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Pattern occupation of HDACs on chromatin determines PI3K/AKT inhibitor resistance in cancers [ChIP-seq]

ABSTRACT: Blocking BRD4 or HDACs induces paradoxically similar gene expression, comparably attenuates PI3K/AKT inhibitor resistance in multiple cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE137207 | GEO | 2020/09/09

REPOSITORIES: GEO

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Pattern occupation of HDACs on chromatin determines PI3K/AKT inhibitor resistance in cancers [RNA-seq]

Project description:Blocking BRD4 or HDACs induces paradoxically similar gene expression, comparably attenuates PI3K/AKT inhibitor resistance in multiple cancer cells.

2020-09-09 | GSE137200 | GEO

Pattern occupation of HDACs on chromatin determines PI3K/AKT inhibitor resistance in cancers [RNA-seq]

Project description:Pattern occupation of HDACs on chromatin determines PI3K/AKT inhibitor resistance in cancers [RNA-seq]

| PRJNA564800 | ENA

Pattern occupation of HDACs on chromatin determines PI3K/AKT inhibitor resistance in cancers [ChIP-seq]

Project description:Pattern occupation of HDACs on chromatin determines PI3K/AKT inhibitor resistance in cancers [ChIP-seq]

| PRJNA564807 | ENA

Genome-wide mapping of HATs and HDACs in human CD4+ T cells

Project description:Histone acetyltransferases (HATs) and deacetylases (HDACs) function antagonistically to control histone acetylation. As acetylation is a histone mark for active transcription, HATs have been associated with active and HDACs with inactive genes. We describe here genome-wide mapping of HATs and HDACs binding on chromatin and ﬁnd that both are found at active genes with acetylated histones. Our data provide evidence that HATs and HDACs are both targeted to transcribed regions of active genes by phosphorylated RNA Pol II. Furthermore, the majority of HDACs in the human genome function to reset chromatin by removing acetylation at active genes. Inactive genes that are primed by MLL-mediated histone H3K4 methylation are subject to a dynamic cycle of acetylation and deacetylation by transient HAT/HDAC binding, preventing Pol II from binding to these genes but poising them for future activation. Silent genes without any H3K4 methylation signal show no evidence of being bound by HDACs. high throughput sequencing: genome-wide analysis of 5 HATs, 4 HDACs in human CD4+ cells, Tip60 and HDAC6 in activated CD4 cells, genome-wide analysis of 2 histone acetylations and RNA Polymerase II after HDAC inhibitor treatment in CD4, histone modification with WDR5 knock-down and HDAC inhibitor treatment in HeLa cells expression profiling: Global change in gene expression in human CD4+ T cells after HDAC inhibitor treatment for 2hours and 12 hours. (9 samples in total)

2009-08-20 | E-GEOD-15735 | biostudies-arrayexpress

Genome-wide mapping of HATs and HDACs in human CD4+ T cells

2009-08-20 | GSE15735 | GEO

Influence of catalytic and non-catalytic functions of class I HDACs on the cellular transcriptome

Project description:We generated a cellular class I HDAC toolbox allowing to discriminate between catalytic and non-catalytic roles of class I HDACs. Our study reveals a comprehensive, functional analysis of class I HDACs.

2022-08-14 | GSE193885 | GEO

PI3K/AKT signaling determines a dynamic switch between distinct KSRP functions favoring skeletal myogenesis.

Project description:Skeletal myogenesis is orchestrated by distinct regulatory signaling pathways, including PI3K/AKT, that ultimately control muscle gene expression. Recently discovered myogenic micro-RNAs (miRNAs) are deeply implicated in muscle biology. Processing of miRNAs from their primary transcripts is emerging as a major step in the control of miRNA levels and might be well suited to be regulated by extracellular signals. Here we report that the RNA binding protein KSRP is required for the correct processing of primary myogenic miRNAs upon PI3K/AKT activation in myoblasts C2C12 and in the course of injury-induced muscle regeneration, as revealed by Ksrp knock-out mice analysis. PI3K/AKT activation regulates in opposite ways two distinct KSRP functions inhibiting its ability to promote decay of myogenin mRNA and activating its ability to favor maturation of myogenic miRNAs. This dynamic regulatory switch eventually contributes to the activation of the myogenic program.

| S-EPMC3278731 | biostudies-literature

HDAC5 is a repressor of angiogenesis and determines the angiogenic gene expression pattern of endothelial cells

Project description:Class IIa histone deacetylases (HDACs) are signal-responsive regulators of gene expression involved in vascular homeostasis. To investigate the differential role of class IIa HDACs for the regulation of angiogenesis, we used siRNA to specifically suppress the individual HDAC isoenzymes. Among the HDAC isoforms tested, silencing of HDAC5 exhibited a unique pro-angiogenic effect evidenced by increased endothelial cell migration, sprouting and tube formation. Consistently, overexpression of HDAC5 decreased sprout formation, indicating that HDAC5 is a negative regulator of angiogenesis. The anti-angiogenic activity of HDAC5 was independent of MEF2 binding and its deacetylase activity, but required a nuclear localization indicating that HDAC5 might affect the transcriptional regulation of gene expression. To identify putative HDAC5 targets, we performed microarray expression analysis. Silencing of HDAC5 increased the expression of fibroblast growth factor 2 (FGF2) and angiogenic guidance factors including Slit2. Antagonization of FGF2 or Slit2 reduced sprout induction in response to HDAC5 siRNA. ChIP assays demonstrate that HDAC5 binds to the promoter of FGF2 and Slit2. In summary, HDAC5 represses angiogenic genes, like FGF2 and Slit2, which causally contribute to capillary-like sprouting of endothelial cells. The de-repression of angiogenic genes by HDAC5 inactivation may provide a useful therapeutic target for induction of angiogenesis.

2009-04-02 | GSE15499 | GEO

A Redox-Dependent Pathway for Regulating Reversible HDACs Synchronizes Crown Root Development in Rice

Project description:As a signal molecular in aerobic organism, how reactive oxygen species (ROS) regulates normal life is a fundamental biological question. Locally accumulated ROS have been reported to balance cell division and differentiation in root apical meristem. However, the underlying molecular mechanism is unclear. Here, we reveal that developmentally produced H2O2 in plant root apical meristem (RAM) triggers reversible acetylation modification of proteins which involved in protein synthesis and cell proliferation. WOX11, an essential transcription factor for crown roots (CRs) formation, modulates ROS homeostasis by directly regulating class III peroxidases. HDACs (histone deacetylases) sense cellular redox status to enhance their enzyme activities, which drives protein acetylation level alterations in rice roots. Oxidation-dependent on WOX11 triggered protein acetylation modification leads to a robust root system in rice. Our study revealed a novel regulatory mechanism which cellular redox status via a WOX11-dependent manner regulates protein acetylation during rice crown root development. The molecular link between the redox status and HDACs activities through WOX11-dependent pathway may provide new insight into which plants exploit developmentally produced ROS to direct organogenesis. Additionally, HDACs reversible enzyme activity via redox-regulated endows with the flexibility of protein modification control in dealing with developmental and changing environmental cues.

2022-08-10 | PXD029260 | Pride

TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression

Project description:This SuperSeries is composed of the following subset Series: GSE28948: TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (gene expression data) GSE28950: TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (ChIP-Seq data) GSE35540: TMPRSS2-ERG, HDACs and EZH2 are involved in an AR centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (gene expression after ERG KD) Refer to individual Series

2012-04-26 | E-GEOD-28951 | biostudies-arrayexpress

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