title: Gene expression profiles upon knocking down Cops2 or Cops5 in mouse embryonic stem cells

status: Public on May 17 2016

city: Tianjin

first: Lingyi

last: Chen

address: 94 Weijin Road

institute: Nankai University

summary: To understand the role of Cops2 in mouse embryonic stem cells, we applied expression microarray analysis with GFP knockdown, Cops2 knockdown (2 different hairpins), and Cops5 knockdown mouse ESCs.

overall_design: Mouse ESCs were transfected with shGFP, shCops2(two different shRNAs), or shCops5 plasmids. 72 hours after transfection, cells were harvested for RNA prep and microarray analysis.

first: Chen

last: Lingyi


title: Cre-ERT mediated antiviral induction

status: Public on May 18 2016

city: Clayton

first: Michael

middle: Paul

last: Gantier

state: VIC

address: Hudson Institute of Medical Research

department: Centre for Innate Immunity and Infectious Diseases

country: Australia

institute: Hudson Institute of Medical Research

summary: In this work, we aimed at studying the impact of microRNAs on     antiviral responses, using inducible deletion of one or two copies of     Dicer1 (in Dicer-floxed x EsrCRE+ MEFs). Unexpectedly, we discovered     that Cre-ERT activation by hydroxytamoxifen (OHT) alone, independent of     Dicer1 deletion, had a strong impact on antiviral responses. These     microarrays were performed on SV40 immortalized Dicer1 fl/fl EsrCRE+     MEFs, Dicer1 fl/wt EsrCRE+ MEFs, 96 h after initial OHT treatment, and     SV40 immortalized Dicer1 wt/wt EsrCRE+ MEFs, Dicer1 wt/wt EsrCRE-neg     MEFs (Wild Type MEFs), 48 h after initial OHT treatment. These analyses     revealed the strong induction of several antiviral genes (Rsad2,     Cxcl10...), following Cre-ERT activation.

overall_design:
SV40 immortalized mouse embryonic fibroblasts from various genotypes were stimulated 24h with 500nM hydroxytamoxifen, and further expanded for 24 or 72h.
Each sample was analyzed on Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray
Each sample is in simplicate - no biological replicates; sample 1-4 were processed/analyzed on a different microarray slide to 5-8 (different day/operator)

middle: P

first: Genevieve

last: Pepin


title: Identifying PD0325901-regulated genes in the J1 mESCs

city: xi'an

first: Zhiying

last: Ai

state: shannxi

address: No.3 Taicheng Road, Yangling

country: China

institute: Northwest A&F University (NWAFU)

summary: It has been demonstrated that PD0325901 promotes self-renewal of mouse embryonic stem cells, however, the target genes of PD0325901 are not fully understood. To better understand the downstream target genes of PD0325901, we performed Microarray analyses to identify their downstream targets. The data show the genes regulated by PD0325901.

overall_design: J1 mESCs maintained in  medium containing 1000 U/mL LIF and supplemented without or with PD0325901 for 24 hours, then total RNA was extracted for analysis.

first: Yongyan

last: Wu

first: Zekun

last: Guo


title: Knockout of Pseudouridine synthase 1 (PUS1) in mice. [M1-Muscle]

status: Public on May 16 2016

city: Columbia

first: Diego

last: Altomare

state: SC

address: 715 Sumter Street, Room 617

department: Department of Drug Discovery and Biomedical Sciences

country: USA

institute: University of South Carolina

summary: In an effort to produce a mouse model of Mitochondrial Myopathy with Lactic acidosis and Sideroblastic Anemia (MLASA), we knocked out the gene for Pseudouridine synthase 1 (PUS1), an enzyme that modifies uridine to pseudouridine in many cytoplasmic and mitochondrial tRNAs, as well as other cellular RNAs. The Pus1-/- mice are viable, are born at the expected Mendelian frequency, and are non-dysmorphic. The PUS1 mRNA and certain pseudouridine modifications are absent in cytoplasmic and mitochondrial tRNAs in the Pus1-/- mice. The Pus1-/- mice display reduce exercise capacity at 14 weeks, with alterations in muscle morphology, histology, and physiology. Red gastrocnemius muscle from Pus1-/- mice shows reduced number and size of mitochondria and reduced Cytochrome C oxidase activity.

overall_design: Two-condition, two-color experiment:  Mouse wild type PUS1 and homozygous mutant PUS1 M1-skeletal muscle (red, slow) tissue samples: 4 biological replicates each.

first: Jeffrey

middle: R

last: Patton


title: Knockout of Pseudouridine synthase 1 (PUS1) in mice. [Liver]

overall_design: Two-condition, two-color experiment:  Mouse wild type PUS1 and homozygous mutant PUS1 liver tissue samples: 4 biological replicates each.


title: Oncogenomics of c-Myc-induced papillary lung adenocarcinoma

status: Public on May 20 2016

city: Hannover

first: Juergen

last: Borlak

state: Lower Saxony

address: Feodor-Lynen-Str. 35

department: Centre for pharmacology and toxicology

country: Germany

institute: Hanover Medical School

summary:
To study a complex network of gene expression changes underlying  c-Myc-triggered carcinogenesis in  lung we performed oligonucleotide array analysis of solid lung adenocarcinomas which developed in transgenic mice due to constitutive expression of c- Myc in alveolar type II epithelial cells and compared them with the non-transgenic lung as a control. The microarray analysis yielded 162 up regulated and 301 down regulated genes. The genes were further analyzed with regard to their biological functions, to known responsiveness to c-Myc and to the presence of potential c-Myc -binding sites in their promoters.
We identified inappropriate expression of a variety of genes involved in the several pathways critical for the development of lung tumor: cell cycle, cell growth, cell death, adhesion, cytoskeleton organization, invasive and angiogenic capacity. Some genes identified in this study were known to be similarly changed in human malignancies and specifically in lung tumors which makes the SPC/c-Myc-transgenic mouse model useful for investigating human lung cancer.  Many other genes differently expressed in lung tumors are novel targets for mechanism based therapies and serve as useful tumor markers. New c- Myc-responsive genes and putative c-Myc -targets identified in this study contributed to the collective examination of distinct c-Myc transcriptomes that are partly cell type- and species- specific
The molecular rules defining c-Myc’s activity in lung cancer remain elusive. We therefore investigated the c-Myc gene networks in a transgenic mouse model of lung cancer. Genome wide gene expression profiling applied to histological well-defined tumors revealed 162 up and 301 repressed genes and identified novel c-Myc targeted cell cycle and apoptosis genes. To better understand transcriptional responses the co-occupancy of different transcription factors (TF) were analyzed. This defined composite modules with 64, 68, 96 and 92, 88 and 96% of tumor associated down-regulated genes having TF-binding sites for either c-Myc, Klf7, Gata3 or c-Myc, Sox18 and P53, respectively. The composite modules fitted 48% and 80% of regulated genes. Likewise, 75, 96, 89 and 44, 59 and 54% of up-regulated genes in tumor or non-tumor transgenic tissue were enriched for Myc, Elf5,Cebp and c-Myc, Hbp1 and Hif1 TF-binding sites, respectively to suggest diverse and distinct TF-clusters at different stages of disease. Importantly, the genes coding for TFs were regulated as well and electrophoretic mobility shift assay (EMSA) confirmed c-Myc DNA-binding activity at targeted promoters of regulated genes. Furthermore, computational biology defined Gata3, mortalin and moesin to function in master regulatory gene networks and experimental validation of the constructed networks was achieved by EMSA, RT-PCR, Western blotting and gene reporter assay. Lastly, evidence for c-Myc DNA binding activity at targeted gene promoters was also derived from published Chip-sequence data of 7 human cell lines and the clinical significance of findings can be demonstrated by their regulation in human lung cancer. In conclusion, novel c-Myc targeted cell cycle and apoptosis genes were identified to function in gene regulatory networks. The results of the present study improve an understanding of c-Myc transforming capacity and provide a molecular rationale for the development of molecularly targeted therapies.

overall_design: To investigate the consequences of oncogenic activation of c-Myc in lung adenocarcinomas we used the surfactant protein C (SPC)- promoter to target c-Myc expression to alveolar epithelium (Ehrhardt et al., 2001). We compared gene expression profiles in c-Myc-induced papillary lung adenocarcinomas (PLACs) of transgenic mice with histologically confirmed normal lung of non transgenic animals of about the same age . To identify key transcriptional events associated with malignant growth RNA was prepared from tumor sets of small, middle and large size and analyzed by oligonucleotide microarrays. Small tumors were pooled into groups of n=3 whereas medium and large size tumors were obtained from n= 4 and n = 3 individual animals, respectively. Normal lung from n= 4 non-transgenic mice of the same age was used as control.

first: Yari

last: Ciribilli

first: Prashant

last: Singh

first: Reinhard

last: Spanel

first: Alberto

last: Inga

first: Tatiana

last: Meier


title: Knockout of Pseudouridine synthase 1 (PUS1) in mice. [Heart]

overall_design: Two-condition, two-color experiment:  Mouse wild type PUS1 and homozygous mutant PUS1 heart tissue samples: 4 biological replicates each.


title: Knockout of Pseudouridine synthase 1 (PUS1) in mice.

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

overall_design: Refer to individual Series


title: Knockout of Pseudouridine synthase 1 (PUS1) in mice. [M2-Muscle]

overall_design: Two-condition, two-color experiment:  Mouse wild type PUS1 and homozygous mutant PUS1 M2-skeletal muscle (white, fast) tissue samples: 4 biological replicates each.


title: Knockout of Pseudouridine synthase 1 (PUS1) in mice. [Kidney]

overall_design: Two-condition, two-color experiment:  Mouse wild type PUS1 and homozygous mutant PUS1 kidney tissue samples: 4 biological replicates each.


status: Public on May 13 2016

city: London

first: Paul

last: Gissen

state: London

address: Gower Street

department: LMCB

country: United Kingdom

institute: UCL

summary:
Mouse IMCD3 cell lines knocked-down for VPS33B, VIPAR and PLOD3 are used as models of ARC syndrome, an autosomal recessive disorder cause by mutations in VPS33B or VIPAR.
Previous work has shown that ARC syndrome causes epithelial cell polarisation defectes and mislocalisation of membrane proteins, so polarised IMCD3 cells were used as an experimental model.
Affymetrix arrays were used to characterise the changes to the transcriptome when protein levels of VPS33B, VIPAR and PLOD3 are reduced.

overall_design: mouse IMCD-3 cell lines, 15 samples in total, three biological repeats of each of: wild type, control shRNA, VPS33B shRNA, VIPAR shRNA, PLOD3 shRNA

first: Blerida

last: Banushi

first: Anna

last: Straatman-Iwanowska

first: Clare

last: Rogerson

first: Anne-Marie

last: Lyne


title: Expression data from mouse hair follicle stem cells at postnatal day 49 in K14-sPLA2-IIA and wild type mice

status: Public on May 09 2016

city: Navi Mumbai

first: SANJEEV

middle: K

last: WAGHMARE

state: MAHARASHTRA

address: Sector 22, Kharghar

department: STEM CELL BIOLOGY GROUP

country: India

institute: ACTREC, TATA MEMORIAL CENTRE

summary:
sPLA2-IIA is involved in lipid catabolism and is deregulated in various human cancers. Our data showed that over expression of sPLA2-IIA in skin disrupts various epidermal lineages, loss of ortho-parakeratotic organization, stem cell depletion/quiescence and increased differentiation potentially associated with global differences in epigenetic status. Our study has provided significant contribution to over existing knowledge of sPLA2-IIA by showing the unexplored role of sPLA2-IIA in hair follicle stem cells and skin homeostasis mediated through JNK/c-Jun signaling mechanism.
We have performed microarray analysis  on hair follicle stem cells in K14-sPLA2-IIA mice to uncover the global  gene expression profile underlying stem cell regulation and tissue homeostasis, and have shown the distinct classes of up-regulated genes involved during this process.

overall_design: To understand the molecular mechanism, we performed the genome-wide expression profiling of hair follicle stem cells in K14-sPLA2-IIA (TG) and wild type (WT) mice. CD34+ α6-intergrin+ (Hair follicle stem cells) were FACS isolated  for RNA extraction and further performed the hybridization by using the mice GeneChip(R) Mouse Gene 2.0 ST arrays (Affymetrix, USA).

first: Sanjeev

last: Waghmare


title: Modulation of LPS-stimulated BV2 microglial cells by Amauroderma rugosum hexane fraction (HF)

status: Public on May 14 2016

city: KUALA LUMPUR

first: PUI MUN

last: CHAN

state: WILAYAH PERSEKUTUAN

address: DEPARTMENT OF BIOMEDICAL SCIENCE

department: DEPARTMENT OF BIOMEDICAL SCIENCE

country: Malaysia

institute: UNIVERSITY OF MALAYA

summary: The anti-inflammatory effects of A. rugosum might be associated with various signalling transduction pathways and therapeutic targets. Therefore, with the aid of microarray technology specific signalling pathways and therapeutic targets by A. rugosum hexane fraction (HF) can be easily identified.

overall_design: Biological replicate (in duplicate) samples were sorted according to four conditions: cells only (control), cells induced with 1 µg/mL of LPS, cells treated with 100 µg/mL of HF, and cells induced with 1 µg/mL of LPS and treated with 100 µg/mL of HF.

first: Pui

middle: M

last: Chan

first: Yee

middle: S

last: Tan

first: Kek

middle: H

last: Chua

first: Umah

last: Kuppusamy

first: V

last: Sabaratnam


title: Knockout of Pseudouridine synthase 1 (PUS1) in mice. [Brain]

first: Diego

last: Altomare

overall_design: Two-condition, two-color experiment:  Mouse wild type PUS1 and homozygous mutant PUS1 brain tissue samples: 4 biological replicates each.

first: Jeffrey

last: Patton


title: p38 alpha activates purine metabolism to initiate hematopoietic stem/progenitor cell cycling

status: Public on Apr 20 2016

city: Tokyo

first: Keiyo

last: Takubo

address: 1-21-1 Toyama Shinjuku-ku

department: Department of Stem Cell Biology

country: Japan

institute: National Center for Global Health and Medicine

summary: Hematopoietic stem cells (HSCs) maintain quiescence by activating specific metabolic pathways, including glycolysis. However, how stress hematopoiesis, including bone marrow transplantation, induces metabolic changes in hematopoietic stem/progenitor cells (HSPCs) remains unclear. Here, we report a critical role for the p38MAPK family isoform p38α in initiating HSPC proliferation during stress hematopoiesis in mouse. We found that p38MAPK is immediately phosphorylated in HSPCs after hematological stress. p38α loss resulted in defective recovery from hematological stress and a delay in initiation of HSPC cycling. Bone marrow transplant altered levels of amino acids and purine-related metabolites in a p38α-dependent manner. Mechanistically, p38α signaling increases expression of inosine-5’-monophosphate dehydrogenase 2 in HSPCs after transplantation, an activity correlated with perturbed cell cycle progression in vitro and in vivo. Overall, we propose a novel mechanism governing HSPC cell cycle initiation via metabolic signaling in response to stress.

overall_design: CD34- Flt3- LSK cells (LT-HSC) or CD34+ Flt3+ LSK cells (MPP) in the bone marrow (femur and tibia) from wild type (WT) or p38 cKO (cKO) C57BL/6J mice (Ly5.2) were sorted using SORP FACS AriaI followed by labbeling with CFSE for 30 minutes at 37℃ and transplanted into lethally (9.5Gy)-irradiated Ly5.1 congenic mice. Sixteen hours later, bone marrow cells were collected from femur and tibia of transplanted mice, and CFSE-positive cells were sorted. Total RNA was then extracted using RNeasy micro kit (Qiagen), and cDNA was synthesized from mRNA and hybridized to gene chip Mouse60k (Agilent Technologies) and expression levels analyzed.

first: Daiki

last: Karigane

first: Hiroshi

last: Kobayashi

first: Toshio

last: Suda


title: Exclusion of non-expressed genes from the Chikungunya RNAi screen hit identification process

city: Berlin

first: Hans-Joachim

last: Mollenkopf

address: Charitéplatz 1

institute: Max-Planck-Institute for Infection Biology

summary: To allow exclusion of non-expressed genes from the hit identification process, microarray analyses of (i) Allstars transfected and Chikungunya (CHIKV) infected, (ii) Allstars transfected and non-infected, (iii) non-transfected and CHIKV infected and (iv) non-transfected and non-infected 293 cells were performed. Transfection was done by adding 4x10e5 293 cells (in complete DMEM medium) to a mixture of serum-free RPMI medium, HiperFect (Qiagen) and Allstars siRNAs (Qiagen, final siRNA concentration: 20 nM). Infection with CHIKV-GFP was performed 72 h p.t. at an MOI of ~3. Cells were lysed 18 h p.i. using Trizol (Invitrogen), followed by RNA isolation, that was subsequently subjected to microarray analysis.

overall_design: Microarray experiments were performed as dual-color hybridizations on Agilent 4x44K human whole genome catalog arrays (Agilent-014850). To compensate for dye-specific effects, a dye-reversal color-swap was applied.

first: Alexander

last: Karlas

first: Thomas

last: Meyer


title: Microarray analysis of peripheral blood mononuclear cells (PBMCs) from IgA nephropathy patients, membranous nephropathy patients and healthy controls.

status: Public on Apr 22 2016

city: Suita

first: Daisuke

last: Okuzaki

state: Osaka

address: Yamadaoka 3-1

department: Immunology Frontier Research Center

institute: Osaka univ.

summary: To search for new markers of active lesions that might help better understand the molecular basis of MN and IgAN and aid in their diagnosis, DNA microarray analysis was performed with peripheral blood mononuclear cells (PBMCs)

overall_design: 1-color microarray experiments were performed on peripheral blood mononuclear cells (PBMCs) from 15 IgAN patients, 8 membranous nephropathy patients and pooled healthy subjects.

last: Nojima


title: Expression data from Tbx1 knockout (KO) palatal shlelves

city: Bunkyo-ku

first: Noriko

last: Funato

state: Tokyo

address: 1-5-45 Yushima

institute: Tokyo Medical and Dental University

summary:
Deletion of Tbx1, a member of the T-box transcription factor gene family, results in abnormal epithelial fusion between the palatal shelves and the mandible, which induces cleft palate by inhibiting elevation of the palatal shelves.
We used microarrays to determine the downstream genes of Tbx1 during palatogenesis and identified distinct classes of dysregulated genes.

overall_design: Wild-type and Tbx1KO head or palatal shelves were collected at Embryonic day (E) 12.5 or 13.5 for RNA extraction and hybridization on Affymetrix Mouse Gene 2.0ST Array.

first: Deepak

last: Srivastava

first: Hiromi

last: Yanagisawa


title: Gene expression in ABHD5-knockdown RAW264.7 cells

status: Public on May 12 2016

city: Chongqing

first: Hongming

last: Miao

state: Chongqing

address: Gaotanyan Street NO.30

department: Department of Biochemistry and Molecular Biology

institute: Third Military Medical University (Army Medical University)

summary: RAW cells or ABHD5-KD RAW cells were subjected to microarray assays. Each group contain 3 samples.

overall_design: To explore the regulatory role of ABHD5 in metabolic pathways, RAW cells or ABHD5-KD RAW cells were subjected to microarray assays.

first: Houjie

last: Liang


title: Cellular dynamics of mouse trophoblast stem cells: Identification of a persistent stem cell type.

status: Public on May 01 2016

city: Tsukuba

first: Kimiko

last: Inoue

state: Ibaraki

address: 3-1-1 Koyadai

department: Bioresource Engineering Division

institute: BRC, RIKEN

summary: Mouse trophoblast stem cells (TSCs) proliferate indefinitely in vitro, despite their highly heterogeneous nature. In this study, we sought to characterize TSC colony types by using methods based on cell biology and biochemistry for a better understanding of how TSCs are maintained over multiple passages. Colonies of TSCs could be classified into four major types: type 1 is compact and dome-shaped, type 4 is flattened but with a large multilayered cell cluster, and types 2 and 3 are their intermediates. A time-lapse analysis indicated that type 1 colonies predominantly appeared after passaging, and a single type 1 colony gave rise to all other types. These colony transitions were irreversible, but at least some type 1 colonies persisted throughout culture. The typical cells comprising type 1 colonies were small and highly motile, and aggregated together to form primary colonies. A hierarchical clustering based on global gene expression profiles suggested that a TSC line containing more type 1 colony cells was similar to in-vivo extraembryonic tissues. Among the known TSC genes examined, Elf5 showed a differential expression pattern according to colony type, indicating that this gene might be a reliable marker of undifferentiated TSCs. When aggregated with fertilized embryos, cells from types 1 and 2, but not from type 4, distributed to the polar trophectoderm in blastocysts. These findings indicate that cells typically found in type 1 colonies can persist indefinitely as stem cells and are responsible for the maintenance of TSC lines. They may provide key information for future improvements in the quality of TSC lines.

overall_design: Comparative gene expression analyses across different colony types in murine trophoblast stem cells. Three cell lines cultured by conventional medium and one cell line cultured by chemically defined medium were used for the analysis. Extraembryonic ectoderm and ectoplacental cone derived from C57BL/6 and ICR strains were used as in vivo control. Two to four replications were performed in each sample.

first: Kaori

last: Motomura

first: Atsuo

last: Ogura


title: Expression data from neonatal mice cardiomyocytes

status: Public on Apr 13 2016

city: Wuhan

first: Xiang

last: Cheng

state: Hubei

address: No.1277 Jiefang Avenue

institute: Institute of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology

summary: FGF21 belongs to the FGF superfamily and the highest expression of the FGF21 transcript was found in the liver. The initial studies identified FGF21 as an endocrine hepatokine with crucial roles in regulating lipid, glucose and energy metabolism. More recent studies have indicated a role for FGF21 in cardiovascular stress and diseases.The goal of our study is to analyze the effect of FGF21 on ischemic cardiomyocytes transcriptome using microarray.

overall_design: Total RNA was extracted from cultured neonatal mice cardiomyocytes after exposure to hypoxia (in 2% oxygen, 5% CO2 and 93% N2) for 12 h in the absence or presence of FGF21. Samples were processed for hybridization to the Mouse Gene 2.0 ST Array (Affymetrix). We sought to find out the differentially expressed genes regulated by FGF21 in hypoxic cardiomyocytes.

first: Ting-Ting

last: Tang

first: Jing-Jing

last: Li

first: Yuan-Yuan

first: Ke

last: Wang

first: Wen-Yong

last: Dong

first: Ni

last: Xia

first: Shao-Fang

last: Nie

first: Min

last: Zhang

first: Zhi-Peng

last: Zeng

first: Bing-Jie

last: Lv

first: Jiao

last: Jiao

first: Yu-Hua

last: Liao

first: Qing

first: Xin

last: Tu

first: Ziad

last: Mallat

first: Guo-Ping

last: Shi


title: Gene expression data from long term hematopoietic stem cells (LT-HSC, Lin-Sca-1+c-kit+CD34-CD135-) isolated from control, MxCre Jak2VF/+ and MxCre Jak2VF/+ EZH2-/- mice

status: Public on Apr 19 2016

city: Syracuse

first: Golam

last: Mohi

state: New York

address: 766 Irving Avenue

department: Pharmacology

institute: SUNY Upstate Medical University

summary: Inactivating EZH2 mutations have been associated with myelofibrosis (MF). Moreover, EZH2 mutations co-exist with the JAK2V617F mutation in a significant cases of MF. To determine the effects of concomitant loss of EZH2 and JAK2V617F mutation in hematopoiesis, we generated Ezh2-deficient Jak2V617F-expressing mice. To gain insights into the mechanisms by which Ezh2 deficiency promotes the development of MF in Jak2V617F knock-in mice, we performed microarray gene expression analysis on sorted LT-HSC from control, MxCre;Jak2VF/+ and MxCre;Jak2VF/+ EZH2-/- mice.

overall_design: Microarray analyses were performed on LT-HSC sorted from control, MxCre Jak2VF/+ and MxCre Jak2VF/+ EZH2-/- mice BM cells at 12 weeks after pI-pC injections. Three biological replicates for each genotype, i.e., a total of nine samples were utilized for microarray analyses.

first: Yue

last: Yang


title: Expression data of endothelial cells from mouse hindbrain and genetic Wnt-medulloblastoma and Shh-medulloblastoma mouse models

status: Public on Apr 05 2016

city: Memphis

first: David

last: Finkelstein

state: TN

address: 332 N. Lauderdale St.

department: Computational Biology

institute: St Jude Children's Research Hospital

summary:
The childhood brain tumour medulloblastoma includes four subtypes with very different prognoses. Here, we show that paracrine signals driven by mutant Beta-Catenin in WNT-medulloblastoma – an essentially curable form of the disease – induce an aberrant fenestrated vasculature that permits the accumulation of high levels of intra-tumoural chemotherapy and a robust therapeutic response. In contrast, SHH-medulloblastoma – a less curable disease subtype – contains an intact blood brain barrier, rendering this tumour impermeable and resistant to chemotherapy. Remarkably, the medulloblastoma-endothelial cell paracrine axis can be manipulated in vivo, altering chemotherapy permeability and clinical response. Thus, medulloblastoma genotype dictates tumour vessel phenotype, explaining in part the disparate prognoses among medulloblastoma subtypes and suggesting an approach to enhance the chemoresponsiveness of other brain tumours.
We used microarrays to detail the global program of gene expression within endothelial cells from normal mouse hindbrain and genetic mouse models of different medulloblastoma subtypes to identify and verify up-regulated and down-regulated genes

overall_design: Endothelial cells were isolated from adult mouse hindbrain and genetic mouse models of Wnt and Shh-medulloblastoma using Cd-144 and Cd-105 antibodies based magnetic sorting. RNA was extracted and used for hybridization on Affymetrix microarrays. We sought to identify changes in endothelial gene expression patterns based on the surrounding microenvironment, so we purified endothelial cells from normal mouse brain or tumors from genetic mouse models. These include the Shh-medulloblastoma model (Ptch+/-; Ink4c -/-) and Wnt-medulloblastoma model (Blbp-Cre; mutant Ctnnb1+/-; p53-/-; mutant Pik3ca +/-)

first: Timothy

last: Phoenix

first: Richard

last: Gilbertson


title: Loss of renal tubular PGC-1α exacerbates diet-induced renal steatosis and age-related urinary sodium excretion in mice

status: Public on Apr 26 2016

city: Basel

first: Christoph

last: Handschin

address: Spitalstrasse 41

country: Switzerland

institute: Biozentrum, University of Basel

summary: The kidney has a high energy demand and is dependent on oxidative metabolism for ATP production. Accordingly, the kidney is rich in mitochondria, and mitochondrial dysfunction is a common denominator for several renal diseases. While the mitochondrial master regulator peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is highly expressed in kidney, its role in renal physiology is so far unclear. Here we show that PGC-1α is a central transcriptional regulator of mitochondrial metabolic pathways in the kidney. Moreover we demonstrate that mice with an inducible nephron-specific inactivation of PGC-1α in the kidney display elevated urinary sodium excretion, exacerbated renal steatosis during metabolic stress but normal blood pressure regulation. Overall, PGC-1α seems largely dispensable for basal renal physiology. However, the central role of PGC-1α in renal mitochondrial biogenesis indicates that activation of PGC-1α in the context of renal disorders could be a valid therapeutic strategy to ameliorate renal mitochondrial dysfunction.

overall_design: We used microarrays to detect changes in gene expression in whole kidney from mice. Nephron-specific inducible PGC-1alpha knockout (NiPKO) or control mice (CTRL) were fed either a chow diet or a high fat diet (HFD 60 kcal% fat, D12492) for 20 weeks. We used 4 biological replicates for each condition. The samples were: CWT – chow fed CTRL mice; CKO – chow fed NiPKO mice; HWT – HFD fed CTRL mice; HKO – HFD fed NiPKO mice.

first: Kristoffer

last: Svensson

first: Bettina

last: Cardel


title: PIR-B negatively regulates IL-13-induced esophageal eosinophil effector functions

status: Public on May 05 2016

city: Cincinnati

first: Marc

middle: E

last: Rothenberg

state: OH

address: 3333 Burnet Ave. MLC-7028

department: Allergy

institute: Cincinnati Children's Hospital Medical Center

summary: Eosinophilic esophagitis (EoE) is a T helper type 2 (TH2) cytokine-associated disease charaterized by eosinophil infiltration, epithelial cell hyperplasia and tissue remodeling.  Recent studies have highlighted a major contribution for IL-13 in EoE pathogenesis.  Paired immunoglobulin-like receptor (PIR)-B is a cell surface immune-inhibitory receptor that is expressed by eosinophils and postulated to regulate eosinophil development and migration.  We report that Pirb is upregulated in the esophagus after inducible overexpression of IL-13 (CC10-IL13 Tg mice) and is overexpressed by esophageal eosinophils.  CC10-IL13Tg/PirB-/- mice displayed increased esophageal eosinophilia and EoE pahtology, including epithelial cell thickening, fibrosis and angiogenesis, compared with CC10-IL13 Tg/PirB+/+ mice.  Transcriptome analysis of primary Pirb+/+ and Prib-/- esophageal eosinophils revealed increased expression of transcripts associated with promoting tissue remodeling in Pirb-/- eosinophils including pro-fibrotic genes, genes promoting epithelial-to-mesenchymal transition (EMT) and genes associated with epithelial growth.  These data identify PIR-B as a molecular checkpoint in IL-13-induced eosinophil accumulation and activation, which may serve as a novel target for future therapy in EoE.

overall_design: 17 samples are analyzed in this experiment.  The experiment was designed with 3 replicates for each treatment/genotype/tissue (Dox and no Dox/wildtype and knockout/bone marrow and esophagus), with the exception of the sample wildtype bone marrow no Dox where 1 replicate was dropped due to low hybridization signal.  The no Dox and wildtype samples are controls for the treatment and background of the mice.

first: Netali

last: Ben Baruch-Morgenstern

first: Melissa

last: Mingler

first: Emily

last: Stucke

first: John

middle: A

last: Besse

first: Ting

last: Wen

first: Hadar

last: Reichman

first: Ariel

last: Munitz


title: LY75 modulates epithelial to mesenchymal transition and metastatic potential of ovarian cancer cells

status: Public on Apr 01 2016

city: Quebec

first: Dimcho

last: Bachvarov

state: Quebec

address: 9, rue McMahon

country: Canada

institute: CHU-Q, Centre de recherche-HDQ

summary: Epithelial ovarian cancer (EOC) accounts for 4% of all cancers in women and is the leading cause of death from gynecologic malignancies. It is well established that cancer invasion and metastasis still represent the major causes of the failure of cancer treatment. Previously, we identified the mannose receptor LY75 (DEC205/CD205) gene as notably hypomethylated in high-grade (HG) serous epithelial ovarian tumors, compared to normal ovarian tissues. LY75 has been identified as a putative antigen-uptake receptor, which is expressed abundantly on dendritic cells, which are specialist antigen presenting cells to T lymphocytes for the initiation of an immune response. The implication of LY75 in EOC tumorigenesis is currently unknown. Here we show that LY75 is strongly overexpressed in HG serous EOC tumors as compared to normal ovarian tissue. Importantly, shRNA-mediated LY75 knockout in the mesenchymal EOC cells (SKOV3) led to mesenchymal to epithelial transition (MET), associated with overexpression of epithelial markers E-cadherin and EPCAM and loss of expression of mesenchymal markers Fibronectin, N-cadherin Snail1 and Twist1. In addition, LY75 suppression significantly inhibited EOC cell migration and invasion in vitro. However, LY75 knockdown led to enhanced tumor cell dissemination and significantly increased lethality in vivo, in xenograft model of advanced peritoneal EOC. Thus, our findings indicate that LY75 could play an essential role in the mesenchymal-to-epithelial transition (MET) of EOC cells and support the hypothesis that, while epithelial-to-mesenchymal transition (EMT) enables the invasiveness of tumor cells, a MET-associated epithelial phenotype could be essential for their metastatic colonization.

overall_design: To better understand the molecular mechanisms of LY75 gene action in epithelial ovarian cancer (EOC), we employed the Agilent Whole Human Genome microarrays, containing ~ 44,000 genes to identify global gene expression changes upon LY75 suppression in SKOV3 EOC cells. We compared the gene expression of the previously selected shRNA-mediated LY75-knockdown clones sh-S3 and sh-S6 against the corresponding control (ctrl) clone. The microarray experiments were performed in duplicates, as two hybridizations were carried out for each of the LY75-suppressing cell clone against the corresponding control, using a fluorescent dye reversal (dye-swap) technique.


title: Compare proB cells from WT, Tp53-/-, Lnk-/-, Tp53-/-Lnk-/- mice and Tp53-/-Lnk-/-B-ALL

city: Philadelphia

first: Wei

last: Tong

state: PA

address: 316A Abramson Bldg., 3615 Civic Center Blvd.

department: Pediatrics

institute: Children's Hospital of Philadelphia, and University of Pennsylvania School of Medicine

summary: The adaptor protein LNK (SH2B3) has emerged as an important protein in regulating B cell development B cell leukemia. Loss-of-function mutations in LNK (SH2B3) are found in Philadelphia chromosome–like acute lymphoblastic leukemia (Ph-like ALL), but how LNK regulates normal B cell development or promotes leukemogenesis remains unclear. We found that combined loss of Lnk and tumor suppressors Tp53 in mice triggers a highly aggressive and transplantable precursor B-ALL. This study aims to investigate the molecular mechanism by which LNK regulates B-ALL development. We performed expression profiling of bone marrow proB progenitors from WT, Tp53-/-, Lnk-/- and preleukemic healthy Tp53/Lnk double knockout (DKO) mice, as well as leukemic bone marrow cells from DKO mice that have developed B-ALL. Results suggest that Tp53-/-Lnk-/- B-ALLs display similar gene expression profiles to human Ph-like B-ALLs, suggesting this model for preclinical and molecular studies.

overall_design: B220+CD19+CD43+AA4.1+IgM-NK1.1-Ly6c- bone marrow proB cells were double sorted from WT, Tp53-/-, Lnk-/- and preleukemic healthy Tp53/Lnk double knockout (DKO) mice, as well as leukemic bone marrow cells from DKO mice that have developed B-ALL.  RNA was isolated using miRNeasy kit from QIAGEN and processed using the NuGEN Pico kit. The microarray analysis was performed at the PENN Molecular Profiling/Genomics Facility using GeneChip Mouse Gene 2.0ST array (Affymetrix).

first: Ying

last: Cheng

first: Kudakwashe

last: Chikwava

first: Chao

last: Wu

first: Haibing

last: Zhang

first: Anchit

last: Bhagat

first: Shane

last: Glasgow

first: Dehua

last: Pei

last: Choi


title: Genome-wide analysis of Estrogen Receptor-mediated response to acute Estradiol treatment in liver (expression)

city: Rennes

first: Raphaël

last: Métivier

address: Campus de Beaulieu

country: France

institute: CNRS UMR 6290

summary: Estrogen-based treatments have numerous extra-reproductive effects. On the one hand, they have protective metabolic actions against abdominal fat accumulation, type 2 diabetes, liver steatosis,… But, on the other hand, the oral route of administration, presumably due to a hepatic impact on liver-derived coagulation factors, appears to increase risks of venous thrombosis and pulmonary embolism. The characterization of liver genes expression regulations by these hormones thereby appears of utmost interest, but the estrogen-sensitive transcriptome of liver and ER cistrome was so far explored under chronic hormonal treatment. To explore the early steps of these mechanisms, we determined here the short-term changes in liver transcriptional responses to acute E2 administration, and aimed to characterize the mechanisms allowing these programs to be engaged. Collectively, through the comparison of mice expressing or not ER, our data demonstrate that acute administration of E2 provokes genes expression variations which fit with a crucial role of ER in the prevention of liver steatosis in mice fed with a high fat diet by E2. They also evidenced higher proportion of ER binding sites (BSs) located at the direct vicinity (distance <3kb) of regulated genes than what is determined in human cancer cell models. Besides this specific aspect of ER cistrome in vivo, we unexpectedly found that 40 % of the BSs of the pioneer factor Foxa2 were dependent upon the expression of ER that indirectly influences the distribution of the nucleosomes harbouring a dimethylated H3K4 around these Foxa2 sites.

overall_design: Analysis of estrogen-sensitive and estrogen receptor (ER)-dependent transcriptomes in livers from wild-type or ERKO mice.

first: Gaëlle

last: Palierne

first: Aurélie

last: Fabre

first: Romain

last: Solinhac

first: Yannick

last: Lippi

first: Pascal

last: Martin

first: Christine

last: Le Péron

first: Stéphane

last: Avner

first: Francoise

last: Lenfant

first: Coralie

last: Fontaine

first: Gilles

last: Salbert

last: Flouriot

first: Jean

middle: F

last: Arnal


title: A Glo1-methylglyoxal pathway that is perturbed in maternal diabetes regulates embryonic and adult neural stem cell pools in offspring

status: Public on Mar 31 2016

city: Toronto

first: Freda

last: Miller

state: Ontario

address: 686 Bay Street

department: Neurosciences and Mental Health

institute: Hospital for Sick Children

summary: We used microarrays to compare the gene expression profile in cultured primary neurospheres derived from the subventricular zone of adult (2 m.o.) offspring of mothers treated with PBS or methylglyoxal during pregnancy

overall_design: Primary neurospheres derived from 2-month-old adult CD1 mice born to mothers treated with PBS or MG twice daily from gestational day 12 until delivery were collected, and total RNA extracted. cDNA was hybridized on Affymetrix Mouse Gene 2.0 ST Array and gene expression was analyzed using Partek software. In total, 3 PBS treated and 3 MG treated mice were used.

first: David

last: Kaplan


title: PHD2/3-dependent hydroxylation of thyroid hormone receptor-α mediates the transcriptional regulation of phospholamban to tune the cardiac response to chronic β-adrenergic stress

city: Chapel Hill

first: Jonathan

middle: C

last: Schisler

state: NC

address: MBRB, Rm 2340C

department: McAllister Heart Institute

institute: The University of North Carolina at Chapel Hill

summary: Ischemic heart disease is the leading cause of heart failure. Both clinical trials and experimental animal studies demonstrate that chronic hypoxia can induce contractile dysfunction even before substantial ventricular damage, implicating a direct role of oxygen in the regulation of cardiac contractile function. Prolyl hydroxylase domain (PHD) proteins are well recognized as oxygen sensors and mediate a wide variety of cellular events by hydroxylating a growing list of protein substrates. Both PHD2 and 3 are highly expressed in the heart, yet their functional roles in modulating contractile function remain incompletely understood. Here, we report that combined deletion of PHD2 and 3 dramatically decreases the expression of phospholamban (PLN), results in sustained activation of CaMKII and sensitizes mice to myocardial injury induced by chronic β-adrenergic stress. We provide evidence that thyroid hormone receptor-α (TR-α), a transcriptional regulator of PLN, interacts with PHD2 and 3 and is hydroxylated at two proline residues. Inhibition of PHDs increases the interaction between TR-α and nuclear receptor co-repressor 2 (NCOR2) and suppresses PLN transcription. These observations provide new mechanistic insights into how oxygen directly modulates cardiac contractility, providing the possibility that cardiac function can be modulated therapeutically by tuning PHD  enzymatic activity.

overall_design: Two-condition experiment comparing gene expression in hearts isolated from PHD2/3f/f; Cre-/- and  PHD2/3f/f; Cre+/- mice. Three biological replicates (mouse hearts) per condition.

first: W

last: Townley-Tilson

first: Liang

last: Xie


title: Expression data of Brain CD45+ cells from WT and STI knockout mice after WNV infection

status: Public on Mar 22 2016

city: NORTH CHICAGO

first: Rahul

last: Vijay

state: IL

address: 3333 GreenBay Road, BSB 2.450

department: Microbiology and Immunology

institute: Rosalind Franklin University

summary: West Nile virus (WNV) is the most important cause of endemic encephalitis in the USA. Strikingly, only a small percentage of patients develop clinical disease and of these patients, approximately 1 out of 150 patients develops encephalitis. The basis for this great variability in disease outcome is unknown, but may be related to the innate immune response. Innate immune responses, critical for control of WNV infection, are initiated by signaling through pathogen recognition receptors (PRR) such as RIG-I and MDA5. IPS-1 is a key adaptor in generating a PRR-dependent interferon response.. Here we show that IPS-1 deficiency in hematopoietic cells resulted in increased mortality and delayed WNV clearance from the brain. In IPS-1-/- mice, a dysregulated immune response was detected, characterized by a massive influx of macrophages and virus-specific T cells into the infected brain. These T cells were multifunctional and were able to lyse peptide-pulsed target cells in vitro. However, virus-specific T cells in the infected IPS-1-/- brain exhibited lower functional avidity than those in C57BL/6 brains, possibly contributing to less efficient virus clearance. The presence of virus-specific memory T cells was also not protective. We also show that macrophages were increased in numbers in the IPS-1-/- brain. Both macrophages and microglia exhibited an activated phenotype. Microarray analyses showed the preferential upregulation of genes associated with leukocyte activation and inflammation. Together, these results demonstrate the critical role that hematopoietic cell expression of Type 1 interferon and other IPS-1-dependent molecules have in WNV clearance and in regulating the inflammatory response.

overall_design: We used 4 mice in each group. STI knockout mice developed lethath encephalitis after WNV infectin. WT mice which have mild disease after WNV were used as controls.

first: Jincun

last: Zhao

first: Stanley

last: Perlman


title: Characterization of genetic variability of Venezuelan equine encephalitis viruses

status: Public on Mar 24 2016

city: Livermore

first: Kevin

last: McLoughlin

state: CA

address: PO Box 808

department: Global Security

institute: Lawrence Livermore National Laboratory

summary:
We performed whole genome single nucleotide polymorphism (SNP) based analysis of all available Venezuelan equine encephalitis (VEE) virus antigenic complex genomes and developed a high resolution genome-wide SNP microarray.
We used the SNP microarray to analyze a broad panel of VEEV isolates, found excellent concordance between array and sequence based genotypes for previously sequenced strains, and genotyped unsequenced strains.

sample_organism:
Venezuelan equine encephalitis virus
Mucambo virus
Pixuna virus
Cabassou virus

overall_design: We analyzed 134 VEEV and VEE antigenic complex isolates with the SNP microarray. 81 of these had genome sequences available and were used to assess concordance between array- and sequence-based genotypes.  4 strains were analyzed with duplicate arrays. In addition, 3 arrays were run on samples of brain tissue from mice that had been infected with VEEV strain TC-83 2 days previously.

first: Shea

middle: N

last: Gardner

first: Nicholas

last: Be

last: Allen

first: Scott

last: Weaver

first: Naomi

last: Forrester

first: Mathilde

last: Guerbois

first: Crystal

last: Jaing


title: Transcriptome profiles of mice intestine and liver upon infection with Salmonella typhimurium (MC71-TT and MC71-DcdtB)

city: Povo

first: Toma

last: Tebaldi

state: Trento

address: via Sommarive n. 9

department: Centre for Integrative Biology

country: Italy

institute: University of Trento

summary:
Bacterial genotoxins, produced by several Gram-negative bacteria, induce DNA damage in the target cells. While the responses induced in the host cells have been extensively studied in vitro, the role of the genotoxins as effectors during the course of acute and chronic infections remains poorly characterized.To address this issue, we assessed the effects of the Salmonella enterica genotoxin, known as typhoid toxin, in in vivo models of murine chronic infections. Immunocompetent mice were chronically infected with isogenic S. enterica, serovar Typhimurium (S. Typhimurium) strains, encoding either a functional (MC71-TT) or an inactive (MC71-DcdtB) typhoid toxin.
Keywords: salmonella typhimurium, bacterial genotoxins, typhoid toxin, chronic infection, mice model

overall_design: Transcriptomic analysis was performed on intestine tissues (colon, jejunum and ileum) and liver collected from 129S6/SvEvTac mice, either uninfected or infected with S. typhimurium MC71 strains (strain MC71-TT, expressing a functional typhoid toxin,  and strain MC71-dcdtB, expressing an inactive typhoid toxin) for 60 days

first: Riccardo

last: Guidi

first: Teresa

last: Frisan

first: Thorbjorn

last: Krejsgaard


title: Circadian regulation of Intellectual Disability genes in the hippocampus, a brain oscillator

status: Public on Mar 12 2016

city: 91400 Orsay

first: Florent

last: Dumont

state: Ile de France

address: 17 avenue des sciences

institute: Université Paris-Saclay

summary:
Sleep has been strongly implicated in learning and especially in the reprocessing of recently acquired memory. Children with intellectual disability (ID) tend to have sleep-wake disturbances, which may contribute to the pathophysiology of the disease. As far as sleep is, in part, a circadian process, we decided to study rhythmic gene expression in hippocampus, a brain structure, which plays a key role in memory in human and rodents.
By investigating the transcriptome of mouse adult hippocampus, we report here the identification of 663 circadian rhythm (CR)-regulated genes, which have been clustered in four categories, based on their temporal pattern of expression. In addition to the standard core-clock genes, enrichment analysis of the hippocampal CR-regulated genes revealed the presence of several transcription factors, underlying the existence of an inter-regulation of genes' expression between clusters. Interestingly, these hippocampal circadian rhythm-regulated genes are very enriched in sleep/wakefulness related genes. We show here that glucocorticoid signaling, already shown to be involved in memory regulation, is a circadian regulated pathway in hippocampus. Furthermore, we identified a list of 30 CR-regulated ID genes. Our results demonstrate that hippocampus can be considered as a peripheral oscillator and illustrate the link between circadian rhythm, sleep, intellectual disability and memory consolidation.

overall_design: In order to identify circadian rhythm-regulated genes in mouse hippocampus, we realized a study in dark-dark conditions, thus allowing to overcome the effects induced by light changes. To systematically identify genes with circadian regulated expression, RNA samples from the hippocampus of three mice at four Circadian Time (CT) points were used for expression profiling using Agilent microarray technology. The dark/dark period started at 7 p.m. The Circadian Time (CT) 18 samples were taken after 30 h of continuous dark; the other circadian times followed at 6-h intervals: CT0, CT6 and CT12 after 36, 42 and 48 h of continuous darkness, respectively.

first: Julie

last: Renaud


title: A serial screen for roadblocks to reprogramming identifies the sumoylation effector protein Sumo2

status: Public on Mar 03 2016

city: boston

first: Marti

middle: Anne

last: Borkent

state: Massachusetts

address: 185 cambridge street

department: Center for Molecular Biology

institute: MGH Boston

summary:
The generation of induced pluripotent stem cells (iPSCs) from differentiated cells following forced expression of Oct4, Klf4, Sox2 and c-Myc (OKSM) is slow and inefficient, suggesting that transcription factors have to overcome somatic barriers that resist cell fate change. Here, we performed an ubiased serial shRNA enrichment screen to identify novel repressors of somatic cell reprogramming into iPSCs. This effort uncovered the sumoylation effector protein Sumo2 as one of the strongest roadblocks to iPSC formation. Depletion of Sumo2 both enhances and accelerates reprogramming, yielding transgene-independent, chimera-competent iPSCs after as little as 36 hours of OKSM expression. We further show that the Sumo2 pathway acts independently of exogenous c-Myc expression and in parallel with small molecule enhancers of reprogramming. Critically, suppression of SUMO2 also promotes the generation of human iPSCs. Together, our results reveal sumoylation as a crucial post-transcriptional mechanism that resists the acquisition of pluripotency from fibroblasts using defined factors.
Microarray analysis was performed during reprogramming or of iPSC lines derived upon Sumo2 knockdown

overall_design: Total RNA was isolated from day 6 reprogramming fibroblasts with or without Sumo2 knockdown; as well as stable iPSC clones derived from Sumo2 knockdown fibroblasts.

first: Ori

last: Bar-Nur

first: Konrad

last: Hochedlinger


title: RISC-mediated control of selected chromatin regulators stabilizes ground state pluripotency of mouse embryonic stem cells (RIP)

status: Public on Mar 29 2016

city: Genova

first: Luca

last: Pandolfini

state: Genova

address: Via Enrico Melen 83, Building B

department: Center for Human Technologies

institute: Istituto Italiano di Tecnologia - I

summary: We performed an integrated analysis of RNA and proteins at the transition between naïve ES cells and cells primed to differentiate. During this transition, mRNAs coding for chromatin regulators were specifically released from translational inhibition mediated by RNA-Induced Silencing Complex (RISC). This suggests that, prior to differentiation, the propensity of ES cells to change their epigenetic status is hampered by RNA interference. The expression of these chromatin regulators was reinstated following acute inactivation of RISC, and it correlated with loss of stemness markers and activation of early cell differentiation markers in treated ES cells.

overall_design: Cytoplasmic RNA-protein complexes from mouse embryonic stem cells at different stages of neural in vitro differentiation were immunoprecipitated with anti-Argonaute antibody and analyzed by microarray hybridization

first: Ettore

last: Luzi

first: Dario

last: Bressan

first: Nadia

last: Ucciferri

first: Michele

last: Bertacchi

first: Rossella

last: Brandi

first: Silvia

last: Rocchiccioli

first: Mara

last: D'Onofrio

first: Federico

last: Cremisi


title: human glioma stem cells (GSC) : undifferentiated versus differentiated in presence or absence of active GSK3beta

status: Public on Mar 23 2016

city: Nice

first: Thierry

last: Girolle

address: parc valrose

institute: INSERM CNRS UNSA iBV

summary:
Transcriptional profilling of human GSC comparing undifferentiated (ND) and differentiated (Diff 0.5%) GSC treated or not with TWS119 (LW) an inhibitor of GSK3beta
Glioblastomas (GBM) are the most common form of primary brain tumors. Highly vascularized, infiltrating, resistant to current therapies, they affect patients at different ages. The median survival is shorter than 18 months. GBM follow the cancer stem cell (CSC) model. This concept proposes that a minority of cells within the tumor mass, with long term self-renewal and differentiation properties, is responsible for the initiation and the growth of tumors. CSCs provide all the subtypes of cells that compose the tumor, including endothelial cells and pericytes. Their functional properties are associated with a molecular signature combining makers of neural and/or embryonic stem cells, and markers of mesenchymal cells. A growing body of evidences supports that tumor’s behavior, including proliferation, progression, invasion and – most importantly - a great part of resistance to therapies are determined by these self-renewing tumor cells. It is becoming therefore evident that failure of current treatments to eliminate glioma-initiating cells (GiCs) contributes to tumor recurrence. Targeting GiCs and their stem-like properties constitutes thus one of the main therapeutic challenges to significantly improve anti-cancer treatments. A relevant solution to target GiCs, is to force them to acquire a non self-renewing state. Under this non stem-like state, the cells lose their tumorigenicity and become vulnerable to therapies.  We observed that GiC differentiation is associated to an increase of active GSK3beta expression. Suppression of this activation using a chemical inhibitor (TWS119) altered the differentiation process. To identify transcroptomic changes due to GSK3beta inhibition during differentiation, we have differentiated two GiC cultures (TG1, and TG6) treated or not with TWS119. Total mRNA have been extracted and compared to mRNA extracted from self-renewing TG1 and TG6 cells. For these experiments we used “Agilent human genome whole 44K” chips.

overall_design: two-condition experiment, undifferentiated GSC (ND) vs. Differentiated (diff 0.5%) and undifferentiated GSC (ND) versus differentiated GSC treated with TWS119 (diff 0.5%LW) in monoplicate in TG1 and in TG6 cells (two different primary cultures of GSC).

first: David

last: Debruynes

last: Virolle


title: Lung adenocarcinoma distally rewires hepatic circadian homeostasis

city: Irvine

first: Paolo

last: Sassone-Corsi

state: CALIFORNIA

address: Sprague Hall

institute: University of California, Irvine

summary: Gene expression was performed in WT and tumor-bearing (TB) mice to determine the effects of a lung tumor on circadian clock of the liver.

overall_design: Livers from WT and TB (KrasLSL-G12D;p53fl/fl) mice were harvested over the circadian cycle at ZT 0, 4, 8, 12, 16 and 20 for gene expression analysis.

first: Selma

last: Masri


title: RISC-mediated control of selected chromatin regulators stabilizes ground state pluripotency of mouse embryonic stem cells (RNA)

overall_design: Comparison between EpiSC derived directly from mouse embryonic stem cells and from Epiblast-Like Aggregates


title: The effect of Lats2 knockout and diet on liver disease in mice

status: Public on Mar 17 2016

city: Rehovot

first: Yael

last: Aylon

address: 234 Herzl St.

department: Department of Molecular Cell Biology

country: Israel

institute: Weizmann Institute of Science

summary:
Liver samples of mice harboring liver-specific deletion of Lats2 (Lats2-CKO) were compared to WT mice.
This effect was tested along with the effect of diet - high cholesterol diet (Paigen-PD) vs. normal chow (ND).

overall_design: Expression array analysis on Affymetrix microarrays was carried out for livers from WT and Lats2-CKO mice fed ND or HCD for 9 weeks.

first: Ron

last: Rotkopf

first: Moshe

last: Oren


title: Gene expression data for MACS-isolated primary splenic T cells

status: Public on Feb 25 2016

city: Zhunan

first: Ching-Yu

last: Huang

state: Miao-Li

address: NO. 35, Keyan Rd.,

department: Immunology Research Center

country: Taiwan

institute: National Health Research Institutes

summary:
We are interested in unveiling potential gene expression alterations underlying the T cell-related phenotypes observed in DUSP4-/- mice.
We used microarray to obtain a macroscopic views of gene profiles comparing freshly isolated splenic T cells from WT and DUSP4-/- mice

overall_design: Magnetic-assisted cell sorting isolating T cells to 90-95% purity from freshly prepared splenocytes, followed by immediate RNA extraction.

first: Ching-yu


title: Aspartoacylase-dependent transcriptome changes in immortalized brown adipocytes

status: Public on Feb 29 2016

city: Graz

first: Andreas

last: Prokesch

state: Styria

address: Harrachgasse 21/7

department: Institute of Cell Biology, Histology, and Embryology

country: Austria

institute: Medical University Graz

summary: Here we investigated the effect of stable knock-down of the NAA-catabolizing enzyme, Aspartoacylase (Aspa), on global gene expression in a brown adipocyte cell line.

overall_design: Immortalized brown adipogenic cells (iBACs) with stable Aspa knock-down and control cells were grown until confluence and then differentiated. Cells were harvested on day 7. Experiment was done in triplicates with three different passages.

first: Helmut

middle: J

last: Pelzmann

first: Ariane

last: Pessentheiner

first: Corina

middle: T

last: Madreiter

first: Matthias

last: Schittmayer

first: Barbara

last: Darnhofer

first: Wolfgang

last: Greier

first: Ruth

last: Birner-Grünberger

first: Juliane

middle: G

last: Bogner-Strauss


title: Global hepatic gene expression data from PPARa liver KO, PPARa liver WT, PPARaKO and WT male mice treated or not with Fenofibrate

status: Public on Feb 20 2016

city: Toulouse

first: Alexandra

last: Montagner

address: 180 Chemin de Tournefeuille

institute: INRA

summary:
Fenofibrate is a specific agonist of the nuclear receptor PPARa. To identify the gene expression under the strict dependence of hepatic PPARa activity, we generated a new mouse strain of PPARa-specific deletion in hepatocyte (albumin-Cre+/- Pparaflox/flox or LKO) and we compared them to total Ppara KO (KO), wild-type (WT) and liver WT (albumin-Cre-/- Pparaflox/flox or LWT) mice.
We used microarrays to detail the global programme of gene expression in liver of Ppara LKO, LWT, Ppara KO and WT male mice.

overall_design: There are 36 liver samples, each from an individual mouse. The samples are from Ppara liver KO (LKO), Ppara KO (KO), wild-type (WT) and liver WT (LWT) male mice of 14 week-old from the same genetic background (C57Bl/6J) treated with Fenofibrate (100 mg/kg/day) or vehicle (aqueous solution of gum Arabic 3%) by daily gavage for 10 days. n= 4 mice for LKO, LWT and WT genotypes treated with vehicle; n=3 for KO mice treated with vehicle; n=5 mice for LWT, LKO and KO genotypes treated with fenofibrate; n=4 WT mice treated with fenofibrate.  All mice were sacrified at ZT14.

first: Arnaud

last: Polizzi

first: Yannick

last: Lippi

first: Walter

last: Wahli

first: Hervé

last: Guillou


title: CARD9 impacts colitis by altering gut microbiota metabolism of tryptophan into aryl hydrocarbon receptor ligands

city: Paris

first: Bruno

last: LAMAS

address: 27 rue Chaligny

department: CHU St Antoine

institute: Unité INSERM 1157/UMR 7203

summary: It is crucial to decipher the host-microbiota interactions as they are involved in intestinal homeostasis and diseases. Caspase Recruitment Domain 9 (Card9) is an inflammatory bowel disease (IBD) susceptibility gene coding for an adapter protein for innate immunity toward many microorganisms. Card9 mediates colitis recovery via interleukin 22 pathway activation and Card9-/- mice have enhanced susceptibility to colitis. To reveal the mechanisms responsible of this defect in Card9-/-mice, we compared colon transcriptomics in WT and Card9-/- mice before and during DSS-induced colitis. Mice transcriptomes clusterized according to the genotype supporting a pattern clearly different in WT and Card9-/- mice. The number of up-regulated genes at day 7 was largely higher in Card9-/- compared to WT mice. Pathway analyses of the induced transcripts showed a dominance of immune-related pathway with a stronger signal in Card9-/- mice. Interestingly, NOD-like receptor signaling pathway, in which CARD9 is involved, was an exception with weaker activation in Card9-/- than in WT mice. During the recovery period at day 12, pathways involved in cell proliferation and replication were significantly activated in WT compared to Card9-/- mice confirming the healing defect in Card9-/- mice. Results published in Nature Medicine, doi:10.1038/nm.4102

overall_design: For the induction of colitis, mice were given drinking water supplemented with 2% (w/v) Dextran sulphate sodium (DSS) for 7 days, then allowed to recover by drinking water alone for 5 additional days. 3 mice of each groups (WT and Card9-/-) were sacrified before DSS administration. 5 WT mice and 5 Card9-/- mice were sacrified 7 days after DSS administration and 5 mice of each group were sacrified at day 12.

last: Lamas

first: Mathias

middle: L

last: Richard

first: Valentin

last: Leducq

first: Hang-Phuong

last: Pham

first: Marie-Laure

last: Michel

first: Gregory

last: Da Costa

first: Chantal

last: Bridonneau

first: Sarah

last: Jegou

first: Thomas

middle: W

last: Hoffmann

first: Jane

last: Natividad

first: Loic

last: Brot

first: Soraya

last: Taleb

first: Aurélie

last: Couturier-Maillard

first: Isabelle

last: Nion-Larmurier

first: Fatiha

last: Merabtene

first: Philippe

last: Seksik

first: Anne

last: Bourrier

first: Jacques

last: Cosnes

first: Bernhard

last: Ryffel

first: Laurent

last: Beaugerie

first: Jean-Marie

last: Launay

last: Langella

first: Ramnik

last: Xavier

first: Harry

last: Sokol


title: Expression data of the NOTCH1 leukemia mouse model

status: Public on Mar 21 2016

city: tian jin

first: hongyan

last: zhang

state: Other(国外)

address: nanjing road 288

department: SKLEH

institute: PUMC

summary:
We established the NOTCH1 leukemia mouse model, and then established the iPS model from the leukemia cells.
We used microarrays to detail the gene expression of  leukemia cells, the partially reprogrammed cells and the iPS cells.

overall_design: Colonies were picked up for RNA extraction on Affymetrix microarrays. We handled the groups at four stages:  Leukemia cells, GFP+ cells, GFP- cells, iPS cells..

first: Hongyan

last: Zhang

first: Tao

last: Cheng


title: Global hepatic gene expression data from PPARa liver KO, PPARa liver WT, PPARaKO and WT male mice fed ad libitum, fasted for 24 hours and re-fed

first: Alexandra

last: Montagner

summary:
If the function of the nuclear receptor PPARa is well-known during a prolongated fasting, its hepatic biological function during feeding and refeeding conditions still needs to be investigated. Moreover, in vivo data collected so far on PPARa function during fasting were obtained using the total Ppara KO transgenic mouse model. To identify genes whose expression is under the strict dependence of hepatic PPARa activity, we generated a new mouse strain of PPARa-specific deletion in hepatocyte (albumin-Cre+/- Pparaflox/flox or LKO) and we compared them to total Ppara KO (KO), wild-type (WT) and liver WT (albumin-Cre-/- Pparaflox/flox or LWT) mice under three nutritional challenges.
We used microarrays to detail the global programme of gene expression in liver of Ppara LKO, LWT, Ppara KO and WT male mice fed ad libitum, fasted for 24 hours and refed.

overall_design: There are 52 liver samples, each from an individual mouse. The samples are from Ppara liver KO (LKO), Ppara KO (KO), wild-type (WT) and liver WT (LWT) male mice of 8 week-old from the same genetic background (C57Bl/6J) fed ad libitum, fasted for 24 hours, fasted for 24 hours and then refed 24 hours more with glucose added in water (200g/l). In fed condition (Fed), n= 3 mice for LKO, LWT genotypes, n= 5 for KO and n= 4 fot WT; in fasting condition (Fas), n=5 for LKO, LWT and WT genotypes and n= 3 for KO; in refeeding condition (Ref), n= 5 for LKO, KO and WT genotypes and n= 4 for LWT. All mice were sacrified at ZT14.

first: Arnaud

last: Polizzi

first: Yannick

last: Lippi

first: Walter

last: Wahli

first: Hervé

last: Guillou


title: Gene expression profiles of OSKH iPSCs, OSK iPSCs and ESC

status: Public on May 26 2016

city: San Francisco

first: Akira

last: Kunitomi

address: 1650 Owens Street

institute: The J. David Gladstone Institutes

summary: Induced pluripotent stem cell (iPSC) generation is similar to somatic cell nuclear transfer in oocytes, and this procedure can be used to generate ESCs, which suggests the contribution of oocyte-specific constituents. Here, we show that the mammalian oocyte-specific linker histone H1foo has beneficial effects on iPSC generation. Induction of H1foo with Oct4, Sox2, and Klf4 (OSKH) significantly enhanced the efficiency of iPSC generation. H1foo promoted in vitro differentiation characteristics with low heterogeneity in iPSCs. H1foo enhanced the generation of germline competent chimeric mice from iPSCs in a manner similar to that for ESCs. These findings indicate that H1foo contributes to the generation of higher-quality iPSCs. This experiment was designed to investigate the similarity of global gene transcriptome profile among OSKH iPSCs, OSK iPSCs and ESC.

overall_design: Undifferentiated four replicates of OSKH iPSCs, three replicates of OSK iPSCs (control group) and ESC were collected and applied in this experiment.

first: Shinsuke

last: Yuasa


title: KDM6 Inhibition induces DNA Damage Response (DDR) during ESC Differentiation but not during self-renewal.

status: Public on Mar 11 2016

city: Würzburg

first: Claus

middle: Juergen

last: Scholz

address: Josef-Schneider-Str. 2

department: Core Unit SysMed

institute: University Hospital Würzburg

summary:
The discovery of the first histone demethylase in 2004 (LSD1/KDM1) opened new avenues for the understanding of how histone methylation impacts cellular functions. A great number of histone demethylases have been identified since, which are potentially linked to gene regulation as well as to stem cell self-renewal and differentiation. KDM6A/UTY and KDM6B/JMJD3 are both H3K27me3/2-specific histone demethylases, which are known to play a central role in regulation of posterior development, by regulating HOX gene expression. So far nothing is known about the role of histone lysine demethylases (KDMs) during early hematopoiesis. We are studying the role of KDM6A and KDM6B on self-renewal, global gene expression and on local and global chromatin states in embryonic stem cells (ESCs) and during differentiation. In order to completely abrogate KDM6 demethylase activity in ESCs we employed a specific inhibitor (GSK-J4, Kruidenier et al. 2012). Treatment of ESCs with GSK-J4 had no effect on viability and proliferation . However, ESC differentiation in the presence of GSK-J4 was completely abrogated. In conclusion we show that ESC differentiation is completely blockend in the absence of any H3K27 demethylase activity.
We used microarrays to detail  the global gene expression program of genes which are differentially expressed during the early differentiation of ESC derived embryoid bodies (EBs) in the presence of GSK-J4 (KDM6 Inhibitor).

overall_design: ESCs (R1) have been cultured and differentiated in the presence of GSK-J4 a KDM6 specific inhibitor.

first: Christine

last: Hofstetter

first: Heike

last: Weber

first: Albrecht

last: Müller

first: Matthias

last: Becker


title: PBX3 cooperates with MEISI in causing rapid acute myeloid leukemia and recapitulates the core transcriptome of MLL-rearranged leukemia

city: Monrovia

first: Jianjun

last: Chen

department: Systems Biology

institute: Beckman Research Institute of City of Hope

summary: To investigate whether co-expression of PBX3/MEIS1 can mimic that of MLL-AF9, HOXA9/MEIS1 or HOXA9/PBX3 in inducing leukemogenesis, we conducted in vivo mouse bone marrow transplantation (BMT) assays. Briefly, normal mouse bone marrow (BM) progenitor (i.e., lineage negative; Lin-) cells collected from B6.SJL (CD45.1) donor mice (CD45.1) were retrovirally co-transduced with MSCVneo-MLL-AF9+MSCV-PIG (MLL-AF9), MSCVneo-HOXA9+MSCV-PIG (HOXA9), MSCVneo-HOXA9+MSCV-PIG-MEIS1 (HOXA9+MEIS1), MSCVneo-HOXA9+MSCV-PIG-PBX3 (HOXA9+PBX3), MSCV-PIG-PBX3+MSCVneo-MEIS1 (PBX3+MEIS1), MSCVneo+MSCV-PIG-PBX3 (PBX3) , MSCVneo+MSCV-PIG-MEIS1 (MEIS1), or MSCVneo+MSCV-PIG (normal control; NC). Retrovirally transduced cells then were cultured with cytokines as well as puromycin and G418. Seven days later, the donor cells were transplanted into lethally irradiated (960 rads) 8- to 10-week-old C57BL/6 (CD45.2) recipient mice. The transplanted mice were watched for leukemogenesis. Then, gene expression profiling was conducted with bone marrow samples collected from leukemia groups and control group.

overall_design: A total of 20 mouse BM samples including 15 mouse AML samples with 3 each of the MLL-AF9, HOXA9+MEIS1, HOXA9+PBX3, HOXA9, and PBX3+MEIS1 groups, along with 5 samples from the normal control (NC) group, were analyzed by use of Affymetrix GeneChip Mouse Gene 2.0 ST Array (Affymetirx, Santa Clara, CA). For each sample, the CD45.1+ cells (i.e., transplanted donor cells) were sorted with flow cytometry from whole BM cells collected from BMT recipient mice at the end stage. Then total RNA was isolated by use of miRNeasy extraction kit (Qiagen, Valencia, CA).

first: Zejuan

last: Li

first: Ping

first: Zhixiang

last: Zuo

first: Abdel

last: Elkahloun

first: Paul

middle: P

last: Liu


title: Non-alcoholic steatohepatitis causes selective CD4+ T cell loss and promotes hepatocarcinogenesis

status: Public on Mar 10 2016

city: BETHESDA

first: PING

last: JIN

state: MD

address: 9000 ROCKVILLE PIKE

department: DTM

institute: CC/DTM/NIH

summary: Hepatocellular carcinoma (HCC) is the second most common cause of cancer related death. NAFLD affects a large proportion of the US population. Its incidence and prevalence are increasing to epidemic proportions around the world and is known to increase the risk of HCC. We studied how intrahepatic lipids affect adaptive immunity and HCC development in different murine models of NASH and HCC. Linoleic acid, a fatty acid found in NAFLD caused a selective loss of hepatic CD4+ but not CD8+ T cells leading to accelerated hepatocarcinogenesis. CD4+ T cells were more dependent on oxidative phosphorylation for energy source than CD8+ T cells, and disruption of oxidative phosphorylation by linoleic acid caused more severe damage in CD4+ T cells leading to selective loss of these cells. In vivo blockade of ROS using n-acetylcysteine reversed the NASH-induced hepatic CD4+ T cell decrease and delayed NASH-promoted HCC. Our results provide a new link between lipid metabolism and impaired anti-tumor surveillance.

overall_design: The samples are isolated CD4 or CD8 T cells co-cultured with linoleic acid or not. The aim of the particular  experiment is to study the any possible different response between CD4 and CD8 T cells to linoleic acid.

first: Chi

last: Ma

first: Aparna

last: Kesarwala

first: Tobias

last: Eggert

first: Jose

last: Medina-Echeverz

first: David

last: Kleiner

last: Jin

last: Stroncek

first: Masaki

last: Terabe

first: Veena

last: Kapoor

first: Giorgio

last: Trinchieri

first: Mei

last: ElGindi

first: Miaojun

last: Han

first: Dean

last: Felsher

first: Daniel

last: McVicar

first: Mathias

last: Heikenwälder

first: Armin

first: Tim

last: Greten


title: Liver tissue from liver specific Vps33b knockout (Vps33bfl/fl-AlfpCre) and control (Vps33bfl/fl) mice

status: Public on Jun 10 2016

city: London

first: Paul

last: Gissen

state: London

address: Gower Street

department: LMCB

institute: UCL

summary:
Liver tissue from Vps33b liver ko (Vps33bfl/fl-AlfpCre) mice is a model of liver disease associated with ARC syndrome, an autosomal recessive inherited metabolic disorder cause by mutations in VPS33B or VIPAS39.
ARC is a multisystem disorder, with liver and kidneys affected in particular. Defects in hepatocyte polarity have been identified.
Affymetrix arrays were used to characterise the changes in the liver transcriptome when Vps33b is not expressed.

overall_design: Mouse liver tissue, 10 samples in total, 4 from control mice, 6 from ko mice.

first: Joanna

last: Hanley

first: Banushi

last: Blerida

first: Anna

last: Straatman-Iwanowska

first: Clare

last: Rogerson

first: Lyne

last: Anne-Marie

first: Holly

last: Smith


status: Public on Mar 01 2016

city: Valencia

first: Francisco

middle: García

last: García

address: Eduardo Primo Yúfera, 3

department: Bionformatics & Biostatistics Unit

country: Spain

institute: CIPF

summary:
Expression data from wild type or Gdap1-null Mouse Embryonic Fibroblasts before and 4 days after transduction with the reprogramming factors Oct4, Sox2, Klf4 and cMyc
We used microarrays to detail the global programme of gene expression underlying cell reprogramming

overall_design: Total RNA from wild type or Gdap1-null Mouse Embryonic Fibroblasts was extracted before or at day 4 of reprogramming and hybridised on affymetrix microarrays

first: Javier

last: Prieto

first: Marian

last: Leon

first: Xavier

last: Ponsoda

last: García-García

first: Eva

last: Serna

first: Roque

last: Bort

first: Joaquín

last: Dopazo

first: Carlos

last: López-García

first: Josema

last: Torres


title: Defining the molecular mechanisms underlying immunological memory in T cells (expression)

status: Public on Feb 02 2016

city: Freiburg

first: Pierre

middle: Daniel

last: Cauchy

state: Baden-Württemberg

address: Breisacher Str. 115

department: Zentrum für Translationale Zellforschung

institute: University Medical Center Freiburg

summary: Immunological memory is a defining feature of animal development, allowing rapid responses to repeat infections, yet the very basis of T cell-dependent memory remains poorly understood. Here we demonstrate that the critical steps in the acquisition of T cell memory occur not after completion of T cell differentiation but during the initial activation phase of naïve T cells, when extensive chromatin remodelling reprograms immune response genes towards a stably maintained primed state. During this process, inducible factors including AP-1 create hundreds of DNase I hypersensitive sites (DHSs), allowing the recruitment of ETS1 and RUNX1 to sites that were previously inaccessible. Significantly, these DHSs remain temporally and mitotically stable long after cessation of AP-1 activation, and function to maintain regions of active chromatin in the vicinity of genes that regulate immune responses. This priming enables increased accessibility and the accelerated induction of other inducible regulatory elements in previously activated T cells.

overall_design: Examination of gene expression patterns in naïve, blast, memory T-cells with or without PMA activation via microarray study.

first: Sarah

last: Bevington

first: Piper

last: Jason

first: Bertrand

last: Elizabeth

first: Lalli

last: Naveen

first: Sascha

last: Ott

first: Constanze

last: Bonifer

first: Peter

last: Cockerill


title: RISC-mediated control of selected chromatin regulators stabilizes ground state pluripotency of mouse embryonic stem cells (RNAi)

first: Luca

last: Pandolfini

summary: We performed an integrated analysis of RNA and proteins at the transition between naïve ES cells and cells primed to differentiate. During this transition, mRNAs coding for chromatin regulators were specifically released from translational inhibition mediated by RNA-Induced Silencing Complex (RISC). This suggests that, prior to differentiation, the propensity of ES cells to change their epigenetic status is hampered by RNA interference. The expression of these chromatin regulators was reinstated following acute inactivation of RISC, and it correlated with loss of stemness markers and activation of early cell differentiation markers in treated ES cells.

overall_design: We assayed the impact of the functional inhibition of chromatin regulators on cell priming inhibiting chromatin remodeling activities by either pharmacological or genetic interference.

first: Ettore

last: Luzi

first: Dario

last: Bressan

first: Nadia

last: Ucciferri

first: Michele

last: Bertacchi

first: Rossella

last: Brandi

first: Silvia

last: Rocchiccioli

first: Mara

last: D'Onofrio

first: Federico

last: Cremisi


title: Unexpected distinct roles of the related histone H3 lysine 9 methyltransferases G9a and G9a-Like Protein in myoblasts

status: Public on Feb 01 2016

first: PONTIS

last: Julien

address: 35, rue Hélène BRION

institute: UMR7216 CNRS

summary: Lysine methyltransferases G9a and GLP (G9a- Like Protein) form functional heterodimeric complexes that establish mono- and dimethylation on histone H3 lysine 9 (H3K9me1, H3K9me2) in euchromatin. Here we describe unexpected opposite individual roles for G9a and GLP during skeletal muscle terminal differentiation. Indeed, gain- or loss-of-function assays in myoblasts showed that in consistency with previous reports that G9a inhibits terminal differentiation. But GLP plays a more complicated role in muscle differentiation since both knockdown and overexpression inhibits terminal differentiation. Unexpectedly, in contrast to G9a, we show that GLP overexpression promotes abnormal expression of muscle differentiationspecific genes in proliferating myoblasts. Transcriptomic analysis indicates that G9a and GLP regulate different sets of genes. GLP, but not G9a, inhibits at the transcriptional level proteasome subunit-encoding genes resulting in an inhibition of the proteasome activities. Subsequently, GLP, but not G9a, overexpression stabilizes MyoD that is likely to be responsible for muscle markers expression in proliferating myoblasts.

overall_design: Microarray has been perform in duplicate or triplicate on total extract RNA from C2C12 cells (siRNA control, siRNA against G9a or Glp)

first: V

last: Batistti


title: Comparison of wt, Krt18+/- and Krt18-/- non-tumorous liver tissues at the age of 3, 6 and 12 months [gene expression]

status: Public on May 04 2016

first: Vendula

last: Svendova

address: Auenbruggerplatz 2

summary: Analysis of the different genotypes of non-tumorous mouse livers in 3 different ages revealed more genetic alterations in Krt18-/- and Krt18+/- compared to wt livers. This speaks in favor of a higher genomic instability being causally related to K-deficiency and aging, even at a preneoplastic stage.

overall_design: Wild type healthy liver tissue vs. healthy Krt18+/- / healthy Krt18-/- at the age of 3, 6 and 12 months (35 samples)

first: Kira

last: Bettermann

first: Johannes

last: Haybaeck


title: Expression data from induced parvalbumin neurons.

status: Public on Mar 12 2016

city: Beijing

first: Jianwei

last: Jiao

state: Beijing

address: 1 Beichen West Road

department: State Key Laboratory of Reproductive Biology

institute: Institute of Zoology, Chinese Academy of Sciences

summary:
Parvalbumin neurons, as an important subtype of inhibitory neurons, play a crucial role in the brain. The dysfunctions of those cells are associated with multiple neural system disorders. We carried out whole gene expression studies for the induction process of parvalbumin neurons.
We used microarrays to detail the global program of gene expression underlying cellularization and identified distinct classes of up-regulated genes during this process.

overall_design: Induced parvalbumin neuron cells were selected at successive stages of induction process for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain homogeneous populations of induced parvalbumin neurons at each developmental stage in order to increase the temporal resolution of expression profiles.

first: Zixiao

last: Shi


title: How C/EBPa creates an elite cell state for reprogramming to pluripotency [array]

status: Public on Feb 19 2016

first: samuel

last: Collombet

address: 46 rue d'Ulm

department: Biology

institute: Ecole Normale Superieure

summary: Mouse Bcell, upon ectopic expression of the transcription factor Cebpa for 18h, can be reprogrammed to iPS with extremely high efficiency. To understand the molecular control of this phenomena we performed multiple high throughtput functional genomic analysis.

overall_design: Transcriptomic by microarray in Bcell, Bcell+Cebpa18h, Bcell+Cebpa18h+OKSM1d, Bcell+Cebpa18h+OKSM2d, ES cells

first: Bruno

last: di Stefano

first: Samuel

first: Janus

last: Jakobsen

first: Andreas

last: Lackner

first: Thomas

last: Graf


title: Expression data from small intestine crypts of Zfp148gt/+APCMin/+ and Zfp148+/+APCMin/+ mice

status: Public on Feb 10 2016

city: Gothenburg

first: Per

last: Lindahl

address: Sahlgrenska University Hospital, Bruna Straket 16

department: Institute of Medicine

country: Sweden

institute: University of Gothenburg

summary:
The transcription factor Zinc finger protein 148 (Zfp148) interacts physically with the tumor suppressor p53, but the siginficance of this interaction is not known. We recently showed that knockout of Zfp148 in mice leads to ectopic activation of p53 in tissues and cultured fibroblasts, suggesting that Zfp148 represses p53 activity.
Here we hypothesized that targeting Zfp148 would unleash p53 activity and protect against cancer development, and test this idea in the APCMin/+ mouse model of intestinal adenomas.

overall_design: Crypt-enriched tissues were isolated by laser microdissection (PALM) from the small intestines (proximal) of Zfp148gt/+APCMin/+ and Zfp148+/+APCMin/+ mice for RNA extraction and hybridization to Affymetrix microarrays.

first: Anna

last: Nilton

first: Volkan

middle: I

last: Sayin


title: Global hepatic gene expression data from germ free and specific pathogen free male mice.

first: Alexandra

last: Montagner

summary:
Liver clock regulates transcription of hepatic genes in response to feeding. To explore the possibility that the microbiome influences this process, we measured the liver transcriptome in normal mice (Specific Pathogen Free or SPF mice) and compared it to the transcriptome in mice lacking microbiota (Germ Free or GF mice) at different time points over 24h.
We used microarrays to detail the global programme of gene expression in liver of GF and SPF 10-12 weeks-old male C57Bl/6 male mice.

overall_design: There are 40 liver samples, each from an individual mouse. The samples are from germ free mice (GF) and specific pathogen free mice (SPF). Mice of both types were sacrificed at four time points: Zeitgeber Time 0, 6, 12, and 18. There are five replicates per condition.

first: Agata

last: Korecka

first: Velmurugesan

last: Arulampalam

first: Hervé

last: Guillou

first: Sven

last: Pettersson

first: Walter

last: Wahli


title: Altered RNA expression in parenteral nutrition mouse model

city: Piscataway

first: Le

last: Zhan

state: NJ

address: 170 Frelinghuysen Rd

department: Pharmacology and Toxicology

institute: Rutgers University

summary:
We reported altered RNA expression profiles in wild-type (WT) C57BL/6J mice upon parenteral nutrition treatment compared to saline infusion controls.
RNA samples used were isolated from the livers of PN or saline infused mice. RNA samples from 3 saline or 3 PN mouse livers were pooled, respectively. Final fold change were calculated by normalize the signal intensity of each probe in PN sample to that of the saline sample.

overall_design:
On day 1, jugular vein catheterization survival surgery was performed on mouse (age 6-10 weeks).On day 2, the catheter was connected to an infusion line and the mouse was transferred to a metabolic cage. Surgical mice then started to receive saline infusion. On day 3, surgical mice started receiving either parenteral nutrion (PN), or saline infusion as control. Food was removed from the cage for mice in the PN group. Mice in saline group continue to have access to food. On day 11, PN and saline control mice were sacrificed and tissues (liver, ileum and colon) were collected for RNA isolation. After RT-qPCR verification, RNA samples from the same tissues from 3 PN mice and 3 saline mice were pooled, respectively. Pooled RNA samples for liver, ileum and colon tissues were then used for microarray analysis.

Please note that only liver samples have been submitted and that sample data table contains the data filtered by 1.5-fold cutoff.

first: Grace

last: Guo


title: Gene expression in fetal aortic arteries of C57BL/6 mice with Nod1 stimulation

status: Public on Jan 31 2016

city: Fukuoka

first: Hirosuke

last: Inoue

state: Fukuoka

address: 3-1-1, Maidashi, Higashi-ku

department: Department of Pediatrics

institute: Graduate School of Medical Sciences, Kyushu University

summary: We previously demonstrated that an innate immune receptor, the nucleotide-binding oligomerization domain-1 (Nod1), was involved in the vascular disease in young and adult mice. However, little is known about the role of Nod1 signaling in fetuses. We administered FK565, one of the Nod1 ligands, to pregnant C57BL/6 mice and examined its effect in the fetuses. Nod1 stimulation increased levels of cytokines in the pregnant mice, placentae and fetuses. We found that FK565 which was administered to the pregnant mice transferred to the fetuses through the placentae, and exerted its effects on fetuses in vivo. Nod1 was abundantly expressed in the arteries, and the vascular tissues predominantly produced CCL2 and IL-6 in response to FK565 compared with other fetal tissues. FK565 induced up-regulation of genes associated with immune response, inflammation and apoptosis in fetal vascular tissues.

overall_design: To explore the molecular mechanism of direct responses of fetal vascular system by Nod1 ligand in vivo, Nod1 -/- females  were mated with Nod1 +/- males , and pregnant mice were subcutaneously injected with 500 μg FK565 at E18.5. Six hours later, aortic arteries of the fetuses were sterilely separated. Microarray analysis was performed on aortic arteries from Nod1 +/- (n=3) and Nod1 -/- (n=3) littermate fetuses.

first: Toshiro

last: Hara


title: Expression data from mouse adrenal glands extracted from wild-type and sf1:Cre; Prkar1a Fl/Fl (KO) adrenals

status: Public on Feb 06 2016

city: Aubiere

first: Pierre

last: Val

address: 24 avenue des Landais

institute: CNRS

summary:
Prkar1a encodes one of the regulatory subunits of PKA. Prkar1a gene ablation in the adrenal cortex is associated with profound phenotypic alterations, constitutive PKA activation and reciprocal inhibition of WNT signallilng pathway
We used microarrays to analyse gene expression in response to Prkar1a gene ablation

overall_design: Adrenal glands were dissected from KO (4) and wild-type littermate (4) mice

first: Antoine

last: Martinez


title: Cell-of-origin specific 3D genome structure acquired during somatic cell reprogramming [Expression]

city: Utrecht

first: Elzo

last: de Wit

address: Uppsalalaan 8

country: Netherlands

institute: Hubrecht Institute

summary: We studied genome topology dynamics during reprogramming of different somatic cell types with highly distinct genome conformations. We find large-scale TAD repositioning and alterations of tissue-restricted genomic neighborhoods and chromatin loops, effectively erasing the somatic cell specific genome structures while establishing an embryonic stem cell-like 3D genome. Yet, early passage iPSCs carry topological hallmarks that enable discerning their cell-of-origin. These hallmarks are not remnants of somatic chromosome topologies. Instead, the distinguishing topological features are acquired during reprogramming, as we also find for cell-of-origin dependent gene expression patterns.

overall_design: Transcriptome analysis was performed in somatic cells (NSC, macrophages, MEFs and pre-B cells) and their corresponding early and late induced pluripotent stem cells. In addition, expression analysis was performed in E14 embryonic stem cells

first: Wouter

last: de Laat


title: Effect of STAT3c on the gene expression of MKN28 gastric cancer cells

status: Public on Feb 27 2016

city: Chia-Yi

first: Jora

middle: Meng-Ju

last: Lin

address: 168 UNiversity Road,Min Hsiung

institute: National Chung Cheng University

summary: To investigate the effect of STAT3 activation on the expression of gastric cancer cells, expression profile was compared in MKN28 cells overexpressed with control vector vs mouse constitutively activated STAT3 mutant (STAT3c).

overall_design: MKN28 gastric cancer cells were transfected with pcDNA3.1 (vector control) or plasmid overexpressing STAT3c (treatment). Stable clones were selected for RNA extraction and expression microarray analysis (Agilent). Experiments were repeated twice.

first: Liang-Yu

last: Chang

middle: M

first: Michael

last: Chan


title: Shear flow vs. static culture of d9 and d12 megakaryocytes

city: Newark

first: Eleftherios

last: Papoutsakis

state: DE

address: 15 Innovation Way

department: Chemical and Biomolecular Engineering

institute: University of Delaware

summary:
d9 and d12 Mks were either cultured statically or subjected to shear flow for 30 min; at d9, half the Mks were placed back in culture for 30 min (60 min time point)
Megakaryocytes (Mks) are exposed to shear flow as they migrate from the bone marrow hematopoietic compartment into circulation thus releasing platelets and pro/preplatelets directly into the blood stream. Shear forces have been now established as promoting Mk maturation and platelet biogenesis. In order to understand the underlying mechanisms that modulate the response of Mks to shear forces, we carried out transcriptional analysis on immature and mature stem cell-derived Mks that were exposed to physiologically-relevant shear (2.5 dyn/cm2). In immature (d9) Mks, shear exposure upregulated genes related to growth and Mk maturation, while in mature (d12) Mks, it upregulated genes involved in apoptosis and intracellular transport. Following shear-flow exposure, 6 AP-1 transcripts (ATF4, JUNB, JUN, FOSB, FOS, and JUND) were upregulated at d9 and two AP-1 proteins (JunD and c-Fos) were upregulated both at d9 and d12. Our data show that MAPK signaling is linked to both the shear-stress response and AP-1 upregulation. JNK phosphorylation increased significantly following shear stimulation, while JNK inhibition reduced shear-induced JunD protein expression. Although p38 phosphorylation did not increase following shear flow, its inhibition reduced shear-induced JunD and c-Fos protein expression. JNK inhibition reduced fibrinogen binding of d9 and d12 platelet-like particle s (PLPs) and P-selectin expression at d12 PLPs, while p38 inhibition reduced fibrinogen binding of d12 PLPs. Here we show  that mechanotransduction of shear forces in Mks results in JNK activation, AP-1 upregulation, and downstream transcriptional changes that promote maturation of immature Mks and platelet biogenesis in mature Mks.

overall_design: Two- and Three-condition experiment (flow vs. static culture condition, d9 vs. d12, and 30 min vs. 60 min at d9); Biological replicates: 3; Technical replicates: 1 (dye-swap)

first: Stephanie

middle: A

last: Luff


title: Expression data from a cell model of Huntington disease

status: Public on Jan 25 2016

city: Boston

first: Guo-Lin

last: Chen

address: 360 Huntington Avenue

institute: Northeastern University

summary:
Huntington disease (HD) is associated with increased nuclear accumulation of the repressor element-1 silencing transcription factor (REST) which govens a huge gene network. An alternative REST splicing event (∆E3) eliminates a motif essential for nuclear targeting of REST.
We used Affymetrix’s GeneChip® Mouse Gene 2.0 ST Array to compare global transcription between STHdhQ111/Q111 cells (a cell model of HD) treated with specific antisense oligos (ASOs) inducing  ∆E3 and a control oligo, with a comparison to normal STHdhQ7/Q7 cells.

overall_design: STHdhQ111/111 cells were treated with specific ASOs (inducing ∆E3) or a control oligo, and STHdhQ7/Q7 cells treated with a control oligo was used for a normal control. 3 representative total RNA samples (one for each group) of high quality were subject to transcriptional profiling.

first: Gregory

last: Miller


title: Autophagy enforces functional integrity of regulatory T cells by coupling environmental cues and metabolic homeostasis

city: Memphis

first: Geoffrey

last: Neale

state: TN

address: 262 Danny Thomas Place

department: Hartwell Center

institute: St Jude Childrens Research Hospital

summary: Regulatory T (Treg) cells respond to immune and inflammatory signals to mediate immunosuppression, but how the functional integrity of Treg cells is maintained under activating environments is unclear. Here we show that autophagy is active in Treg cells and supports their lineage stability and survival fitness. Treg cell–specific deletion of Atg7 or Atg5, both essential genes in autophagy, leads to loss of Treg cells, greater tumor resistance and development of inflammatory disorders. Atg7-deficient Treg cells show increased apoptosis and readily lose expression of the transcription factor Foxp3, especially after activation. Mechanistically, autophagy deficiency upregulates mTORC1 and c-Myc and glycolytic metabolism, which contributes to defective Treg function. Therefore, autophagy couples environmental signals and metabolic homeostasis to protect lineage and survival integrity of Treg cells in activating contexts.

overall_design: We used microarrays to explore the gene expression profiles differentially expressed in CD4+Foxp3-YFP+ Treg cells from untreated and rapamycin-treated Atg7+/- (Atg7-het; Atg7 +/fl crossed with Foxp3-Cre) and Atg7-/-  (Atg7-KO; Atg7 fl/fl mice crossed with Foxp3-Cre) mice

first: Jun

last: Wei

first: Hongbo

last: Chi


title: Human melanocytes: Control vs. RAS or BRAF Infected

city: heidelberg

first: Lionel

last: Larribere

address: im neuenheimer Feld

institute: DKFZ

summary: Transcriptional profiling of human melanocytes comparing control untreated cells with cells infected with different oncogenic mutations. Goal was to determine the effects of melanoma-associated mutation overexpression on global melanocyte gene expression.

overall_design: Two-condition experiment, non infected vs. infected cells. Two time points. Biological replicates: 2

first: Marisol

last: Soengas


title: EphA4 is Involved in Sleep Regulation But Not in the Electrophysiological Response to Sleep Deprivation

status: Public on Jan 29 2016

city: Montreal

first: Valerie

last: Mongrain

state: QC

address: 333 rue Saint-Antoine Est

department: Research center

institute: CRCHUM

summary: Here, we investigated the role of EphA4 in the molecular response to sleep deprivation by measuring forebrain gene expression in EphA4 KO mice. More precisely, we measured the effect of the mutation and of a 6-h sleep deprivation on genome-wide forebrain gene expression using microarray. Please cite the original paper when you use these data (Freyburger et al., Sleep, 2016)

overall_design:
Molecular response of EphA4 knockout (KO) mice and littermates were studied under a 12 h light: 12 h dark cycle, under undisturbed conditions or 6 h sleep deprivation (SD) by using a Mouse Gene 2.0 ST Array (Affymetrix, Santa Clara, CA, USA)

*** WARNING : The Sample data tables report incomplete data.***

first: M

last: Freyburger

first: N

last: Cermakian

first: V


title: Transmission of survival signals through Delta-like 1 on activated CD4+ T cells

status: Public on Jan 09 2016

city: Tokushima

first: Takahiro

last: Furukawa

address: Kuramoto-Cho 2-50-1

institute: Tokushima University

summary: Notch expressed on CD4+ T cells transduces signals that mediate their effector functions and survival by interacting with Notch ligands on adjacent cells. Although Notch signaling is known to be cis-inhibited by Notch ligands expressed on the same cells, the role of Notch ligands on T cells remain unclear. In this report we demonstrate that the Notch ligand Dll1 on CD4+ T cells transduces signals required for the maintenance of activated CD4+ T cells without affecting Notch signaling in the same cells. T cell-specific Dll1-deficient (Dll1-/-) mice did not show any defect in T cell development in thymus or spleen. Co-transfer of CD4+ T cells from Dll1-/- and control mice into recipient mice followed by immunization revealed a rapid decline of CD4+ T cells from Dll1-/- mice compared with control cells. Dll1-/- mice exhibited lower clinical scores of experimental autoimmune encephalitis than control mice. The expression of Notch target genes in CD4+ T cells from Dll1-/- mice was not affected, suggesting that Dll1 deficiency in T cells does not affect cis Notch signaling. Overexpression of the intracellular domain of Dll1 in Dll1-deficient CD4+ T cells partially rescued impaired survival. Our data highlight Dll1 as an independent regulator of Notch-signaling for the survival of activated CD4+ T cells, and provide new insight into the physiological roles of Notch ligands as well as a regulatory mechanism important for maintaining adaptive immune responses

overall_design: The mRNA expression in activated CD4+ T cells from mouse was obtained by DNA microarray analysis. These mRNA expression was compared.

first: Koji

last: Yasutomo

first: Hideaki

last: Horikawa


title: DNA microarray analysis of PBMCs from Behçet’s disease (BD) patients

status: Public on Jan 21 2016

city: Suita

first: Daisuke

last: Okuzaki

state: Osaka

address: Yamadaoka 3-1

department: Immunology Frontier Research Center

institute: Osaka univ.

summary: To examine if gene expression profiles of many Behçet’s disease (BD) patients are commonly abnormal compared to those of healthy volunteers, we performed a genome-wide complementary DNA microarray analysis using an Agilent Hu44K array; RNA samples were isolated from the PBMCs of 41 individual BD patients (32 females and 9 males) and 17 normal volunteers.

overall_design: A total of 41 two color arrays were performed and each individual array included a target sample and a control sample.

first: Hiroshi

last: Nojima