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Expression data from mouse perigonadal white adipose tissue - various mutant conditions

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Pierre de la Grange

PROVIDER: E-GEOD-51204 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Antagonistic functions of LMNA isoforms in energy expenditure and lifespan.

Lopez-Mejia Isabel C IC de Toledo Marion M Chavey Carine C Lapasset Laure L Cavelier Patricia P Lopez-Herrera Celia C Chebli Karim K Fort Philippe P Beranger Guillaume G Fajas Lluis L Amri Ez Z EZ Casas Francois F Tazi Jamal J

EMBO reports 20140317 5

Alternative RNA processing of LMNA pre-mRNA produces three main protein isoforms, that is, lamin A, progerin, and lamin C. De novo mutations that favor the expression of progerin over lamin A lead to Hutchinson-Gilford progeria syndrome (HGPS), providing support for the involvement of LMNA processing in pathological aging. Lamin C expression is mutually exclusive with the splicing of lamin A and progerin isoforms and occurs by alternative polyadenylation. Here, we investigate the function of lam ...[more]

PMID: 24639560

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ABT-737 treatment induces regulation and activation of pathways implicated in cell survival, proliferation and stem cells in treated AML mice survival, proliferation and stem cells in treated AML mice

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2013-11-06 | E-GEOD-48601 | biostudies-arrayexpress

Expression data from mouse perigonadal white adipose tissue - various mutant conditions [exon-level analysis]

Project description:Progerin-expressing mice (HGPS-like) demonstrated increased energy metabolism and lipodystrophy. Increased mitochondrial biogenesis was found in adipose tissue from HGPS-like mice, whereas lamin C-only mice had fewer mitochondria. Thus we analyse which molecular pathways mediated the changes in adipose tissue caused by lamin C and progerin expression and the roles of these pathways in energy metabolism and aging. 10 cDNAs samples were analysed. We compared the mean fold change of 2 to 4 biological replicates. We performed an unpaired Student’s t-test to compare intensities in the different biological replicates. Genes were considered significantly regulated when the fold change was ? 1.5, and the p-value was ?0.05.

2015-06-05 | E-GEOD-51203 | biostudies-arrayexpress

Argonaute proteins couple chromatin silencing to alternative splicing (exon array)

Project description:While Argonaute (AGO) proteins play a major role in transcriptional gene silencing (TGS) in many organisms, their role in the nucleus of somatic mammalian cells remains elusive. Here, we have purified AGO1 and AGO2 chromatin-embedded complexes, and found these proteins associated with previously described partners, but also with chromatin modifiers and, rather unexpectedly, with different splicing factors. Using the CD44 gene as a model for alternative splicing, we show that both AGO1 and AGO2 are required for Protein Kinase C (PKC)-dependent variant exon inclusion. AGO proteins facilitate the spliceosome recruitment and modulate the elongation rate of RNA polymerase II (RNAPII). The recruitment of AGO proteins to CD44 transcribed region is dependent on both the endonuclease Dicer and the chromodomain-containing protein HP1g, and results in locally increased levels of histone H3 lysine 9 (H3K9) methylation on variant exons. Genome wide analysis of splicing in either AGO2 or Dicer null cells showed that the two proteins have similar effects on many splicing events. Finally, sRNAs associated with nuclear AGO2 are mostly in sense orientation relative to protein-coding genes, supporting a role for intragenic antisense non-coding RNAs in the recruitment AGO and splicing factors. Together, our data demonstrate for the first time that the endogenous RNAi pathway is involved in alternative splicing decisions, unravelling a new model in which AGO proteins couple RNAPII elongation and chromatin modification. Study of AGO2 or Dicer knock-out on gene expression and splicing regulation in MEF cells Transcriptome analysis of AGO2 and Dicer null MEF cells on GeneChipM-BM-. Mouse Exon 1.0 ST Arrays (Affymetrix). Dicer null MEF cells and wild-type MEF cells were from M. Otsuka. AGO2 null MEF cells were from A. Tarakhovsky. Experiment has been done in experimental triplicates. 9 Total samples were analyzed.

2012-09-10 | E-GEOD-39746 | biostudies-arrayexpress

Expression data from mouse perigonadal white adipose tissue - various mutant conditions [gene-level analysis]

2015-06-05 | E-GEOD-51202 | biostudies-arrayexpress

Identification of the altered transcripts in the NMF291–/– cerebellum by exon array.

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2011-10-19 | E-GEOD-33069 | biostudies-arrayexpress

The data of differentially regulated exons from mouse testes - wild-type and Dazap1 mutant

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2013-06-01 | E-GEOD-42603 | biostudies-arrayexpress

Differentially regulated exons from wild-type and Dazap1 mutant mouse testes

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-06-01 | E-GEOD-42604 | biostudies-arrayexpress

Expression data of CD4+T cells from Idiopathic CD4+ T cells lymphopenia (ICL) patients, Sarcoidosis (SARC) and Healthy individuals

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2015-05-15 | E-GEOD-56998 | biostudies-arrayexpress

hCAF1/CNOT7 regulates interferon signaling by targeting STAT1

Project description:Stringent regulation of the interferon signaling pathway is essential for maintaining the immune response to pathogens and tumors. The transcription factor STAT1 is a crucial mediator of this response. Here we show that hCAF1/CNOT7 regulates class I and II interferon pathways at different crucial steps. In resting cells hCAF1 can control STAT1 trafficking by interacting with the latent form of STAT1 in the cytoplasm. IFN treatment induces STAT1 release, suggesting that hCAF1 may shield cytoplasmic STAT1 from undesirable stimulation. Consistent, hCAF1 silencing enhances STAT1 basal promoter occupancy associated with increased expression of a subset of STAT1-regulated genes. Consequently, hCAF1 knockdown cells exhibit an increased protection against viral infection and reduced viral replication. Furthermore, hCAF1 participates in the extinction of the IFN signal, through its deadenylase activity, by speeding up the degradation of some STAT1-regulated mRNAs. Since abnormal and unbalanced JAK/STAT activation is associated with immune disorders and cancer, hCAF1 could play a major role in innate immunity and oncogenesis, contributing to tumor escape. mRNAs from cells expressing the siRNA siRNA duplexes targeting hCAF1, corresponding to the coding region 941-961 (kd) (hCAF1 NCBI Reference Sequence: NM_013354.5) and one non-targeting control siRNA (mock).

2013-12-31 | E-GEOD-43334 | biostudies-arrayexpress

Activation of IFN/STAT1 signaling is a hallmark of response to chemotherapy in patient-derived xenografts of triple-negative breast cancer

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