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Transcriptome analysis of naïve or stimulated WT and TRIM28 KO CD4 T cells (Affymetrix)

ABSTRACT: Critical role for TRIM28 and HP1b/g in the epigenetic control of T cell metabolic reprogramming and effector differentiation The study explores the role of gene silencing by TRIM28, an adaptor protein for histone binding modules , in CD4 T cell function.

ORGANISM(S): Mus musculus

PROVIDER: GSE140444 | GEO | 2019/11/16

REPOSITORIES: GEO

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Transcriptome analysis of naïve or stimulated WT and TRIM28 KO CD4 T cells (RNA-seq)

Project description:Critical role for TRIM28 and HP1b/g in the epigenetic control of T cell metabolic reprogramming and effector differentiation The study explores the role of gene silencing by TRIM28, an adaptor protein for histone binding modules , in CD4 T cell function.

2019-11-16 | GSE140445 | GEO

Transcriptome analysis of WT and TRIM28 KO CD4 T cells, naïve or stimulated with anti-CD3 (plate-bound) and anti-CD28 (soluble) in Th0, Th1, Th2, Th17 or Treg conditions

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PolII ChIP-Seq performed on naïve WT and TRIM28KO CD4 T cells

Project description:Critical role for TRIM28 and HP1b/g in the epigenetic control of T cell metabolic reprogramming and effector differentiation

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H3K9me3 and H3K9Ac ChIP-Seq performed on naïve WT and TRIM28KO CD4 T cells

Project description:Critical role for TRIM28 and HP1b/g in the epigenetic control of T cell metabolic reprogramming and effector differentiation

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Transcriptome analysis of naïve or stimulated WT and TRIM28 KO CD4 T cells (Affymetrix)

Project description:Transcriptome analysis of naïve or stimulated WT and TRIM28 KO CD4 T cells (Affymetrix)

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Comparison of gene expression in Wild type and T cell-specific conditional Trim28 KO in TCR stimulated and un-stimulated naive CD4 positive and T regulatory cells

Project description:A microarray study was performed in unstimulated and TCR-stimulated CD4 + T cells and Treg in wild type and conditional Trim28 KO mice to identify genes that are regulated by Trim28. These experiments constitute a portion of the study described below: Paper Abstract: Peripheral T cell activation and differentiation into specialized effectors are regulated by TCR- and cytokine-mediated signals that induce clonal expansion and unique transcriptional factors. These processes may include active chromatin modification by nuclear factors. In search of such molecules, we found Trim28, a component of large nuclear chromatin-regulatory complex is tightly controlled upon TCR stimulation at the level of phosphorylation, and examined global impact of Trim28 loss in especially CD4+ T cells, by generating T cell-specific conditional Trim28 KO mice (CKO). CD4+ T cells from CKO mice showed defective IL-2 production and T cell proliferation associated with defective upregulation of cell-cycle associated proteins. Accordingly, young CKO showed T-lymphopenia. Surprisingly, Trim28 CKO mice eventually accumulated auto-reactive memory-phenotype T cells that produced inflammatory IL-17. CKO mice are also susceptible to induced auto-inflammatory disease with TH-17 dominant immune response. Loss of Trim28 showed aberrant accumulation of TH-17 and FoxP3+ T cells, two key T cells in inflammation vs. tolerance. We found CKO T cells showed a cell-extrinsic promotion of TH-17 and FoxP3+ T cell development by a mechanism involving overproduction of TGF-beta. Our study revealed unexpected roles of Trim28, a global chromatin regulator in both T cell activation and tolerance. Trim28 conditional KO mice and age-matched control mice were sacrificed, and neive CD4+ T cells (CD4+CD62+CD25-) and Treg (CD4+CD62+CD25+) were sorted. Stimulation of naive T cells was done with anti-CD3 and anti-CD28 for 13 hours. We collected quadruplicates for each group.

2012-04-28 | E-GEOD-32224 | biostudies-arrayexpress

Transcriptome data after TRIM28 knockdown in A375 melanoma cells

Project description:TRIM28 is a bromodomain protein implicated in the regulation of tumor growth. TRIM28 regulates gene expression by recruiting epigenetic writers including HDACs, SETDB1 and HP1. To determine the role of TRIM28 in melanoma cells we knocked down TRIM28 using lentiviral shRNA constructs followed by gene expression analysis using HTA 2.0 GeneChip.

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TRIM28 is essential for erythroblast differentiation in the mouse

Project description:We discovered that Trim28 genetic loss in the adult mouse leads to defective immature erythropoiesis in the bone marrow and consequently to anemia.We further found that TRIM28 controls erythropoiesis in a cell-autonomous manner by inducibly deleting Trim28 exclusively in hematopoietic cells. Finally, in the absence of TRIM28 we observed increased apoptosis as well as diminished expression of multiple erythroid transcription factors and heme biosynthetic enzymes in immature erythroid cells. Thus, TRIM28 is essential for the cell-autonomous development of immature erythroblasts in the bone marrow. To induce Cre recombinase from the Mx1Cre transgene, poly(I:C) was injected 5 times every other day. Mice were analyzed two weeks after completion of poly(I:C) administration. TRIM28 mutant mice generate two distinct types of immature erythroid cells; KOa, with 5-8% of the Trim28 gene remaining undeleted (still bearing 26% of residual mRNA), and KOb, with 1-4% of the gene remaining undeleted (and with 18% of mRNA remaining).

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RNA-seq of gonadal adipose tissue from male and female Trim28-WT and Trim28 adipose specific KO mice

Project description:Many genes have been implicated in WAT lipid metabolism, including tripartite motif containing 28 (Trim28), a gene proposed to primarily influence adiposity via epigenetic mechanisms in embryonic development. We set out to determine if adipose specific deletion of Trim28 led to changes in adipose tissue function and molecular phenotype. We performed transcriptomics analysis on adipose tissue taken from WT and adipose specific Trim28 KO mice to investigate their molecular phenotype, and to identify pathways altered in KO animals.

2020-11-25 | E-MTAB-9809 | biostudies-arrayexpress

TRIM28 silences endogenous retroviruses in neural progenitor cells

Project description:Here we show that in neural progenitor cells (NPCs) TRIM28 silences transcription of two groups of endogenous retroviruses (ERVs): IAP1 and MMERVK10C. Derepression of ERVs in Trim28-deficient NPCs was associated with a loss of H3K9me3 and resulted in transcriptional upregulation and reverse transcription. These findings demonstrate a unique dynamic transcriptional regulation of ERVs in NPCs. Analysis of upregulation of ERVs in Trim28-deficient NPCs

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