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HDAC6 deacetylates IDH1 to regulate the homeostasis of hematopoietic stem/progenitor cells [WGBS-seq]

ABSTRACT: In order to further explore the mechanism by which increased 5hmC inhibits expansion of LSK cells from Hdac6-/- murine primary BM cells, we performed WGBS-seq and oxWGBS-seq analysis using LSK cells isolated from Hdac6-/- and WT mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE234147 | GEO | 2023/06/06

REPOSITORIES: GEO

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HDAC6 deacetylates IDH1 to regulate the homeostasis of hematopoietic stem/progenitor cells

Project description:In order to further explore the mechanism by which increased 5hmC inhibits expansion of LSK cells from Hdac6-/- murine primary BM cells, we performed RNA sequencing (RNA-seq) analysis using LSK cells isolated from Hdac6-/- and WT mice.

2022-05-21 | GSE203239 | GEO

HDAC6 deacetylates IDH1 to regulate the homeostasis of hematopoietic stem/progenitor cells

Project description:HDAC6 deacetylates IDH1 to regulate the homeostasis of hematopoietic stem/progenitor cells

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Acute loss of TET function results in aggressive myeloid cancer in mice [WGBS]

Project description:To evaluate the DNA methylation in LSK cells from the bone marrow of wildtype or Tet2/3 DKO mice. In order to address the impact of the loss of Tet2/3 proteins in DNA methylation in LSK cells, we compared by WGBS the methylome of wild and, Tet2/3 DKO LSK cells in bone marrow.

2015-11-26 | E-GEOD-72629 | biostudies-arrayexpress

Hdac6 regulates Tip60-p400 function in stem cells (sequencing)

Project description:The Tip60 (also known as Kat5) lysine acetyltransferase functions broadly as a transcriptional co-activator that acetylates histones. In contrast, Tip60 functions in embryonic stem cells (ESCs) both to silence genes that promote differentiation and to activate genes required for proliferation. The mechanism by which Tip60 functions as a repressor is unknown. Here we show that the class II histone deacetylase Hdac6 co-purifies with Tip60-p400 complex from ESCs and is necessary for complete silencing of most differentiation genes targeted by Tip60. In contrast to differentiated cells, where Hdac6 is mainly cytoplasmic and does not interact with Tip60, Hdac6 is largely nuclear in ESCs and neural stem cells (NSCs) and interacts with Tip60-p400 in both cell types. Hdac6 is enriched at promoters bound by Tip60-p400 in ESCs, but while Tip60 binds on both sides of transcription start sites (TSSs), Hdac6 binding overlaps with only the downstream Tip60 peak. Surprisingly, Hdac6 does not deacetylate histones at these sites, but rather is required for Tip60 binding. These data suggest that nuclear exclusion of Hdac6 during differentiation plays a major role in modulation of Tip60-p400 function. We determined the genome-wide localization of Tip60 and Hdac6 in mouse ES cells, and examined genomic binding profiles of Tip60 and Hdac6 upon indicated knockdown by ChIP-seq. We examined genomic binding profiles of p400 upon indicated knockdown by ChIP-seq.

2013-11-20 | E-GEOD-42209 | biostudies-arrayexpress

HDAC6 and HSP90 control the functions of Foxp3+ T regulatory cells

Project description:Foxp3+ T-regulatory cells (Tregs) are key to immune homeostasis such that their diminished numbers or function can cause autoimmunity and allograft rejection. Foxp3+ Tregs express histone/protein deacetylases (HDACs) that regulate chromatin remodeling, gene expression and protein function. Pan-HDAC inhibitors developed for oncology enhance Treg production and suppression but have limited non-oncologic applications given their broad effects. We show, using HDAC6-deficient mice and WT mice treated with HDAC6-specific inhibitors, that HDAC6 inhibition promotes Treg suppressive activity in models of inflammation and autoimmunity, including multiple forms of experimental colitis and fully MHC-incompatible cardiac allograft rejection. Many of the beneficial effects of HDAC6 targeting are also achieved by inhibition of the HDAC6-regulated protein, HSP90. Hence, selective targeting of a single HDAC isoform, HDAC6, or its downstream target, HSP90, can promote Treg-dependent suppression of autoimmunity and transplant rejection. RNA from three independent samples from magnetically separated CD4+CD25+ Treg of HDAC6 knock out, compared to wild type (C57BL6) control

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HDAC6 deacetylates IDH1 to promote the homeostasis of hematopoietic stem and progenitor cells

Project description: Not available

| S-SCDT-10_15252-EMBR_202256009 | biostudies-other

HDAC6 overexpression effect on mouse ESCs

Project description:Analysis of mouse ESCs overexpressing HDAC6. Histone deacetylase 6 (Hdac6) was discovered as a deacetylase of α-tubulin and functions in cell migration, immunity and resistance to virus infection in vitro. HDAC6 overexpression ESCs and control ESCs were selected for RNA extraction and hybridization on Agilent microarrays. Results provide insight into the role of HDAC6 in the mouse ESCs.

2016-12-01 | GSE81710 | GEO

Hdac6 is a stem-cell specific modulator of Tip60-p400 function (gene expression)

Project description:To identify the functional role of Hdac6 in embryonic stem cells, we examined gene expression changes in mouse ES cells upon Tip60, Hdac6 and double knockdown. Two biological replicates each for control (GFP), Tip60, Hdac6 and double KD in E14 mouse ESCs. Lentiviral-based shRNA was used and gene expression changes were determined 3 days after KD. The global gene expression profiles of Tip60, Hdac6 and double KD were compared to control KD cells.

2013-11-20 | E-GEOD-42208 | biostudies-arrayexpress

WGBS-seq and oxWGBS-seq Atlas for Oral Squamous Cell Carcinoma

Project description:Whole genome bisulfite sequencing (WGBS‑seq) and whole-genome oxidative bisulfite sequencing (oxWGBS‑seq) in four paired OSCC tumor and its NAT were performed to obtain precise, genome-wide, single-base resolution maps of 5mC and 5hmC. Based on these maps, the genomic content of 5mC and 5hmC in these paired samples were observed, as well as the distributions of 5mC and 5hmC in genic regions and histone-marked gene regulatory regions.

2023-04-05 | GSE212634 | GEO

ARID1A-mutated ovarian cancers depend on HDAC6 activity

Project description:ARID1A, encoding a subunit of the SWI/SNF chromatin remodeling complex, is the most mutated epigenetic regulator in human cancers. ARID1A and TP53 mutations are typically mutually exclusive. Therapeutic approaches that correlate with ARID1A mutational status remain a challenge. Here, we show that HDAC6 activity is essential in ARID1A-mutated ovarian cancers. Inhibition of HDAC6 activity using a clinically applicable small molecule inhibitor significantly improved the survival of mice bearing ARID1A-mutated ovarian tumors. This correlated with the suppression of growth and dissemination of ARID1A-mutated, but not wild-type, tumors. The dependence on HDAC6 activity in ARID1A-mutated cells correlated with a direct transcriptional repression of HDAC6 by ARID1A. HDAC6 inhibition selectively promoted apoptosis of ARID1A-mutated cells. HDAC6 directly deacetylated the Lysine 120 residue of p53, a pro-apoptotic post-translational modification. Thus, ARID1A mutation inactivates p53’ apoptotic function by upregulating HDAC6. These results indicate that pharmacological inhibition of HDAC6 is a novel therapeutic strategy involving ARID1A-mutation

2017-07-14 | GSE84405 | GEO

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