Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inhibition of cancer cell self-renewal through an epigenetic HDACi-histone H1.0 axis.

ABSTRACT: Identification of HDACi-responsive, H1.0-dependent genes inhibiting self-renewal of HCC1569 breast cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE119369 | GEO | 2020/02/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Inhibition of cancer cell self-renewal through an epigenetic HDACi-histone H1.0 axis.

Project description:Inhibition of cancer cell self-renewal through an epigenetic HDACi-histone H1.0 axis.

| PRJNA488996 | ENA

Selective inhibition of cancer cell self-renewal through a Quisinostat-histone H1.0 axis.

Project description: Not available

| S-EPMC7156485 | biostudies-literature

Genome Wide Distribution of Linker Histone H1.0 is Independent of MeCP2 II

Project description:Previous studies suggested that MeCP2 binds to linker DNA and competes with linker histone H1 to regulate chromatin structure, but this hypothesis has never been tested in vivo. Here, we expressed Flag-tagged H1.0 in forebrain excitatory neurons in mice and performed ChIP-Seq to reveal H1.0 distribution and its relationship with MeCP2. Unexpectedly, we detected no major change in H1.0 upon MeCP2 depletion, revealing that MeCP2 functions independent of linker H1.0.

2018-05-28 | GSE107519 | GEO

Genome Wide Distribution of Linker Histone H1.0 is Independent of MeCP2 I

2018-05-28 | GSE95471 | GEO

Linker Histone H1.0 Couples Cellular Stiffness to Chromatin Structure [RNA-seq]

Project description:Eukaryotic nuclei encase the genome and differentially package it for the various needs of distinct cell types. Tuning of genome structure and function is accomplished by chromatin binding proteins, which are responsive to cellular stress, determining the transcriptome and phenotype of the cell. We sought to investigate the connection between extracellular stress and chromatin structure to regulate cellular stiffness. We demonstrate that the linker histone H1.0, which compacts nucleosomes into higher order chromatin fibers, controls genome structure and cellular response to stress. Histone H1.0 has privileged expression in tension-responsive fibroblasts across tissue types in mouse and humans, and is necessary and sufficient to mount a myofibroblast phenotype in these cells. Loss of histone H1.0 prevents transforming growth factor beta (TGF-b)-induced fibroblast contraction, proliferation and migration in an isoform-specific manner via inhibition of a transcriptome targeting extracellular matrix molecules. Histone H1.0 is associated with local regulation of gene expression by chromatin fiber compaction and histone acetylation, rendering the nucleus and cell stiffer in response to cytokine stimulation. Knockdown of H1.0 decreased levels of HDAC1 and the chromatin reader BRD4, thereby preventing transcription of a fibrotic gene program. Transient depletion of histone H1.0 in vivo decompacts chromatin and prevents fibrosis in cardiac muscle, lung, and kidney, thereby linking chromatin structure with fibroblast phenotype in response to extracellular stress. Our work identifies an unexpected role of linker histones to sense and respond to cellular stress, directly coupling cellular tension, nuclear organization and gene transcription.

2024-02-28 | GSE215267 | GEO

Linker Histone H1.0 Couples Cellular Stiffness to Chromatin Structure [ChIP-seq]

2024-02-28 | GSE215266 | GEO

The Lin28b-let-7-Hmga2 axis determines the higher self-renewal potential of fetal haematopoietic stem cells

Project description:Mouse haematopoietic stem cells (HSCs) undergo a post-natal transition in several properties, including a marked reduction in their self-renewal activity. We now show that the developmentally timed change in this key function of HSCs is associated with their decreased expression of Lin28b and an accompanying increase in their let-7 microRNA levels. Lentivirus(LV)-mediated overexpression of Lin28 in adult HSCs elevates their self-renewal activity in transplanted irradiated hosts, as does overexpression of Hmga2, a well-established let-7 target that is upregulated in fetal HSCs. Conversely, HSCs from fetal Hmga2-/- mice do not display the heightened self-renewal activity that is characteristic of wild-type fetal HSCs. Interestingly, overexpression of Hmga2 in adult HSCs does not mimic the ability of elevated Lin28 to activate a fetal lymphoid differentiation program. Thus Lin28b may act as a master regulator of developmentally timed changes in HSC programs with Hmga2 serving as its specific downstream modulator of HSC self-renewal potential. Lin-Sca1+cKit+ cells were isolated from E14.5 fetal livers (of wild-type of Hmga2-/- embryos) or the bone marrow of 8-12 week old mice by fluorescence activated cell sorting. The RNA was extracted and hybridized on Affymetrix mpuse gene 1.0 ST microarrays.

2013-06-27 | E-GEOD-41758 | biostudies-arrayexpress

The linker histone H1.0 generates epigenetic and functional intratumor heterogeneity

Project description:Identification of H1.0 genome wide distribution in in-vitro transformed fibroblast before its silencing in tumor CSCs and the localization of the histone modifications H3K27me3 and H3K4me3.

2016-09-29 | GSE66169 | GEO

The linker histone H1.0 generates epigenetic and functional intratumor heterogeneity [FAIRE-Seq]

Project description:Identification of nucleosome-free, active regulatory regions in in vitro generated CSCs, following the knockdown of the histone linker H1.0

2016-09-30 | GSE73600 | GEO

The linker histone H1.0 generates epigenetic and functional intratumor heterogeneity [ChIP-Seq]

Project description:Identification of enrichment for H3K27ac and H3K27me3 in in vitro generated CSCs, following the knockdown of the histone linker H1.0

2016-09-30 | GSE73580 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data