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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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ChIP-seq analysis of H3K9 acetylation enrichment in hESCs and day 8 neural progenitor cells

ABSTRACT: H3K9 acetylation was enriched in pluripotency genes in hESCs and in neural genes in neural progenitor cells Examination of H3K9 acetylation distributions in hESCs and neural progenitor cells

ORGANISM(S): Homo sapiens

SUBMITTER: Naihe Jing

PROVIDER: E-GEOD-66778 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dual roles of histone H3 lysine 9 acetylation in human embryonic stem cell pluripotency and neural differentiation.

Qiao Yunbo Y Wang Ran R Yang Xianfa X Tang Ke K Jing Naihe N

The Journal of biological chemistry 20141217 4

Early neurodevelopment requires cell fate commitment from pluripotent stem cells to restricted neural lineages, which involves the epigenetic regulation of chromatin structure and lineage-specific gene transcription. However, it remains unclear how histone H3 lysine 9 acetylation (H3K9Ac), an epigenetic mark representing transcriptionally active chromatin, is involved in the neural commitment from pluripotent embryonic stem cells (ESCs). In this study, we demonstrate that H3K9Ac gradually declin ...[more]

PMID: 25519907

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ChIP-seq analysis of H3K9 acetylation enrichment in hESCs and day 8 neural progenitor cells

Project description:H3K9 acetylation was enriched in pluripotency genes in hESCs and in neural genes in neural progenitor cells

2015-03-11 | GSE66778 | GEO

Mouse ES cells expressing catalytically inactive Ring1B display impaired Ring1B and H3K27me3 deposition.

Project description:ChIP-seq for H3K27me3 and Ring1B was performed in WT mESCs and mESCs containing catalytically inactive Ring1B (I53A mutant). Cells expressing catalytically inactive Ring1B maintain the spatial distribution of Ring1B and H3K27me3 but at reduced levels. These findings support the notion that PRC2 recruitment is, in part, dependent on H2A ubiquitination (H2AK119ub). Two biological replicates were performed for Ring1B and H3K27me3 ChIPs in WT and Ring1B I53A/I53A mouse ESCs. Input chromatin was sequenced for each replicate as a control for ChIP enrichment.

2015-09-20 | E-GEOD-69955 | biostudies-arrayexpress

Oct6 promotes neural commitment via activation of neural lineage genes and inhibition of BMP/Wnt signals

Project description:The neural fate commitment of pluripotent stem cells requires repression of extrinsic inhibitory signals and activation of intrinsic positive transcription factors. However, it remains elusive how these two events are integrated to ensure appropriate neural conversion. Here, we show that Oct6 functions as an essential positive factor for neural differentiation of mouse embryonic stem cells (ESCs), specifically during the transition from epiblast stem cells (EpiSCs) to neural progenitor cells (NPCs). Chimera analysis showed that Oct6 knockdown leads to markedly decreased incorporation of ESC in neuroectoderm. By contrast, Oct6-overexpressing ESC derivatives preferentially contribute to neuroectoderm. Genome-wide ChIP-seq and RNA-seq analyses indicate that Oct6 is an upstream activator of neural lineage genes, and also a repressor of BMP and Wnt signalings. Our results establish Oct6 as a critical regulator that promotes neural commitment of pluripotent stem cells through a dual role: activating internal neural induction programs and antagonizing extrinsic neural inhibitory signals. RNA-seq was performed to examine Oct6 function in ESC neural differentiation at Day2, Day4 and Day6 after dox induction. On Day4 EB, ChIP-seq assay was ultilized to characterize the targets of Oct6.

2014-01-31 | E-GEOD-54569 | biostudies-arrayexpress

ATF4 Licenses C/EBPb Activity in Human Mesenchymal Stem Cells Primed for Adipogenesis

Project description:We report ChIP-seq for C/EBPb and ATF4 in human mesenchymal stem cells and in a cell-free system using naked genomic DNA. ChIP-Seq for GR, RNA Polymerase II, and H3K27 acetylation in hMSCs cultured under different adipogenic conditions are also presented. hMSCs cultured at high or low cell seeding densities in the presence or absence of adipogenic induction cocktail

2015-06-25 | E-GEOD-68864 | biostudies-arrayexpress

Homo sapiens

Project description:ChIP-seq analysis of H3K9 acetylation enrichment in hESCs and day 8 neural progenitor cells

| PRJNA277946 | ENA

Tribbles-1 regulates hepatic lipogenesis through post-transcriptional regulation of C/EBP? [ChIP-Seq]

Project description:We report ChIP-Seq data for C/EBPa in livers of mice with liver-specific KO (LSKO) of Trib1 as compared to WT controls, or in livers of mice overexpressing C/EBPa via adeno-associated virus (AAV) as compared to controls. 8-10 week old Trib1 flox/flox mice treated with AAV_Null (WT) or AAV_Cre (LSKO); 8-10 week old C57B/6 WT mice treated with AAV_Null or AAV_Cebpa.

2015-07-14 | E-GEOD-70716 | biostudies-arrayexpress

ChIP-seq analysis of Gli1 and Sox2 input to neural progenitor program and integration with actve histone marks

Project description:In the vertebrate neural tube, regional Sonic hedgehog (Shh) signaling invokes a time- and concentration-dependent induction of six different cell populations mediated through Gli transcriptional regulators. Elsewhere in the embryo, Shh/Gli responses invoke different tissue appropriate regulatory programs. To elucidate Shh/Gli regulation of neural fate sepcification, we performed Gli1 ChIP-Seq analysis. We further analyzed two transcription factors whose motifs were enriched in Gli1 ChIP data (Sox2 and Foxa2). Two active histone marks (H3K4me2 and H3K27ac) were additionally analyzed to study activity status of Shh-responsive cis-elements. Active enhancer histone marks and transcription factor binding patterns were obtained from neuralized emrbyoid bodies. Biological replicates were performed for Gli1 and mock FLAG chips. Histone profiling for enhancer marks were taken from time course experiment performed in parallel.

2012-12-15 | E-GEOD-42132 | biostudies-arrayexpress

Comparison non-targeting hRNA hESCs versus UBE2K shRNA hESCs

Project description:Histones modulate gene expression by chromatin compaction, regulating numerous processes such as differentiation. However, the mechanisms underlying histone degradation remain elusive. When compared with their differentiated counterparts, immortal human embryonic stem cells (hESCs) have a unique chromatin architecture and low levels of trimethylated histone H3 at lysine 9 (H3K9me3), a heterochromatin-associated modification. Here we assess a link between the intrinsic epigenetic landscape and ubiquitin-proteasome system of hESCs. We find that hESCs exhibit high expression of UBE2K, a ubiquitin-conjugating enzyme. Loss of UBE2K increases the levels of H3K9 trimethyltransferase SETDB1, resulting in H3K9 trimethylation and repression of neurogenic genes during differentiation. Concomitantly, loss of UBE2K impairs the ability of hESCs to differentiate into neural progenitors with neurogenic properties. Besides H3K9 trimethylation, we find that UBE2K binds histone H3 to induce its polyubiquitination and degradation by the proteasome. Notably, ubc-20, the worm orthologue of UBE2K, also regulates both histone H3 levels and H3K9 trimethylation in C. elegans germline. Thus, our results indicate that UBE2K crosses evolutionary boundaries to promote histone H3 degradation and reduce H3K9me3 repressive marks in immortal cells.

2020-06-01 | PXD018625 | Pride

Identification of ubiquitination sites of purified histone H3

2020-06-01 | PXD018621 | Pride

Expression data of neural progenitor cells differentiation from human embryonic stem cells

Project description:Mocetinostat (MGCD) which is a kind of histone deacetylase inhibitors (HDACi) promotes human embryonic stem cells (hESCs) differentiation towards neural progenitor cells (NPCs). Application of HDAC inhibitors (HDACi) increased the expression of neuroectodermal markers once neural differentiation was initiated, thereby leading to more NPC generation. We used microarrays to detail the global gene expression during NPC differentiaton upon MGCD treatment and identified the transcript changes effected by MGCD during this process. Undifferentiated H9 hESCs (D0), as well as H9 cells with or without MGCD treatment on day 3 (D3C and D3M) and on day 7(D7C and D7M) of NPC generation were collected for RNA extraction and hybridization on Affymetrix microarrays.

2014-09-03 | E-GEOD-61050 | biostudies-arrayexpress

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