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Genome-wide localization maps of JMJD1A, SWI/SNF components, and PPARγ in brown adipocytes treated with isoproterenol

ABSTRACT: We analyzed ChIP-seq profiles for H3K4me3, H3K27ac, BRG1, ARID1A, PPARγ and JMJD1A and FAIRE-seq open chromatin profile in immortalized brown adipocytes (iBATs) treated with 1 μM isporoterenol (ISO) or vehicle for 2 hr

ORGANISM(S): Mus musculus

PROVIDER: GSE67586 | GEO | 2015/04/15

SECONDARY ACCESSION(S): PRJNA280378

REPOSITORIES: GEO

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Genome-wide localization maps of JMJD1A, SWI/SNF components, and PPAR? in brown adipocytes treated with isoproterenol

Project description:We analyzed ChIP-seq profiles for H3K4me3, H3K27ac, BRG1, ARID1A, PPAR? and JMJD1A and FAIRE-seq open chromatin profile in immortalized brown adipocytes (iBATs) treated with 1 ?M isporoterenol (ISO) or vehicle for 2 hr ChIP-seq profiles for H3K4me3, H3K27ac, BRG1, ARID1A, PPAR? and JMJD1A and FAIRE-seq open chromatin profile in iBATs at Day 8 of differentiation treated with 1 ?M isporoterenol (ISO) or vehicle for 2 hr

2015-04-15 | E-GEOD-67586 | biostudies-arrayexpress

Genome-wide analysis of JMJD1A and PPARγ binding in immortalized, differentiated preadipocytes derived from inguinal subcutaneous white adipose tissue.

Project description:In acute cold stress in mammals, JMJD1A, an H3K9 demethylase, up-regulates thermogenic gene expressions through β-adrenergic signaling in brown adipose tissue (BAT). Aside BAT-driven thermogenesis, mammals also have another mechanism to cope with long-term cold stress by inducing the browning of subcutaneous white adipose tissue (scWAT). Here, we show that this occurs through a two-step process that requires both β-adrenergic dependent phosphorylation of S265 and demethylation of H3K9me2 by JMJD1A. The histone demethylation independent acute Ucp1 induction in BAT and demethylation dependent chronic Ucp1 expression in beige-scWAT provide complementary molecular mechanisms to ensure an ordered transition between acute and chronic adaptation to cold stress. JMJD1A mediates two major signaling pathways, namlely β-adrenergic receptor and PPARγ activation, via PRDM16-PPARγ-P-JMJD1A complex for beige adipogenesis.

2018-02-16 | GSE107899 | GEO

Jmjd1a / Jmjd2c RNAi expression profile

Project description:Global gene expression effects of silencing Jmjd1a and Jmjd2c genes We used microarrays to detail the global programme of gene expression after silencing Jmjd1a gene and Jmjd2c gene separately Keywords: dose response

2007-09-29 | GSE8937 | GEO

JMJD1A inhibits proliferation and aggressiveness of gastric cancer by up-regulating RUNX3

Project description:The histone demethylase JMJD1A（Jumoji domain containing 1A） is overexpressed in multiple cancers and promotes cancer progression. However, the role and mechanism of JMJD1A in gastric cancer remains poorly understood.Here, we found that JMJD1A could suppress gastric cancer cell proliferation, migration, invasion and xenograft tumor growth. Using RNA sequencing, we identified RUNX3 as a novel target gene of JMJD1A.

2020-02-12 | GSE145105 | GEO

DNA microarray analysis of Jmjd1a and/or Jmjd1b knockout embryonic stem cells

Project description:Histone H3 lysine 9 (H3K9) methylation is an epigenetic mark of transcriptionally repressed chromatin. During mammalian development, H3K9 methylation levels seem to be spatiotemporally regulated by the opposing activities of methyltransferases and demethylases to govern correct gene expression. However, the combination(s) of H3K9 methyltransferase(s) and demethylase(s) that contribute to this regulation and the genes regulated by them remain unclear. Herein, we demonstrate the essential roles of H3K9 demethylases Jmjd1a and Jmjd1b in the embryogenesis and viability control of embryonic stem (ES) cells. Mouse embryos lacking Jmjd1a/Jmjd1b died after implantation. Depletion of Jmjd1a/Jmjd1b in mouse ES cells induced rapid cell death accompanied with a massive increase in H3K9 methylation. Jmjd1a/Jmjd1b depletion induced an increase in H3K9 methylation in the gene-rich regions of the chromosomes, indicating that Jmjd1a/Jmjd1b removes H3K9 methylation marks in the euchromatin. Importantly, the additional disruption of the H3K9 methyltransferase G9a in a Jmjd1a/Jmjd1b-deficient background rescued not only the H3K9 hypermethylation phenotype but also the cell death phenotype. We also found that Jmjd1a/Jmjd1b removes H3K9 methylation marks deposited by G9a in the Oct4 and Ccnd1 loci to activate transcription. In conclusion, Jmjd1a/Jmjd1b ensures ES cell viability by antagonizing G9a-mediated H3K9 hypermethylation in the gene-rich euchromatin.

2018-03-14 | GSE98761 | GEO

Epigenetic regulation of sex determination by the histone demethylase Jmjd1a

Project description:Developmental gene expression is defined through cross-talk between the function of transcription factors and epigenetic status including histone modification. Although several known transcription factors play crucial roles in mammalian sex determination, how chromatin regulation contributes to this process is unknown. We observed male-to-female sex reversal in mice lacking the H3K9 demethylase Jmjd1a, and found that Jmjd1a directly regulates expression of the mammalian Y chromosome sex-determining gene Sry, by regulating H3K9me2 marks. These studies reveal a pivotal role for epigenetic regulation in mammalian sex determination, and provide new impetus for identifying additional causes of disorders of sex determination by environmental factors. Gene expression patterns were measured in gonadal somatic cells of Jmjd1a mutant and control embryos at E11.5. Three biological replicates were performed in each group.

2013-08-03 | E-GEOD-49513 | biostudies-arrayexpress

Identification of JMJD1A and JMJD2B target genes in renal cell Carcinoma

Project description:The Hypoxia-Inducible Factors induce the expression of the histone demethylases JMJD1A (KDM3A) and JMJD2B (KDM4B), linking the hypoxic tumor microenvironment to epigenetic mechanisms that may foster tumor progression. Using transcript profiling, we have identified genes that are regulated in RCC4 with siRNA-mediated knockdown of JMJD1A and JMJD2B. This dataset includes expression data obtained from renal cell Carcinoma being loss or mutation of the von Hippel-Lindau (VHL) tumor suppressor gene combination with siRNA-mediated knockdown of histone demethylases JMJD1A and JMJD2B.

2021-11-03 | GSE167025 | GEO

The histone demethylase JMJD1A is essential to prostate cancer cells through regulation of c-Myc expression

Project description:Analysis of gene expresssion altered upon knockdown of histone demethylase JMJD1A in human prostate cancer cells. The objective is to elucidate the transcriptional programs that are controlled by JMJD1A in human prostate cancer. CWR22Rv1 prostate cancer cells were transduced with lentiviral particles encoding control pLKO.1 or JMJD1A shRNA (shJMJD1A). After 48 h, total RNAs were collected for the microarray analysis to determine the differentially expressed genes between Rv1 pLKO.1 and Rv1 shJMJD1A samples.

2015-09-08 | E-GEOD-70498 | biostudies-arrayexpress

Gene expression in HCT116 cells after JMJD1A/1B depletion

Project description:Using microarrays to explore the global programme of gene expression after depeltion of JMJD1A and JMJD1B

2017-06-01 | GSE71785 | GEO

Genome-wide analysis of JMJD1A and PPARγ binding in immortalized, differentiated preadipocytes derived from inguinal subcutaneous white adipose tissue.

Project description:Genome-wide analysis of JMJD1A and PPARγ binding in immortalized, differentiated preadipocytes derived from inguinal subcutaneous white adipose tissue.

| PRJNA421900 | ENA

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