of human MM cell lines. In this analysis, we evaluated the molecular changes triggered in MM.1S myeloma cells by their in vitro treatment with MLN4924. The transcriptional profiles of each experimental condition were characterized by oligonucleotide microarray analysis, using the human U133 plus 2.0 Affymetrix GeneChip.

overall_design: The human multiple myeloma (MM) cells MM.1S were cultured in vitro in the presence or absence of the NEDD8 activating enzyme (NAE) inhibitor MLN4924 for 8, 16 or 24hrs. The gene expression profiles of drug treated cells were compared with the profiles of control MM.1S cells.

first: Douglas

middle: W

last: McMillin


title: The peripheral genome-wide gene expression profiles in humans after prolonged wakefulness and sleep recovery

city: Sao Paulo

first: Renata

last: Pellegrino

address: Rua NApoleao de Barros 925

country: Brazil

institute: UNIFESP

summary: Although the specific functions of sleep have not been completely elucidated, the literature has suggested that sleep is essential for proper homeostasis. Sleep loss is associated with changes in behavioral, neurochemical, cellular, and metabolic function as well as impaired immune response. We evaluated the gene expression profiles of healthy male volunteers who underwent 60 hours of prolonged wakefulness (PW) followed by 12 hours of sleep recovery (SR) using high-resolution microarrays. Peripheral whole blood was collected at 8 am in the morning before the initiation of PW (baseline), after the second night of PW, and one night after SR. We identified over 500 genes that were differentially expressed. Notably, these genes were related to DNA damage and repair and stress response as well diverse immune system responses such as natural killer pathways including killer cell lectin-like receptors family, as well granzymes and T-cell receptors which play important roles in host defense. These results support the idea that sleep loss can lead to alterations in molecular processes that result in perturbation of cellular immunity, induction of inflammatory responses, and homeostatic imbalance. Moreover, expression of multiple genes was down-regulated following PW and up-regulated after SR compared to PW, suggesting an attempt of the body to re-establish internal homeostasis. In silico validation of alterations in the expression of CETN3, DNAJC and CEACAM genes, confirmed previous findings related to the molecular effects of sleep deprivation. Thus, the present findings confirm that the effects of sleep loss are not restricted to the brain and can occur intensely in peripheral tissues.

overall_design: The peripheral blood from each  volunteer (nine individuals) were collected in the baseline night and every morning after PW and after the night of SR.

first: R

first: D

last: Sunaga DY

first: C

last: Guindalini

last: Martins

last: Mazzotti

first: Z

last: Wei

first: J

last: Daye

first: M

middle: L

last: Andersen

first: S

last: Tufik


title: Polycomb function during oogenesis is required for mouse early embryonic development

first: Antoine

last: Peters


title: The gamma secretase inhibitor MRK-003 attenuates pancreatic cancer growth in preclinical models

city: Rahway

first: Oscar

last: Puig

state: NJ

address: 126 East Lincoln Ave

department: Molecular Profiling Research Informatics

institute: Merck Research Laboratories

summary: Pancreatic ductal adenocarcinoma (PDAC) is a nearly uniformly lethal malignancy, with most patients facing an adverse clinical outcome.  Given the pivotal role of aberrant Notch signaling in the initiation and progression of PDAC, we investigated the effect of MRK-003, a potent and selective γ-secretase inhibitor, in preclinical PDAC models.  We used a panel of human PDAC cell lines, as well as patient-derived PDAC xenografts, to determine whether pharmacological targeting of the Notch pathway could inhibit pancreatic tumor growth and potentiate gemcitabine sensitivity.  In vitro, MRK-003 treatment downregulated the canonical Notch target gene Hes-1, significantly inhibited anchorage independent growth, and reduced the subset of CD44+CD24+ and aldehyde dehydrogenase (ALDH)+ cells that have been attributed with tumor initiating capacity.  Ex vivo pretreatment of PDAC cells with MRK-003 in culture significantly inhibited the subsequent engraftment in immunocompromised mice.  In vivo, MRK-003 monotherapy significantly blocked tumor growth in 5 of 9 (56%) patient-derived PDAC xenografts.  Moreover, a combination of MRK-003 and gemcitabine showed enhanced antitumor effects compared to gemcitabine alone in 4 of 9 (44%) PDAC xenografts. Baseline gene expression analysis of the treated xenografts indicated that upregulation of nuclear factor kappa B (NFκB) pathway components was associated with the sensitivity to single MRK-003, while upregulation in B-cell receptor (BCR) signaling and nuclear factor erythroid-derived 2-like 2 (NRF2) pathway correlated with response to the combination of MRK-003 with gemcitabine. The preclinical findings presented here provide further rationale for small molecule inhibition of Notch signaling as a therapeutic strategy in PDAC.

overall_design: Pancreatic ductal adenocarcinoma xenografts were grown in Athymic Nude-Foxn1nu mice. RNA was extracted and profiled in Affymetrix platform to identify genes correlating with sensitivity to MRK-003

first: Anirban

last: Maitra

first: Rajesh

last: Kumar


title: Gene Expression Profiles of IL17RC+ and IL17RC- THP1 Cells

status: Public on May 01 2012

city: Bethesda

first: Lai

state: MD

address: 10 Center Dr. Room 2B47

institute: NIH/NEI/NCCAM

summary: Age related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly population worldwide. While recent studies have demonstrated strong genetic associations of single nucleotide polymorphisms within a number of genes and AMD, other modes of regulation are also likely to play a role in its aetiology. We undertook DNA methylation microarray analysis on monozygotic and dizygotic twins who were discordant for AMD and identified methylated IL17RC promoters as being present only in non-AMD control individuals rather than in AMD patients. We validated this finding of a significantly decreased level of methylation on the IL17RC promoter in AMD siblings as well as in a case control study involving 202 genetically unrelated AMD patients and 96 controls (95% CI, 0.03-0.17, P=3.1x10-8). Further, we showed that hypomethylation of the IL17RC promoter in AMD patients led to an elevated expression of its protein and mRNA in peripheral blood as well as in the retina and choroid, suggesting that the DNA methylation pattern and expression of IL17RC may potentially serve as a biomarker for the diagnosis of AMD and likely plays a role in disease pathogenesis.

overall_design: Affymetrix U133 plus 2.0 GeneChip was used to detect gene expression patterns of IL17RC+ and IL17RC- THP1 cells.

first: Baoying

last: Liu


title: Expression data from Top2β KO cells as well ICRF-193 treatment of in vitro derived neurons and cortical glutamatergic neurons

first: Dirk

last: Schuebeler

address: Fabrikstrasse 24

institute: Friedrich Miescher Institute for Biomedical Research

summary: Expression profiling of from Top2β knokout and ICRF-193 treated neurons reveals a significant number of genes that are transcriptionally deregulated

overall_design: Gene expression in the Top2β knocnout ES, NP and TN stages of stem cell differention to the corresponidng wild type cells. In vitro derived neurons and cortical glutamatergic neurons were either treated with DMSO or ICRF-193 and were compared to reveal differentially expressed genes.

first: Vijay

last: Tiwari

first: Lukas

last: Burger


title: Topoisomerase IIbeta occupies H3K4 methylated sites  and regulates neuronal survival via repression of the neurotrophin receptor p75

type: Genome binding/occupancy profiling by genome tiling array


title: Inhibition of miR-9 regulates HuR and DICER1 and blocks Hodgkin Lymphoma tumor outgrowth

city: Berlin

first: Lea

middle: Haarup

last: Gregersen

address: Robert-Rössle-Str. 10

institute: Max-Delbrück-Centrum für Molekulare Medizin (MDC)

summary: An Hodgkin Lymphoma cell line have been treated with an LNA inhibitor for miR-9 or with a scramble LNA to identify miR-9 regulated pathways that could be important for Hodgkin Lymphoma pathogenesis.

overall_design: L428 cells were transfected with a miR-9 LNA inhibitor or a scrambled LNA. Total RNA was harvested 9 hours post-transfection and analyzed on Affymetrix HG-U133 Plus 2.0 human arrays. A total of six arrays were analyzed. For filtering, uninformative genes with the same expression level across all arrays (including non-expressed genes) were removed and the differentially expressed genes, their corresponding p-values and false discovery rates were calculated using limma.

first: E

last: Leucci

first: A

last: Zriwil

first: L

first: K

middle: T

last: Jensen

last: Obad

first: Y

last: Chen

last: Bellan

last: Sadelin

last: Leoncini

last: Kauppinen

last: Lund


title: Identification of genes induced on nitrate, role of OxyR

city: Cleveland

first: Divya

last: Seth

state: OH

address: 2106 Cornel Road

institute: Case Western Reserve University

summary: The study aimed to identify role of OxyR during growth on different electron acceptors when E. coli are growing anaerobically.

sample_organism: Escherichia coli str. K-12 substr. MG1655

overall_design: Wt and OxyR null cells were grown on nitrate and fumarate medium anaerobically. Each condition was done in duplicate. RNA was extracted using Qiagen RNeasy kit after stabilization of RNA with RNA protect bacteria reagent. Hybridization and further processing was done based on Affymetrix protocols on E. coli Genome 2.0 arrays.


title: Gene expression profiles of triple-negative breast cancer cells under the condition of 3D proliferation

city: Fukuoka

first: Fusanori

last: Yotsumoto

address: 7-45-1, Nanakuma, Jonan-ku

department: Department of Biochemistry, School of Medicine

institute: Fukuoka University

summary:
Triple-negative breast cancer (TNBC) is defined by the absence of estrogen and progesterone receptors and human epidermal growth factor receptor 2, and is the most lethal and aggressive subtype of breast cancer. However, the genes which relate to promote tumor aggressiveness in TNBC remain unclear.
In order to investigate specific genes and pathways involved in TNBC tumorigenesis, we compared genes differentially expressed between 3D cultures (3DC) or tumor xenograft models and control two-dimensional cultures (2DC).

overall_design: Total RNA was prepared from the TNBC cells under the condition of 2DC, 3DC and tumor xenograft models, and applied to Affymetrix Human Genome U133 Plus 2.0 Array.

first: Shingo

last: Miyamoto


title: Hydroxylation of 5-methylcytosine by TET2 maintains the active state of the mammalian HOXA cluster (Infinium HumanMethylation450 Beadchip)

city: heidelberg

first: michael

middle: thomas

last: bocker

address: Im Neuenheimer Feld

institute: DKFZ Heidelberg

type: Methylation profiling by genome tiling array

summary: Differentiation is accompanied by extensive epigenomic reprogramming, leading to the repression of stemness factors and the transcriptional maintenance of activated lineage-specific genes. Here we used the mammalian Hoxa cluster of developmental genes as a model system to follow changes in DNA modification patterns during retinoic acid induced differentiation. We found the inactive cluster to be marked by defined patterns of 5-methylcytosine (5mC). Upon the induction of differentiation, the active anterior part of the cluster became increasingly enriched in 5-hydroxymethylcytosine (5hmC), following closely the colinear activation pattern of the gene array, which was paralleled by the reduction of 5mC. Depletion of the 5hmC generating dioxygenase Tet2 impaired the maintenance of Hoxa activity and partially restored 5mC levels. Our results indicate that gene specific 5mC-5hmC conversion by Tet2 is crucial for the maintenance of active chromatin states at lineage-specific loci.

overall_design: Genome wide DNA methylation profiling of uninduced and retinoic acid (RA) induced NTera2/D1 embryocarcinoma cells (NT2). Bisulphite converted DNA of uninduced, 7d RA and 14d RA treated NT2 cells  were hybridised to the Illumina Infinium HumanMethylation450 Beadchip.

first: Michael

last: Bocker

first: Francesca

last: Tuorto

first: Günter

last: Raddatz

first: Tanja

last: Musch

first: Feng-Chun

last: Yang

first: Mingjiang

last: Xu

first: Frank

last: Lyko

first: Achim

last: Breiling


title: Differential regulation of Twist1-responsive genes in 4T1 cells

first: Gongda

last: Xue

summary:
Twist1 variants including wildtype Twist1, a non-phosphorylatable mutant Twist1/S42A and a phospho-mimicking mutant Twist1/S42D were expressed in 4T1 cells in which the endogenous Twist1 was depleted.
We wanted to use microarray analysis to evaluate those genes that are differentially regulated by Twist1 variants.

overall_design: All cell lines were grown to 70% confluency and total RNA was isolated with Qiagen kit. Each sample was prepared as triplicates. Parental 4T1 cells were used as control.

first: David

last: Restuccia


title: Blood biomarkers of pancreatic cancer associated diabetes identified by peripheral blood-based gene expression profiles

city: Hangzhou

first: Yulian

last: Wu

state: Zhejiang

address: 88 Jiefang Road

department: surgey

country: China

institute: Second Affiliated Hospital, School of Medicine, Zhejiang University

summary: The prognosis of pancreatic cancer is still very poor, how to detect pancreatic cancer from high-risk group in an early stage is essential for improving its long-time survival. Therefore, the purpose of this study was to explore specific biomarkers that can differentiate pancreatic cancer-associated diabetes from type-2 diabetes for the early detection of pancreatic cancer. In the current study, we used global gene transcription analysis with affymetrix gene chip to identify genes specifically expressed in pancreatic cancer-associated diabetes mellitus from peripheral blood samples in stead of from tissue samples.

overall_design: 32 peripheral blood samples were collected for microarray experiments to find differentially expressed genes specific for pancreatic cancer associated diabetes, which included 8 patients diagnosed as pancreatic cancer with diabetes, 8 patients of pancreatic cancer without diabetes, 8 patients with diabetes mellitus>5years and 8 healthy controls. the comparision was done between pancreatic cancer with diabetes vs normal, pancreatic cancer vs normal and diabetes vs normal to identify a small group of genes that differently expressed in the pancreatic cancer with diabetes group.


title: Gene expression profile of regulatory T cells (Tregs) isolated from visceral adipose tissue and lymph nodes of mice sufficient and deficient of Pparg expression in Tregs

first: CBDM

last: Lab

summary: We identified Pparg as a major orchestrator of the phenotype of adipose-tissue resident regulatory T cells (VAT Tregs). To establish the role of Pparg in shaping the VAT Tregs gene profile and cell dynamics, Tregs from lymph nodes and visceral adipose tissue of mice sufficient and deficient of Pparg expression in Tregs were double sorted for microarray analysis.

overall_design: All gene expression profiles were obtained from highly purified (double-sorted) T cell populations sorted by flow cytometry. To reduce variability, cells from multiple mice were pooled. Triplicates were generated for all groups. Raw data were preprocessed with the RMA algorithm in GenePattern and averaged expression values were used for analysis.

first: Daniela

last: Cipolletta

first: Diane

last: Mathis

first: Christophe

last: Benoist


title: Expression Data from HNF1b-knockdown RMG2-ovarian cancer cells

city: Kyoto

first: TAKAKO

last: OKAMOTO

address: 54 Kawahara-cho, shogoin,sakyo-ku,

institute: Kyoto University

summary: Ovarian clear cell carcinoma (OCCC) is a morphologically and biologically distinct subtype of ovarian carcinomas. We previously reported a gene expression profile characteristic of OCCC (OCCC signature), which contains hepatocyte nuclear facter-1b ( HNF-1b). To elucidate the biological role of HNF-1b in OCCC, we performed the suppression of the HNF-1b expression in human ovarian cancer cell line RMG2 using short hairpin RNA. We are now evaluating the functional effect using these cells.

overall_design: Affimetrix Human Genome U133A plus 2.0 chips was conducted for HNF1b knockdown and non-silencing cells (five replicates each for RMG2-HNF1b-sh1 and RMG2-HNF1b-sh2, ten replicates for the RMG2-control). All specimens were arrayed in parallel and used for RMA normalization.

first: Takako

last: Okamoto

first: Noriomi

last: Matsumura

first: Ken

last: Yamaguchi

first: Seiiichi

last: Mori

first: Masaki

last: Mandai

first: Konishi

last: Ikuo


title: Silencing of AEBP1 in U87MG glial cells and Chip-chIP with AEBP1 antibody

status: Public on Apr 30 2012

city: Bangalore

first: Jayashree

last: Ladha

address: Jakkur

country: India

institute: JNCASR

summary:
AEBP1 has been identified as a transcriptional repressor playing a
significant role in adipogenesis. Recently, we have found that AEBP1 is
specifically upregulated in primary glioblastoma. We have used gene
silencing to identify genes perturbed upon AEBP1 downregulation and
ChIP-chip technique to identify its genomic targets of binding and
regulation to understand the un-annotated/undescribed role of this
transcription factor in gliomagenesis.

overall_design:
Cells either mock silenced or silenced using siRNA against AEBP1 were harvested at 46hrs post transfection. Gene expression was profiled for control and AEBP1 silenced cells.

comparison of AEBP1/Rabbit IgG/ Glial cells

first: M

last: Rao


title: Comparison of gene expression profiles in diploid and transformed tetraploid MEF cells

city: Duarte

first: Xiwei

address: 1500 E. Duarte Rd.

department: Computational and Quantitative Medicine

institute: City of Hope National Medical Center

summary:
We propose that abnormal DNA content in tetraploid cells can alter the gene expression profile, contributing to the cellular transformation. To test this hypothesis, we employ mRNA microarray to compare the gene expression profile in transformed tetraploid cells with that in the parent diploid cells.

Keywords: gene expression profile determination

overall_design: Total RNA were extracted from diploid or tetraploid cells (n = 3 for each cell lines. mRNA microarray hybridization was conducted. Data were collected and analyzed.

first: Li

last: Zheng

first: Mian

last: Zhou

first: Huifang

last: Dai

first: Binghui

last: Shen


title: A chemical genetic approach identifies piperazine antipsychotics as promoters of CNS neurite growth on inhibitory substrates.

city: Miami

first: Andrea

last: Johnstone

state: FL

address: 1095 NW 14th Terrace

department: The Miami Project to Cure Paralysis

institute: University of Miami Miller School of Medicine

summary: Injury to the central nervous system (CNS) may result in lifelong loss of function due, in part, to the regenerative failure of CNS neurons.  Major barriers to regeneration faced by injured CNS neurons include inhibitory proteins derived from myelin and the astroglial scar.  Previously, we described the identification of a novel compound, F05, which promotes neurite growth from neurons challenged with inhibitory substrates in vitro, and promotes axonal regeneration in vivo (Usher et al., 2010).  To identify additional regeneration promoting compounds, we used the microarray derived gene expression signature of F05 to query the Broad Institute Connectivity Map, a database of gene expression profiles for cells treated with >1,300 compounds.  Unexpectedly, F05 induced changes in gene expression remarkably similar to those seen with a group of piperazine phenothiazine antipsychotics (PhAPs).  We found that, in contrast to antipsychotics of other structural classes, PhAPs were able to promote neurite growth of CNS neurons cultured on two different glial-derived inhibitory substrates, but did not promote growth on a permissive substrate.  Pharmacological studies suggest that the ability of PhAPs to promote growth depends on antagonism of calmodulin signaling, but not on dopamine receptor antagonism.  Our findings shed light on mechanisms underlying neurite-inhibitory signaling, and suggest a potential pathway for development of novel treatments for CNS injury.

overall_design: 3 Biological Replicates of Vehicle Treated (0.05% DMSO) + 3 Biological Replicates of F05 Treated (5 μM)

first: Gillian

last: Reierson

first: Robin

middle: P

last: Smith

first: Jeffrey

last: Goldberg

first: Vance

last: Lemmon

first: John

last: Bixby


title: Mice lacking circadian transcriptional activator Clock exhibit dramatic changes in renal excretory rhythms

city: Lausanne

first: Sylvain

last: Pradervand

address: Genopode

department: CIG

institute: UNI Lausanne

summary: Recent evidence suggest that the circadian timing system plays an important role in the control of renal function and maintaining blood pressure. Here, we analyzed circadian rhythms of urinary excretion of sodium and potassium in wild-type mice and mice lacking circadian transcriptional activator clock. Analysis of urines collected at hourly intervals over a 24-hour period revealed dramatic changes in rhythms of sodium and potassium excretion in clock(-/-) mice. In parallel, significant differences in circadian pattern of plasma aldosterone levels, but not in the 24-hour mean aldosterone levels, were observed. Microarray-based profiling of renal transcriptomes demonstrated that clock(-/-) mice exhibit dysregulation in multiple mechanisms involved in maintaining sodium and potassium balance by the kidney. The most significant changes were detected in the expression levels of several key enzymes (Cyp4a14, Cyp4a12a and Cyp4a12b) required for the conversion of arachidonic acid to 20-hydroxyeicosatetraenoic acid (20-HETE), a powerful regulator of renal sodium and potassium excretion, renal vascular tone and blood pressure. The 20-HETE levels measured in kidney microsomes of wild-type mice followed a circadian-like temporal pattern. In clock(-/-) mice, the acrophase of this rhythm was shifted by 8 hours and the 24-hour mean levels of 20-HETE were significantly decreased. These results demonstrate that circadian rhythms of urine electrolyte excretion are largely dependent on the circadian clock activity and indicate that circadian oscillations in renal 20-HETE content could be an important mechanism of blood pressure regulation.

overall_design: We examined the temporal profiles of gene expression in mouse whole kidney. Animals were sacrificed for microdissection every 4 hours, i.e. at ZT0, ZT4, ZT8, ZT12, ZT16 and ZT20 (ZT – Zeitgeber (circadian) time, indicates time of light-on as ZT0 and time of light-off as ZT12). The microarray hybridization was performed in duplicates on pools of RNA composed of equivalent amounts of RNA prepared from teo or three animals at each ZT time-point.

first: Svetlana

last: Nikolaeva

first: Gabriel

last: Centeno

first: Vlasta

last: Zavadova

first: Natsuko

last: Tokonami

first: Marc

last: Maillard

first: Olivier

last: Bonny

first: Dmitri

last: Firsov


title: Epigenome analysis of normal and DDX20 knockdown HepG2 cells

status: Public on Apr 27 2012

city: Tokyo

first: Motoyuki

last: Otsuka

address: 7-3-1 Hongo Bunkyo-ku

institute: The University of Tokyo

summary: MicroRNAs (miRNAs) are small RNAs that regulate the expression of specific target genes. While deregulated miRNA expression levels have been detected in many tumors, whether miRNA functional impairment is also involved in carcinogenesis remains unknown. We investigated whether deregulation of miRNA machinery components and subsequent functional impairment of miRNAs are involved in hepatocarcinogenesis. Among miRNA-containing ribonucleoprotein complex components, reduced expression of DDX20 was frequently observed in human hepatocellular carcinomas, in which enhanced NF-kB activity is closely linked to carcinogenesis. Because DDX20 normally suppresses NF-kB activity by preferentially regulating the function of the NF-kB suppressing miRNA-140, we hypothesized that impairment of miRNA-140 function may be involved in hepatocarcinogenesis. Dnmt1 was identified as a direct target of miRNA-140, and increased Dnmt1 expression in DDX20-deficient cells hypermethylated the promoters of metallothionein genes, resulting in decreased metallothionein expression leading to enhanced NF-kB activity and hepatocarcinogenesis. MiRNA-140 knockout mice were prone to hepatocarcinogenesis and showed phenomena similar to those of DDX20 deficiency, suggesting that miRNA-140 plays a central role in DDX20 deficiency–related pathogenesis. Conclusion: These results indicate that miRNA-140 acts as a liver tumor suppressor, and that impairment of miRNA-140 function due to a deficiency of DDX20, a miRNA machinery component, could lead to hepatocarcinogenesis.

overall_design: Genome wide DNA methylation profiling of control and DDX20-knockdown HepG2 cells. Bisulphite converted DNA from the 2 samples were hybridised to the Illumina HumanMethylation450 BeadChip.

first: Akemi

last: Takata


title: Gene expression data of human primary keratinocytes with control, EXOSC9 or EXOSC9+GRHL3 knockdown

status: Public on Apr 28 2012

first: Devendra

last: Mistry

address: 9500 Gilman Drive MC#0869

department: Medicine

institute: University of California-San Diego

summary:
Stem and progenitor cells maintain the tissue they reside in for life by regulating the balance between proliferation and differentiation. How this is done is not well understood. Here, we report that the human exosome maintains progenitor cell function. The expression of several subunits of the exosome were found to be enriched in epidermal progenitor cells, which were required to retain proliferative capacity and to prevent premature differentiation. Loss of PM/Scl-75 also known as EXOSC9, a key subunit of the exosome complex, resulted in loss of cells from the progenitor cell compartment, premature differentiation, and loss of epidermal tissue. EXOSC9 promotes self-renewal and prevents premature differentiation by maintaining transcript levels of a transcription factor necessary for epidermal differentiation, GRHL3, at low levels through mRNA degradation. These data demonstrate that control of differentiation specific transcription factors through mRNA degradation is required for progenitor cell maintenance in mammalian tissue.
Refer to publication (Mistry et. Cell Stem Cell 2012) for more detail

overall_design: For gene expression profiling, cultured primary human keratinocytes were knocked down for EXOSC9, EXOSC9 and GRHL3, or control. RNA was harvested from the cells 5 days after knockdown. Microarray analysis using Affymetrix HG-U133 2.0 plus arrays was performed on duplicate samples. Significantly changed genes were identified as previously described(Sen et al., 2010).

first: Yifang

last: Chen

first: George

last: Sen


title: A Systems Biology Approach Reveals Common Metastatic Pathways in Osteosarcoma

status: Public on Apr 25 2012

city: Houston

first: Alexander

last: Yu

state: TX

department: Pediatrics

institute: Baylor College of Medicine

summary:
Background
Osteosarcoma (OS) is the most common malignant bone tumor in children and adolescents. The survival rate of patients with metastatic disease remains very dismal.  Nevertheless, metastasis is a complex process and a single-level analysis is not likely to identify its key biological determinants.  In this study, we used a systems biology approach to identify common metastatic pathways that are jointly supported by both mRNA and protein expression data in two distinct human metastatic OS models.

Results
mRNA expression microarray and N-linked glycoproteomic analyses were performed on two commonly used isogenic pairs of human metastatic OS cell lines, namely HOS/143B and SaOS-2/LM7.  Pathway analysis of the differentially regulated genes and glycoproteins separately revealed pathways associated to metastasis including cell cycle regulation, immune response, and epithelial-to-mesenchymal-transition.  However, no common significant pathway was found at both genomic and proteomic levels between the two metastatic models, suggesting a very different biological nature of the cell lines.  To address this issue, we used a topological significance analysis based on a “shortest path” algorithm to identify topological nodes, which uncovered additional biological information with respect to the genomic and glycoproteomic profiles but remained hidden from the direct analyses.  Pathway analysis of the significant topological nodes revealed a striking concordance between the models and identified significant common pathways, including “Cytoskeleton remodeling/TGF/WNT”, “Cytoskeleton remodeling/Cytoskeleton remodeling”, and “Cell adhesion/Chemokines and adhesion”.  Of these, the “Cytoskeleton remodeling/TGF/WNT” was the top ranked common pathway from the topological analysis of the genomic and proteomic profiles in the two metastatic models.  The up-regulation of proteins in the “Cytoskeleton remodeling/TGF/WNT” pathway in the SaOS-2/LM7 and HOS/143B models was further validated using an orthogonal Reverse Phase Protein Array platform.

Conclusions
In this study, we used a systems biology approach by integrating genomic and proteomic data to identify key and common metastatic mechanisms in OS.  The use of the topological analysis revealed hidden biological pathways that are known to play critical roles in metastasis.  Wnt signaling has been previously implicated in OS and other tumors, and inhibitors of Wnt signaling pathways are available for clinical testing.  Further characterization of this common pathway and other topological pathways identified from this study may lead to a novel therapeutic strategy for the treatment of metastatic OS.

overall_design: In this study we analyzed two human metastatic OS cell lines and their parental non-metastatic lines. The two human metastatic OS cell line models were HOS/143B and SaOS-2/LM7.  The HOS cell line, originally known as M.T. and later as TE-85, was derived from an OS of a 13 year-old girl.  The 143B metastatic subline was generated from HOS by a Ki-RAS oncogene transformation [Rhim, J.S., et al., Characterization of human cells transformed in vitro by N-methyl-N'-nitro-N-nitrosoguanidine. Int J Cancer, 1977. 19(4): p. 505-10.].  The SaOS-2 cell was derived from an OS of an 11 year-old girl, and its metastatic subline LM7, was developed by multiple in vivo selection of SaOS-2 cells in mice with pulmonary metastases [ Jia, S.F., L.L. Worth, and E.S. Kleinerman, A nude mouse model of human osteosarcoma lung metastases for evaluating new therapeutic strategies. Clin Exp Metastasis, 1999. 17(6): p. 501-6.].  No replicates were included.

first: Ricardo

middle: J

last: Flores

first: Yiting

last: Li

first: Jianhe

last: Shen

first: Pulivarthi

last: Rao

first: Serrine

last: Lau

first: Marina

last: Vannucci

first: Ching

first: Tsz-Kwong

last: Man


title: Expression Data of Treg and Tconv Cells from FoxP3-GFP Chimeric and FoxP3-ires-GFP B6 and NOD Mice

city: Boston

first: CBDM

last: Lab

address: 77 Avenue Louis Pasteur

institute: Harvard Medical School

summary: The aim of this study was to quantify the impact of chimeric Foxp3-GFP protein on the Treg cell transcriptional program.

overall_design: Duplicate samples of Tconv (CD3+CD4+GFP-) and Treg (CD3+CD4+GFP+) splenocytes were double-sorted to achieve > 99.0% purity, from 6 weeks old male Foxp3-Fusion-GFP and Foxp3-ires-GFP mice of both B6 and NOD backgrounds. Following cell sorting into Trizol, RNA was purified, labeled and hybridized to Affymetrix arrays.

first: Jaime

last: Darce

first: Diane

last: Mathis

first: Christophe

last: Benoist


title: Gene expression data from obatoclax-treated SEM-K2 and RS4:11 cell lines

status: Public on Apr 24 2012

city: Philadelphia

first: Li-San

last: Wang

state: PA

address: 1424 Blockley Hall, 423 Guardian Drive

department: Pathology and Laboratory Medicine

institute: University of Pennsylvania

summary: Effects of the pan-anti-apoptotic BCL-2 family small molecule inhibitor, obatoclax mesylate (GeminX Pharmaceuticals), on gene expression were evaluated by microarray analysis in order to gain insights into the killing mechanism by this compound in two human MLL-AF4 cell lines. The results of the gene expression profiling substantiated other lines of evidence derived from genetic and chemical cell death pathway inhibition, Western blot analysis, flow cytometric apoptosis assays, and electron microscopic analyses, showing triple apoptosis, autophagy, and necroptosis death pathway activation by this agent. The results also demonstrated modulation of a number of novel targets of obatoclax encoding various cell death factors at the gene expression level.

overall_design: SEM-K2 and RS4:11 cells were treated with obatoclax or vehicle for 6 hours.  After treatment, total RNA was extracted and cRNA was prepared and hybridized with Affymetrix U133 Plus 2 microarrays. There were a total of 3 treatments per cell line (vehicle, obatoclax at the 72 h EC50, and obatoclax 3x 72 h EC50) and 2 biologic replicates per condition.

first: Alena

middle: Y

last: Edwards

first: Karen

last: Urtishak

first: Kajia

last: Cao

first: I-Ming

first: Susan

last: Atlas

first: Cheryl

last: Willman

first: Carolyn

last: Felix


title: Effect of CTHRC1 knockdown on gene expression of HCCLM3 cells

status: Public on Apr 23 2012

city: Shanghai

first: zhigang

last: zhang

address: No. 800, Dong Chuan Road

department: Shanghai cancer Institute

institute: Shanghai Jiaotong University

summary: Collagen triple helix repeat containing 1 (CTHRC1) has been found to be up-regulated in many human solid tumors. In this study, we investigated the changes of gene expression by comparing CTHRC1-siRNA and Scramble-siRNA control in hepatocellular carcinoma cell line HCCLM3, which has high expression levels of CTHRC1.

overall_design: Differential gene expression was assessed by Affymetrix microarray experiments for 2 samples: CTHRC1-siRNA-treated HCCLM3 cells and Scramble-siRNA-treated HCCLM3 cells.

first: Bing

last: Yu

first: Yun

last: Deng

first: Xiaomei

last: Yang

first: Zhigang

last: Zhang

first: Wenxin

last: Qin


title: Compare gene expression profiles of mouse iNSC, WT-NSC, and MEF

status: Public on Jun 07 2012

city: San Francisco

first: Yadong

last: Huang

address: 1650 Owens Street

institute: Gladstone Institute of Neurological Disease

summary:
The iNSC cells are two clones generated from the same MEF line.  Therefore, we conducted one analysis that compared the two clonal lines and a separate analysis that compared iNSC vs. NSC, iNSC vs. MEF, and NSC vs. MEF.  Both were single factor ANOVAs, the first compared two
groups (the iNSC lines) and the second had three groups.  For the second analysis, we then used linear contrasts to extract the information about differences between all pairs (e.g. iNSC vs. NSC). Looking at the iNSC lines, the correlations between samples from different clonal lines are as high as the correlations between samples from within a clonal line.  Given this, we think that the analysis that combines all 6 of them to compare against the other cell types is appropriate.

overall_design: Array Platform: Affymetrix Mouse Gene 1.0 ST    Samples: A total of 12 arrays    array# filename genotype  1 01.iNSC1.1.CEL iNSC  2 02.iNSC1.2.CEL iNSC  3 03.iNSC1.3.CEL iNSC  4 04.iNSC2.1.CEL iNSC  5 05.iNSC2.2.CEL iNSC  6 06.iNSC2.3.CEL iNSC  7 07.WT.NSC.1.CEL NSC   8 08.WT.NSC.2.CEL NSC   9 09.WT.NSC.3.CEL NSC   10 10.WT.MEFs.1.CEL MEF   11 11.WT.MEFs.3.CEL MEF   12 12.WT.MEFs.5.CEL MEF

last: Ring


title: Expression data from Arid4b knockdown cell lines

city: Bethesda

first: Scott

last: Winter

address: 37 Convent Dr., Bldg 37 Rm 5046

department: CCR

institute: NCI

summary:
High Arid4b promotes mammary tumor growth and metastasis in mouse model systems, and is associated with poor metastasis-free survival in human breast cancer patients. Through shRNA-mediated knockdown, we demonstrated that loss of Arid4b significantly inhibits the ability of mouse breast cancer cells to metastasize to the lungs.
We performed microarray expression and subsequent network analysis to identify genes diferentially regulated as a consequence of Arid4b knockdown.

overall_design: The highly metastatic mouse breast cancer cell line 6DT1 was transduced with lentiviral shRNAs targeting Arid4b (RMM4534-NM_194262, Open Biosystems) or scrambled control in the same pLKO.1 vector backbone. Stably transduced cells were selected with puromycin, then total RNA was isolated from pooled clones.

first: Kent

last: Hunter


title: Expression data from ethanol-tolerant E. coli strain and wild type under ethanol stress

city: Beijing

first: Tingjian

last: Chen

address: One Tsinghua Garden Road

department: Department of Chemical Engineering

institute: Tsinghua University

summary:
Cellular tolerance toward ethanol is a complex phenotype involved many genes, and hard to be improved by manipulating individual genes. We previously established exogenous global regulator IrrE mutants that confer Escherichia coli with significantly enhanced tolerance to stresses, including ethanol.
In order to elucidate the mechanism for enhancement of ethanol tolerance in the mutants and to identify new genes and pathways that can be possible targets for engineering of ethanol tolerance, we carried out comparative transcriptomic and proteomic analyses with the representative strains E1 and E0 (harboring the ethanol-tolerant mutant E1 of IrrE and the wild type IrrE, respectively). The data from transcriptome analyses were deposited here.

overall_design: Cells of ethanol-tolerant mutant E1 and wild-type strain E0 were grown in 1.5% ethanol, and the samples for both of these two strains were prepared in triplicate with biological replicates

first: Zhanglin

last: Lin


title: Effect of ablation of Sfrp5 on gene expression in gonadal white adipose tissue

city: Ann Arbor

first: Ormond

last: MacDougald

state: MI

address: 6458 Brehm Center, 1000 Wall Street

department: Molecular and Integrative Physiology

institute: University of Michigan

summary: We identified secreted frizzled-related protein-5 (Sfrp5) as a transcript that is upregulated during adipocyte differentiation and that is increased in white adipose tissue (WAT) of obese mice, compared to lean mice. To investigate the function of sFRP5 in adipose tissue biology, we studied sFRP5Q27stop mice, in which ENU mutagenesis was used to create a premature stop codon at Gln27, thereby creating a likely null allele.

overall_design: Male wild-type or Sfrp5 KO (Q27Stop) mice were fed a high-fat diet from the ages of four weeks to twelve weeks. At twelve weeks of age, mice were euthanized. Total RNA was then isolated from gonadal WAT and RNA was analyzed by Affymetrix microarrays. Seven wild-type and eight Sfrp5 KO mice were used.

first: Tyler

last: Prestwich

first: Hiroyuki

last: Mori


title: Syntenin-1 is expressed in uveal melanoma and correlates with metastatic progression

status: Public on Apr 18 2012

city: Genova

first: Valentina

last: Mirisola

address: Largo Benzi 10

department: Functiona Genomics

country: Italy

institute: National Cancer Institute

summary: Uveal melanoma is an aggressive cancer that metastasizes to the liver in about half of patients, being at that time almost always fatal. Identification of patients at high risk of metastases may provide indication for a frequent follow-up for early detection of metastases and treatment. The analysis of the gene expression profiling of primary human uveal melanomas showed high expression of SDCBP (encoding for syndecan-binding protein-1 or syntenin-1), which appeared higher in patients with recurrence, whereas expression of syndecans was lower and unrelated to progression. Moreover,  we found that high expression of SDCBP gene was related to metastatic progression in two  additional independent dataset of uveal melanoma patients. More importantly, immunohistochemistry showed that high expression of syntenin-1 protein in primary tumours was significantly related to metastatic recurrence in our cohort of patients. Syntenin-1 expression was confirmed by RT-PCR, immunofluorescence and immunohistochemistry in cultured uveal melanoma cells or primary tumours. A pseudo-metastatic model of uveal melanoma to the liver was developed in NOD/SCID/IL2R null mice and the study of syntenin-1 expression in primary and metastatic lesions revealed higher syntenin-1 expression in metastases. The inhibition of SDCBP expression by siRNA impaired the ability of uveal melanoma cells to migrate in a wound–healing assay. These results suggest that SDCBP is involved in uveal melanoma progression and that it represents a candidate molecular marker of metastases and a potential therapeutic target.

overall_design: Gene expression profiles of 29 unique samples from uveal melanoma patients were measured.

first: Rosaria

last: Gangemi

first: Gaia

last: Barisione

first: Antonella

last: Brizzolara

first: Francesco

last: Lanza

first: Carlo

last: Mosci

first: Sandra

last: Salvi

first: Marina

last: Gualco

first: Mauro

last: Truini

first: Giovanna

last: Angelini

first: Simona

last: Boccardo

first: Michele

last: Cilli

first: Irma

last: Airoldi

first: Paola

last: Queirolo

first: Matrine

last: Jager

first: Antonio

last: Daga

first: Ulrich

last: Pfeffer

first: Silvano

last: Ferrini


title: IL-12 induces myeloid cells in situ to cross-present antigen

city: Doha

middle: Maria

last: Marincola

address: Al Nasr Tower, AL Corniche Street, PO Box 26999

country: Qatar

institute: Sidra Medical and Research Center

summary: Myeloid-derived cells comprising the tumor stroma represent a heterogeneous population of cells critical to the structure, function and growth of established cancers. We have recently found that engineering tumor-specific CD8+ T cells to secrete IL-12 (IL-12TD) can lead to striking improvements in T-cell activity against established melanomas in murine models. Surprisingly, IL-12-dependent enhancement of CD8+ T-cell anti-tumor function did not occur through direct ligation of receptors on lymphocytes or NK cells. Instead, IL-12 sensitized host bone marrow-derived tumor-stromal cells, partly through interferon-gamma, to indirectly enhance the effects of adoptively-transferred T cells. Direct presentation of antigen by tumor was not necessary, but MHC class I expression on endogenous cells was essential for IL-12 mediated anti-tumor enhancements. Upon successful treatment with IL-12TD cells, we observed the selective elimination of tumor-infiltrating CD11b+ F4/80+ macrophages, CD11b+/ClassII+/CD11c+ dendritic cells and CD11b+/Ly6C+/Ly6G- but not CD11b+/Ly6C+/Ly6G+ myeloid-derived suppressor cells within regressing lesions. These results are consistent with a model whereby IL-12 triggers the maturation of myeloid-derived cells into competent antigen cross-presenting cells. Licensed recognition of these antigens by effector T cells may in turn trigger the collapse of the tumor stroma and aid in the regression of large vascularized lesions.

overall_design: Samples were collected at 3 days and 7 days from tumors treated in-vivo with no treatment, Mock pmel-1 CD8+ cell treatment, or IL-12 pmel-1 CD8+ cell treatment. There were 4 biological replicates of each sample type. There were a total of 24 samples.


title: Global gene expression change in the cerebellum of Niemann-Pick disease type C mice with deletion of Ccl3 or Purkinje neuron-specific NPC1 rescue

status: Public on Apr 17 2012

city: Stanford

first: Manuel

last: Lopez

address: Clark Center W200 318 Campus Dr.

institute: Stanford University

summary:
Macrophage inflammatory protein 1alpha/CCL3 protein is a known pro-inflammatory cytokine that can mediate chemotaxis of monocytes and promote cell degranulation. Ccl3 gene expression is elevated in the CNS and visceral tissue of many lysosomal storage disorders. The deletion of Ccl3 in a mouse model of Sandhoff disease was reported to result in reduced monocyte-associated pathology in the brain, delayed neurodegeneration, and prolonged health. However, deletion of Ccl3 in a mouse model of Niemann-Pick C disease was dentrimental or neutral instead of beneficial. Prevention of neuronal loss was instead mediated by providing NPC1 to neurons.
We used microarrays to detail the global change in gene expression of the cerebellum in Niemann-Pick C disease animals, Niemann-Pick C disease animals with Ccl3 gene deletion, and Niemann-Pick C disease animals with Purkinje neuron-specific NPC1-YFP rescue.

overall_design: To identify the top ~50 genes elevated in NPC disease Npc1-/- (NPC) and Npc1+/- (WT) mice were compared at age P50; To profile changes in gene expression as a result of Ccl3 gene deletion Ccl3-/-;Npc1-/- mice were compared against Npc1-/- mice across various ages; To profile changes in gene expression as a result of Purkinje neuron-sepcific NPC1 rescue P;N;Npc1-/- mice were compared against Npc1-/- mice across various ages.

middle: E

first: Matthew

last: Scott


title: Expression data of CD44loCD8+ T cells from sanroque versus wild-type mice

city: Canberra

first: Pheh Ping

last: Chang

state: ACT

address: The Australian National University

department: Pathogens and Immunity

country: Australia

institute: The John Curtin School of Medical Research

summary: We used microarrays to detect the primary changes caused by the 'san' mutation in Roquin gene by comparing the gene expression profiles of naive (CD44lo) CD8+ T cell population.

overall_design: Sorted CD44loCD8+ T cells of age-matched sanroque (Roquinsan/san) and wild-type (Roquin+/+) mice in C57BL/6 background were subjected to RNA extraction and hybridization on Affymetrix microarrays.

first: Pheh

first: Carola

last: Vinuesa


title: Comparison of diploid and transformed tetraploid MEF cells: gene expression and DNA methylation profiling

first: Xiwei

last: Wu

institute: City of Hope National Medical Center

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

overall_design: Refer to individual Series


title: Retinoic acid pathway activity in Wilms tumors and characterization of biological responses in vitro

status: Public on Apr 21 2012

city: Wuerzburg

first: Susanne

middle: Elma

last: Kneitz

address: Biozentrum, Am Hubland

department: Physiologigcal Chemistry

institute: University of Wuerzburg

summary: Wilms tumor (WT) is one of the most common malignancies in childhood. With current therapy protocols up to 90 % of patients can be cured, but there is still a need to improve therapy for patients with aggressive WT and to reduce treatment intensity where possible. Prior data suggested deregulation of the retinoic acid (RA) pathway in high-risk WT. This could be validated in a large independent tumor set. Reduced RA pathway activity and MYCN overexpression were found in high risk tumors as opposed to tumors with low/intermediate risk, suggesting a beneficial impact of RA on advanced WT. To investigate the possible mode of action of retinoids as a novel therapeutic agent we treated primary tumor cell cultures with all-trans-RA (ATRA), 9cis-RA, fenretinide and combinations of retinoids and a histone deacetylase (HDAC) inhibitor. Genes deregulated in high risk tumors showed opposite changes upon treatment suggesting a positive effect of retinoids. 6/7 primary cultures tested reduced proliferation, irrespective of prior RA signaling levels. The only variant culture was derived from mesoblastic nephroma, a distinct childhood kidney neoplasm. Retinoid / HDAC inhibitor combinations provided no synergistic effect. ATRA and 9cis-RA induced morphological changes suggestive of differentiation, while fenretinide induced apoptosis in several cultures tested. Microarray analysis of ATRA treated WT cells revealed differential expression of many genes involved in extracellular matrix formation and osteogenic, neuronal or muscle differentiation. Although some of the effects appear to be reversible, these findings provide further evidence of a potential utility of retinoids in Wilms tumor treatment.

overall_design: total samples analysed are 2

first: Jenny

last: Wegert

first: Sabrina

last: Bausenwein

first: Sabine

last: Roth

first: Norbert

last: Graf

first: Eva

last: Geissinger

first: Manfred

last: Gessler


title: Discovery of genes regulated by the metastasis suppressor gene, RhoGDI2

status: Public on Apr 15 2012

city: Charlottesville

first: Steven

last: Smith

state: VA

department: Urology

institute: University of Virginia

summary:
A number of studies find that metastasis suppressor proteins, including RhoGDI2, may function in part though controlling expression of genes regulating metastasis (reviewed in Smith and Theodorescu, Nature Reviews Cancer, 2009, PMID: 19242414). To uncover systematically gene expression patterns dependent on RhoGDI2 expression, we profiled gene expression in stably transfected control (GFP empty vector) UM-UC-3 bladder carcinoma cells (which have lost endogenous expression of RhoGDI2, as occurs commonly in the progression of bladder cancer PMID: 15173088), as well as stably transfected GFP-tagged RhoGDI2 expressing UM-UC-3 cells.

References:

Moissoglu K, McRoberts KS, Meier JA, Theodorescu D et al. Rho GDP dissociation inhibitor 2 suppresses metastasis via unconventional regulation of RhoGTPases. Cancer Res 2009 Apr 1;69(7):2838-44. PMID: 19276387

Wu Y, Moissoglu K, Wang H, Wang X et al. Src phosphorylation of RhoGDI2 regulates its metastasis suppressor function. Proc Natl Acad Sci U S A 2009 Apr 7;106(14):5807-12. PMID: 19321744

Smith SC, Theodorescu D. Learning therapeutic lessons from metastasis suppressor proteins. Nat Rev Cancer 2009 Apr;9(4):253-64. PMID: 19242414

Theodorescu D, Sapinoso LM, Conaway MR, Oxford G et al. Reduced expression of metastasis suppressor RhoGDI2 is associated with decreased survival for patients with bladder cancer. Clin Cancer Res 2004 Jun 1;10(11):3800-6. PMID: 15173088

overall_design: Two paired biological replicates of GFP (control) and GFP-RhoGDI2 (experimental) UM-UC-3 cells were prepared at different times, isolated during log phase growth, and subjected to gene expression profiling using the Affymetrix HG-U133 Plus 2.0 oligonucleotide microarray platform.

first: Dan

last: Theodorescu


title: Expression data of the iPSCs derived from foreskin fibroblast cells of normal person and KS patient

status: Public on Apr 14 2012

first: Yu

last: Ma

address: 225 South Chongqing Road

institute: Institute of Health Sciences

summary:
Klinefelter’s Syndrome (KS) is one of the common chromosome aneuploidy diseases in males with unexplained physiological mechanism. iPSCs, are similar to ESCs in terms of indefinitive self-renewal and pluripotency, provided an alternative choice for modeling disease to facilitate the disease research in vitro.
We used microarray to detect the global reprogramming of KS and normal fibroblast cells to iPSCs. Also we used microarray to explore the possible molecular varieties between KS patient and normal person in the early development.

overall_design: Fibroblast cells from both normal person and KS patient were reprogrammed into iPSCs by ectopic expression of OCT4, SOX2, KLF4 and C-MYC. The expression profiles of normal and KS fibroblast cells, a line of normal iPSCs and two lines of KS iPSCs as well as a line of human ESCs were detected.

first: Ying

last: Jin


title: Expression data from LysMCre/Cre and KLF2∆/∆ (LysMCre/Cre: KLF2 FL/FL) primary peritoneal macrophages treated with LPS for 6hours

status: Public on Apr 16 2012

city: Cleveland

first: Patrick

last: Leahy

address: 2103 Cornell Rd

department: Cancer Center

institute: Case Western Res. U.

summary:
Gene expression profile of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages following 6 hours of LPS treatment.
We used microarrays to detail the global program of gene expression following LPS stimulation of  LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages. We identified distinct classes of  genes that were altered following LPS stimulation.

overall_design: We injected 3 pairs of LysMCre/Cre (n=3) and KLF2∆/∆ (n=3) mice with 2 ml of thioglycolate broth intraperitoneally.  After 72 hours of thioglycolate injection, total cell suspension from peritoneal cavity were collected. These cells were seeded on 100mm tissue culture plates. Cells were allowed to attach for 4 hours and unattached cells were removed by washing with cell culture medium. These cells were placed in humidified incubator for additional 24 hours before LPS treatment. LPS was diluted to final concentration of 100ng/ml in culture medium and this medium was placed on peritoneal macrophages derived from LysM Cre/Cre and KLF2∆/∆ mice for 6hours. Cells were lysed and total RNA was isolated and subjected to  hybridization on Affymetrix microarrays.

first: Ganapati

middle: H

last: Mahabeleshwar

first: Mukesh

middle: K

last: Jain


title: DNA microarrays (time course) in the iPS process treated with microRNA clusters

status: Public on Apr 13 2012

city: Guangzhou

first: Duanqing

last: Pei

state: Guangdong

address: Room 301, International Business Incubator, Guangzhou science park

department: Center for Molecular Medicine

institute: Guangzhou Institute of Biomedicine and Health, Chinese Academy of Sciences(GIBH.CAS)

summary:
Treatment with MicroRNA cluster B and C increase the iPS efficiency
We used microarrays to identify changes induced by MicroRNA clusters in the iPS process

overall_design: One group were MEFs infected with SKO factors, plus MicroRNA cluster B, C or control blank virus. The other group were MEFs infected with MicroRNA cluster B, C or control blank virus only.TRIZOL cell lysates were prepared at D4 and D8.

first: Baojian

last: Liao

first: Wenzhi

last: He

first: Xichen

last: Bao


title: Gene expression changes in Ahnak knockout mice

city: Seoul

first: Seong

last: Je kyung

country: South Korea

institute: Seoul National University

summary: Transcriptional profiling of WAT comparing wild-type control with Ahnak Knockout mice fed regular chow and high fat diet

overall_design: We obtained white adipose tissue from mice fed regular chow and high fat diet for Affymetrix microarrays

first: Je

last: Seong

first: Sanghyuk

last: Lee


title: The effect of Crem absence on gene expression in mouse testis.

status: Public on Apr 11 2012

city: Ljubljana

first: Peter

last: Juvan

address: Zaloska 4

department: Institute of Biochemistry

country: Slovenia

institute: Faculty of Medicine, University of Ljubljana

summary:
CREM (cAMP responsive element modulator) together with CREB and ATF-1 belong to the CREB family of transcriptional factors, that respond to cyclic AMP signaling and bind to cAMP responsive element (CRE) sites in promoters of selected genes. CREM can produce isoforms that have either activating or repressing functions, depending on the transcription of specific exons. In testis, it is involved in the regulation of spermatogenesis.
In this dataset, we include the expression data obtained from wild-type and Crem knock-out mouse testis.

overall_design: 2 condition experiment: 2 strains (WT, Crem-/-). 5 biological replications per condition.

first: Rok

last: Košir

first: Martina

last: Perše

first: Gregor

last: Majdič

last: Fink

first: Damjana

last: Rozman


title: Gene expression timecourse from Dengue virus infected human endothelial cells

city: Stony Brook

first: Nadine

last: Dalrymple

state: NY

address: 126 Life Sciences Building

department: Molecular Genetics and Microbiology

institute: Stony Brook University

summary:
Dengue viruses cause two severe diseases that alter vascular fluid barrier functions, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). While the mechanisms that lead to vascular permeability are unknown, the endothelium plays a central role in regulating fluid and cellular efflux from capillaries. Thus, dysregulation of endothelial cells functions by dengue virus infection may contribute to pathogenesis and severe disease.
We used microarrays to investigate the effect of dengue virus infection on gene expression within primary human endothelial cells at various times post infection and identified numerous upregulated antiviral and immune response genes.

overall_design: Early passage primary endothelial cells (HUVECs) were mock infected (no virus) or infected with dengue virus and total RNA collected at 3 timepoints: 12, 24, and 48 hours post infection. Multiple timepoints were analyzed to identify changes in gene expression levels over time. Gene expression from both mock infected and dengue virus infected endothelial cells was evaluated to determine fold induction at each timepoint.

first: Erich

middle: R

last: Mackow


title: Assessment of Ex Vivo Prostaglandin pathway activation in HSCs

city: San Diego

first: Dave

last: Robbins

address: 3535 General Atomics Court Ste. 200

institute: Fate Therapeutics

summary: Transplantation with low numbers of hematopoietic stem cells (HSCs), found in many of the publically accessible cryopreserved umbilical cord blood (UCB) units, leads to delayed time to engraftment, high graft failure rates, and early mortality in many patients.  A chemical screen in zebrafish identified the prostaglandin compound, 16,16 dimethyl prostaglandin E2 (dmPGE2), to be a critical regulator of hematopoietic stem cell homeostasis.  We hypothesized that an ex vivo modulation with dmPGE2 prior to transplantation would lead to enhanced engraftment by increasing the “effective” dose of hematopoietic stem cells (HSCs) in cord blood.  A phase I trial of reduced-intensity double UCB transplantation was performed to evaluate safety, rates of engraftment and fractional chimerism of dmPGE2 enhanced UCB units.  To explore potential causes of the lack of enhanced efficacy in the first cohort, we characterized HSCs to determine whether the prostaglandin pathway was being activated under the ex vivo incubation conditions (4°C, 10µM dmPGE2, 60 minutes).  Incubation conditions were identified (37°C, 10µM dmPGE2, 120 minutes) that maximize the activation of the prostaglandin pathway by dmPGE2 in human CD34+ cells.

overall_design: Isolated human CD34+ from umbilical cord blood were incubated ex vivo in Stem Span media with 10uM 16,16-dmPGE2 or DMSO.  Two treatment conditions were evaluated (4 deg C for 1 hour, 37 deg C for 2 hours) with either 3 or 7 biological replicates at each condition.  Total RNA was isolated post incubation and analyzed on Affymetrix microarrays for pathway activation.

first: David


title: Ganglioside GD2 identifies Breast Cancer Stem Cells: Targeting GD3 Synthase Inhibits GD2 Expression and Tumor Growth

city: Houston

first: Kurt

last: Evans

address: 1515 Holcombe Blvd.

institute: MDACC

summary: We FACS sorted Ras-transformed human mammary epithelial cells (HMLER cells) into GD2+ and GD2- as well as CD44high/CD24low and  CD44low/Cd24highcells and comapred the four different population by array.

first: V

last: Battula

first: K


title: Expression data from uremic patients and 20 healthy controls (normals)

city: Vancouver

first: Bruce

middle: Maxwell

last: McManus

state: BC

address: 1081 Burrard Street

department: UBC James Hogg Research Centre

country: Canada

institute: PROOF Centre of Excellence

summary: Renal failure is characterized by important biological changes resulting in profound pleomorphic physiological effects termed “uremia”, whose molecular causation is not well understood. The data was used to study gene expression changes in uremia using whole genome microarray analysis of peripheral blood from subjects with end-stage renal failure (n=63) and healthy controls (n=20) to obtain insight into the molecular and biological causation of this syndrome.

overall_design: The study was conducted at the University of British Columbia and approved by the human ethics research board. A 3:1 case-control design was employed to compare gene expression in patients with chronic renal failure and healthy controls. Patients with stage 5 renal disease aged 18 to 75 years, who were clinically stable awaiting renal transplantation, were not receiving immunosuppressive medications, and who provided written informed consent were enrolled into the study. Patients were treated according to Canadian Guidelines for Chronic Kidney Disease (13). Normal controls of comparable age and gender to the patients who were screened to ensure freedom from known illness and medical therapy served as comparators.

first: Paul

last: Keown

middle: M

first: W

last: McMaster


title: DNA methylation regulates lineage-specifying genes in the human vascular system [methylation array].

status: Public on Apr 10 2012

city: Bergisch Gladbach

first: Silvia

last: Rueberg

address: Friedrich-Ebert-Str. 68

department: Genomic Services Department

institute: Miltenyi Biotec GmbH

summary: During embryonic development, the lymphatic system emerges by transdifferentiation from the cardinal vein. Although lymphatic and blood vasculature share a close molecular and developmental relationship, they display distinct features and functions. However, even after terminal differentiation, transitions between the two endothelial cell types have been reported. Since changes in phenotypic plasticity and cellular differentiation processes frequently involve epigenetic mechanisms, we wondered whether DNA methylation might play a role in regulating cell type-specific expression in endothelial cells. By analyzing global gene expression and methylation patterns of primary human dermal lymphatic and blood endothelial cells, we identified a highly significant set of genes, which were differentially methylated and expressed. Pathway analyses of the differentially methylated and upregulated genes in lymphatic endothelial cells revealed involvement in developmental and transdifferentiation processes. We further identified a set of novel genes, which might be implicated in regulating BEC-LEC plasticity and could serve as therapeutic targets and/or biomarkers in vascular diseases associated with alterations in the endothelial phenotype.

overall_design: Bisulphite converted DNA from the 16 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip v1.1

first: Simone

last: Broenneke

first: Bodo

last: Brueckner

first: Nils

last: Peters

first: Thomas

middle: C

last: Bosch

first: Franz

last: Stäb

first: Horst

last: Wenck

first: Sabine

last: Hagemann

first: Marc

last: Winnefeld


title: Expression data from Paneth cells isolated from mice on calorie restricted or ad libitum diet

status: Public on Apr 12 2012

city: Cambridge

first: Pekka

last: Katajisto

address: ) Cambridge center

institute: Whitehead Institute for Biomedical Research

summary:
Paneth cells recide in the intestinal crypt bottom and are part of the innate immunity and of the intestinal stem cell niche.
We used microarrays to detail the global changes in gene expression following reduced calorie intake.

overall_design: Mice were kept on ad libitum or calorie restricted (60% of calories of ad libitum) diets for 4-7 weeks and paneth cells were isolated using flowcytometry

first: Omer

last: Yilmaz

last: Sabatini


title: Expression profile of mutant U2AF35 transduced cells

city: Tokyo

first: Aiko

last: Sato-Otsubo

address: 7-3-1, Hongo, Bunkyo-ku

institute: University of Tokyo


title: DNA methylation regulates lineage-specifying genes in the human vascular system.


title: Gene expression in skeletal muscle of cancer patients before and after potentially curative surgery

city: Stirling

first: Iain

last: Gallagher

address: Room 4B133 Cottrell Building, University of Stirling, Airthrey Road

department: Faculty of Health Sciences and Sport

country: United Kingdom

institute: University of Stirling

summary: The mechanisms underlying muscle wasting in cancer patients remain poorly understood, and consequently there remains an unmet clinical need for new biomarkers and treatment strategies.

overall_design: Microarrays were used to examine the transcriptome in single biopsies from healthy controls (n=6) and in paired biopsies [pre-resection baseline (weight-loss 7%) and 8 month post-resection follow-up (disease-free /weight-stable for previous 2 months)] from quadriceps muscle of patients with upper gastrointestinal cancer (UGIC) (n=12).

first: James

middle: A

last: Timmons


title: The effect of sleep restriction on transcriptome rhythmicity in mice

city: Göttingen

first: Johanna

last: Barclay

address: Am Fassburg 11

institute: MPI-BPC

summary: Timed sleep restriction designed to mimic human shift work was performed over a 2 week period in mice. On the final day, tissues were collected at 6 hour intervals to exmaine the effects of sleep restriction on circadian gene expression.

overall_design: 3 mice were used at each time point, for both controls and sleep restricted groups.

middle: L

first: Jana

last: Husse

first: Brid

last: Bode

first: Nadine

last: Naujokat

first: Judit

last: Meyer-Kovac

first: Sebastian

last: Schmid

first: Hendrik

last: Lehnert

first: Henrik

last: Oster


title: Gene expression profiling of imatinib-treated and untreated human Hematopoetic progenitors expressing the ETV6-PDGFRB oncogene

city: Brussels

first: Jean-Baptiste

last: Demoulin

address: av Hippocrate 75, B1.74.05

department: de Duve Institute

country: Belgium

institute: Université catholique de Louvain

summary: In order to investigate the mechanism whereby TEL-PDGF-beta (ETV6-PDGFRB) interferes with human hematopoietic progenitors proliferation and differentiation, we analyzed the gene expression response downstream this oncogene. CD34+ cells infected with lentivirus coding for TEL-PDGFRb were cultured for 7 days in the absence of cytokines. Using Affymetrix microarrays, we compared gene expression in these cells and in cells treated for 4 h with low dose imatinib (Glivec), a potent PDGFR inhibitor, to switch off TEL-PDGFRb signaling.

overall_design: This experiment was performed in three biological replicates. In each replicate gene expression profiling from CD34+ HSCs expressing TEL-PDGFRb untreated with Glivec was compared to the corresoniding treated condition. Total RNA were extracted from transduced CD34+ cells using Trizol reagent (Invitrogen) and the RNeasy kit (QIAGEN).

first: Carmen

last: Montano-Almendras

first: Ahmed

last: Essaghir


title: Penetrance of biallelic SMARCAL1 mutations is associated with environmental and genetic disturbances of gene expression (1)

status: Public on Apr 05 2012

first: Alireza

last: Baradaran-Heravi

address: 950 West 28th Avenue, Room 218

department: Medical Genetics

institute: UBC

summary: Biallelic mutations of the DNA annealing helicase SMARCAL1 (SWI/SNF-related  matrix-associated actin-dependent regulator of chromatin, subfamily a-like 1) cause  Schimke immuno-osseous dysplasia (SIOD, MIM 242900), an incompletely penetrant  autosomal recessive disorder. Using human, Drosophila, and mouse models, we show  that the proteins encoded by SMARCAL1 orthologues localize to transcriptionally active  chromatin and modulate gene expression. We also show that similar to SIOD patients,  deficiency of the SMARCAL1 orthologues alone is insufficient to cause disease in fruit  flies and mice although such deficiency causes modest diffuse alterations in gene  expression. Rather, disease manifests when SMARCAL1 deficiency interacts with genetic  and environmental factors that further alter gene expression. We conclude that the  SMARCAL1 annealing helicase buffers fluctuations in gene expression and that  alterations in gene expression contribute to the penetrance of SIOD.

overall_design: For analysis of gene expression in primary cultured human dermal fibroblasts, 5.0 μg of total RNA from three biologically independent replicates was extracted from two SIOD (SD8 and SD60) and a control skin  fibroblast cell lines, labeled and hybridized to Affymetrix Human Genome U133 Plus 2.0 Arrays.

first: Cornelius

middle: F

last: Boerkoel


title: Gene expression analysis of bone biospies from nine patients with endogenous Cushings syndrome before and after  treatment

status: Public on Apr 08 2012

city: Oslo

first: Tove

last: Lekva

address: Sognsvannsveien 20

department: Section of Specialized Endocrinology and Institute for Internal Medicine

country: Norway

institute: OUS-HF, Rikshospitalet

summary: Glucose intolerance and diabetes mellitus are classical parts of endogenous Cushing’s syndrome (CS), and insulin resistance is a feature of cortisol excess. CS patients display characteristics including hyperglycemia, abdominal obesity, reduced high-density lipoprotein cholesterol levels and elevated triglycerides, and arterial hypertension. Hypercortisolism is a well known cause of bone loss, and patients with CS frequently display low bone mass and fragility fractures. Cortisol excess inhibits bone formation, increases bone resorption, impairs calcium absorption from the gut, and affects the secretion of several hormones, cytokines, and growth factors with potential influence on bone metabolism. Bone biopsies from nine CS patients, before and mean 3 months after surgery, were screened for expressional candidate genes using Affymetrix human Gene Plus 2.0 Arrays. Analyses were performed to identify genes in glucocorticoid-induced osteoporosis and genes in glucose metabolism and energy homeostasis.

overall_design: Expression levels were examined in bone biopsy samples from 9 patients with endogenous cushing syndrome, before and mean three months after surgery.

first: Thor

last: Ueland

first: Jens

last: Bollerslev

first: Ole

last: Olstad


title: The Histone Methyltransferase Wbp7 Controls Macrophage Function through GPI Glycolipid Anchor Synthesis. [Expression Profile]

status: Public on Apr 09 2012

city: Vienna

first: Iros

last: Barozzi

address: Borschkegasse 8a

country: Austria

institute: Medical University Vienna

summary:
Histone methyltransferases catalyze site-specific deposition of methyl groups, enabling recruitment of transcriptional regulators. In mammals, trimethylation of lysine 4 in histone H3, a modification localized at the transcription start sites of active genes, is catalyzed by six enzymes (SET1a and SET1b, MLL1–MLL4) whose specific functions are largely unknown. By using a genomic approach, we found that in macrophages, MLL4 (also known as Wbp7) was required for the expression of Pigp, an essential component of the GPI-GlcNAc transferase, the enzyme catalyzing the first step of glycosylphosphatidylinositol (GPI) anchor synthesis. Impaired Pigp expression in Wbp7-/- macrophages abolished GPI anchor-dependent loading of proteins on the cell membrane. Consistently, loss of GPI-anchored CD14, the coreceptor for lipopolysaccharide (LPS)
and other bacterial molecules, markedly attenuated LPS-triggered intracellular signals and gene expression changes. These data link a histone-modifying enzyme to a biosynthetic pathway and indicate
a specialized biological role for Wbp7 in macrophage function and antimicrobial response.

overall_design: Gene expression profiles for bone marrow-derived macrophages (BMDM) from either Wbp7+/- (HET) or Wbp7-/- (KO). Cells were left untreated or challenged with lipopolysaccharide (LPS) for 2hrs or 4hrs. Each genotype-treatment combination were performed in triplicate.

first: Liv

last: Austenaa

first: Agniezska

last: Chronowska

first: Alberto

last: Termanini

first: Renato

last: Ostuni

first: Elena

last: Prosperini

first: Francis

last: Stewart

first: Giuseppe

last: Testa

first: Gioacchino

last: Natoli


title: Efficient derivation of purified lung and thyroid progenitors from embryonic stem cells

city: New York

first: steve

last: shen

address: 545 First Ave

department: Biochemistry

country: USA

institute: New York University

summary: Two populations of Nkx2-1+ progenitors in the developing foregut endoderm give rise to the entire post-natal lung and thyroid epithelium, but little is known about these cells, as they are difficult to isolate in a pure form. We demonstrate here the purification and directed differentiation of primordial lung and thyroid progenitors derived from mouse embryonic stem cells (ESCs). Inhibition of TGFβ and BMP signaling, followed by combinatorial stimulation of BMP and FGF signaling can specify these cells efficiently from definitive endodermal precursors. When derived using Nkx2-1GFP knock-in reporter ESCs, these progenitors can be purified for expansion in culture and have a transcriptome that overlaps with developing lung epithelium. Upon induction, they can express a broad repertoire of markers indicative of lung and thyroid lineages and can recellularize a 3D lung tissue scaffold. Thus, we have derived a pure population of progenitors able to recapitulate the developmental milestones of lung/thyroid development.

overall_design: Comparison between Nkx2-1 positive and Nkx2-1 negative cells derived after 14 days of differentiation of mouse ES cells carrying a knock-in reporter gene, Nkx2-1GFP.

first: Tyler

last: Longmire

first: Laertis

last: Ikonomou

first: Finn

last: Hawkins

first: Constantina

last: Christodoulou

first: Hongmei

last: Mou

first: Yuxia

last: Cao

first: J

last: Jean

first: Letty

middle: W

last: Kwok

first: Jayaraj

last: Rajagopal

first: Steven

last: Sehn

first: Anne

last: Dowton

first: Maria

last: Serra

first: Daniel

middle: I

last: Weiss

first: Michael

middle: N

last: Green

first: Hans-Willem

last: Snoeck

last: Ramirez

first: Darrell

last: Kotton


title: Expression data comparing PLC8024 CD133+ and CD133- HCC cells

city: Hong Kong

first: Stephanie

last: Ma

address: Rm 47, 1/F, Lab Block, Faculty of Medicine Bldg, 21 Sassoon Rd, Pok Fu Lam

department: School of Biomedical Sciences

country: Hong Kong

institute: The University of Hong Kong

summary:
To identify candidate genes involved in enhanced tumorigenicity of CD133+ liver tumor-initiating cells
Affymetrix Human Genome U133 Plus GeneChip 2.0

overall_design: HCC cell line PLC8024 was sorted into CD133+ and CD133- populations by flow cytometry


title: DNA methylation in peripheral blood from individuals with Crohns' disease or ulcerative colitis and normal controls

first: R.

middle: Alan

last: Harris

address: 1 Baylor Plaza

department: Molecular and Human Genetics

institute: Baylor College of Medicine

summary: Genome wide DNA methylation profiling of Crohn's disease, ulcerative colitis, and normal peripheral blood samples. The Illumina Infinium HumanMethylation450 BeadChip v1.1 was used to obtain DNA methylation profiles across 482,421 CpGs in peripheral blood samples. Samples came from 17 Crohn's disease affected, 11 ulcerative colitis affected, and 20 normal individuals. Within these samples were three twin sets discordant for Crohn's disease and three twin sets discordant for ulcerative colitis.

overall_design: Bisulfite converted DNA from the 48 samples were hybridized to the  Illumina Infinium HumanMethylation450 BeadChip v1.1

first: Richard

last: Kellermayer

first: R


title: Gene expression profiling in BCR/ABL-expressing LSCs and BCR/ABL-expressing Hif1a-/-LSCs

status: Public on Apr 04 2012

city: Worcester

first: shaoguang

last: li

address: 364 Plantation street

department: medicine

institute: Umass medical school

summary: Using a mouse model of chronic myelogenous leukemia (CML), here we report that HIF1α plays a crucial role in survival maintenance of leukemia stem cells (LSCs). Deletion of HIF1α impairs the propagation of CML through impairing cell cycle progression and inducing apoptosis of LSCs. Deletion of HIF1α results in elevated expression of p16Ink4a and p19Arf in LSCs, and knockdown of p16Ink4a and p19Arf rescues the defective colony-forming ability of HIF1α-/- LSCs. To further identify the pathways in which Hif1a regulates function of LSCs, we performed a comparative DNA microarray analysis using total RNA isolated from BCR-ABL-expressing wild type LSCs and BCR-ABL-expressing Hif1a-/- LSCs. The result was validated by quantitative real-time PCR analysis of non-BCR-ABL-expressing Lin-Sca-1+c-Kit+ cells, BCR-ABL-expressing wild type LSCs, and BCR-ABL-expressing Hif1a-/- LSCs.

overall_design: To identify genes that are regulated by BCR-ABL in LSCs and LSCs without the Hif1a gene, we compared the gene profile between wild type (WT) LSCs and Hif1a-/- LSCs.

first: Shaoguang

last: Li

first: Haojian

last: Zhang


title: Gene expression profiling in WT and Hif1a-/- HSCs

summary: To understand the underlying mechanism by which the Hif1a gene is required by hematopoietic stem cells (HSCs), we performed a comparative DNA microarray analysis using total RNA isolated from wild type Lin-Sca-1+c-Kit+ cells and Hif1a-/- Lin-Sca-1+c-Kit+ cells. The result was validated by quantitative real-time PCR analysis of wild type Lin-Sca-1+c-Kit+ and Hif1a-/- Lin-Sca-1+c-Kit+ cells.

overall_design: We compared the gene profile of HSCs between WT mice and Hif1a-/- mice.


title: Gene expression profiling in wild type and Hif1a-deficient normal and leukemia stem cells

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

overall_design: Refer to individual Series


title: BW25113 H202 and delta rpoS persister cells vs. stationary phase BW25113 wild-type

status: Public on Apr 03 2012

city: State College

first: Thomas

middle: K.

last: Wood

address: Room 161 Fenske Laboratory, University Park

department: Chemical Engineering & Biochemistry and Molecular Biology

institute: Pennsylvania State University

summary: E. coli K-12 BW25113 persister cells generated via H202 pre-treatment and deletion of rpoS, relative to BW25113 wild-type stationary phase gene expression. Persister cells were generated following exposure to ampicillin 20 ug/mL.

overall_design:
Strains: BW25113 wild-type, pre-treated with H202 10 min, ampicillin 5 h;  BW25113 delta rpoS, ampicillin 5 h; BW25113 wild-type OD at 600 nm of 3.0, ampicillin 30 mins.
Medium: LB
ampicillin 20 ug/mL used to generate persisters; ampicillin 5 ug/mL added to stationary phase BW25113 wild-type

first: Hazel

last: O'Connor

last: Benedik


title: Transcriptional responses of uropathogenic E. coli to stresses caused by sodium chloride or urea.

city: Dayton

first: Oleg

last: Paliy

address: 3640 Colonel Glenn

department: Biochemistry and Molecular Biology

institute: Wright State University

summary:
E. coli which cause urinary tract infections must respond to high osmolarity in the urinary tract as well as the presence of urea.
We used microarrays to measure the differntial gene expression of uropathogenic strain CFT073 in conditions of high osmolarity of urea v. minimal media

overall_design: RNA was extracted from CFT073 in each growth condition and hybridized to an Affymetrix microarray. The differentially expressed genes were analyzed by expression pattern and function.

last: Agans

first: Thusitha

last: Gunasekera

first: Ben

last: Withman


title: Krüppel-like Factor 9 and Progesterone Receptor Co-Regulation of Decidualizing Endometrial Stromal Cells: Implications for its Loss in the Pathogenesis of Endometriosis

city: Little Rock

first: Rosalia

middle: CM

last: Simmen

state: Arkansas

address: 15 Children's Way Slot 512-20B

department: Physiology and Biophysics

institute: University of Arkansas for Medical Sciences

summary: Endometriosis is characterized by progesterone resistance and is associated with infertility. Krüppel-like Factor 9 (KLF9) is a progesterone receptor (PGR)-interacting protein, and mice null for Klf9 are subfertile. Whether loss of KLF9 contributes to progesterone resistance of eutopic endometrium of women with endometriosis is unclear. The aim of this study was to investigate KLF9 and PGR co-regulation of human endometrial stromal cell (HESC) transcriptome network.

overall_design:
Microarray gene expression analysis was conducted in decidualizing HESC by silencing the expression of KLF9 and PGR, alone or in combination by a siRNA approach, to identify additional KLF9 and PGR co-regulated genes and signaling networks/pathways.
HESC also treated with 8-bromo-cAMP, 17ß-estradiol, and medroxyprogesterone acetate (cAME) to mimic stromal progression from a proliferative to a differentiated state.

first: John

last: Pabona

first: Frank

first: Mikhail

last: Nikiforov

first: DaZhong

last: Zhuang

first: Kartik

last: Shankar

first: Zara

last: Zelenko

first: Linda

last: Giudice