Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Histone modifications in LncMyoD-KD mouse muscle stem cells by ChIP-seq

ABSTRACT: We report the application of ChIPmentation on examination of H3K27ac histone mark in cultured satellite cells with siRNA treatment targeting LncMyoD. We observed no difference of H3K27ac mark around transcription start sites (TSS) after LncMyoD KD.

ORGANISM(S): Mus musculus

PROVIDER: GSE159131 | GEO | 2020/12/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome sequencing analysis of LncMyod-knockdown satellite cells by RNA-seq

Project description:To understand the effect of LncMyod knockdown on cultured satellite cells, we isolated satellite cells from mouse hindlimb and cultured them in vitro with siRNA treatment targeting LncMyod. Following RNA-seq showed that loss of LncMyod leads to difficiencies in myogenic differentiation.

2020-12-08 | GSE129766 | GEO

Histone modifications in activated and quiescent mouse muscle stem cells by ChIP-seq

Project description:We report the application of ChIPmentation on examination of H3K27me3 and H3K4me3 histone marks in freshly isolated satellite cells (QSC) and satellite cells isolated after 2.5 days post-injury (ASC). We observed increase of H3K4me3 marks around transcription start sites (TSS) and decrease of H3K27me3 marks around TSS during satellite cell activation.

2020-12-08 | GSE129749 | GEO

Histone modifications in LncMyoD-KD mouse muscle stem cells by ChIP-seq

Project description:Histone modifications in LncMyoD-KD mouse muscle stem cells by ChIP-seq

| PRJNA667737 | ENA

Chromatin structure profiling of mouse muscle stem cells by ATAC-seq

Project description:By comparing ATAC-seq from freshly isolated satellite cells (QSC), satellite cells isolated 2.5 days post-injury (ASC), and satellite cells cultured for differentiation, we observed a gradual opening of satellite cell chromatin structure during activation and differentiation process. We used ATAC-seq to study the functional role of LncMyod during satellite cell differentiation and identified genes that exhibited decrease of accessibilities to their transcription start sites (TSS). The majority of the regions are myogenesis-related genes, suggesting LncMyod plays a critical role in establishing permissive chromatin environment for myogenic progression.

2020-12-08 | GSE129745 | GEO

Global examination of LncMyoD binding sites using ChIRP-seq

Project description:We report the application of ChIRP-seq on examination of LncMyoD binding sittes in differentiated myotubes We observed the global binding sites of LncMyoD in differentiated myotubes.

2020-12-08 | GSE159132 | GEO

A Long Non-coding RNA, LncMyoD, Regulates Skeletal Muscle Differentiation by Blocking IMP2-mediated mRNA Translation

Project description:Increasing evidence suggests that Long non-coding RNAs (LncRNAs) represent a new class of regulators of stem cells. However, the roles of LncRNAs in stem cell maintenance and myogenesis remain largely unexamined. For this study, hundreds of novel intergenic LncRNAs were identified that are expressed in myoblasts and regulated during differentiation. One of these LncRNAs, termed LncMyoD, is encoded next to the Myod gene and is directly activated by MyoD during myoblast differentiation. Knockdown of LncMyoD strongly inhibits terminal muscle differentiation largely due to a failure to exit the cell cycle. LncMyoD directly binds to IGF2-mRNA-binding-protein 2 (IMP2) and negatively regulates IMP2-mediated translation of proliferation genes such as N-Ras and c-Myc. While the RNA sequence of LncMyoD is not well-conserved between human and mouse, its locus, gene structure and function is preserved. The MyoD-LncMyoD-IMP2 pathway elucidates a mechanism as to how MyoD blocks proliferation to create a permissive state for differentiation. In order to perform an unbiased search for downstream signaling pathways perturbed by LncMyodD downregulation, microarrays were performed on myoblasts treated with control vs LncMyoD shRNAs. Total RNA was extracted using the TRIzol reagent (Invitrogen) and purified with Qiagen RNeasy separation columns (Qiagen) from myoblasts treated with control vs. LncMyoD shRNA. First-strand cDNA was synthesized and hybridized to GeneChip Mouse Genome 430 2.0 Array (Affymetrix).

2015-08-11 | E-GEOD-68842 | biostudies-arrayexpress

A Long Non-coding RNA, LncMyoD, Regulates Skeletal Muscle Differentiation by Blocking IMP2-mediated mRNA Translation

2015-08-11 | GSE68842 | GEO

Transcriptome sequencing analysis of LncMyod-knockdown satellite cells by RNA-seq

Project description:Transcriptome sequencing analysis of LncMyod-knockdown satellite cells by RNA-seq

| PRJNA532653 | ENA

Regulation of Histone Acetylation by SUMOylation Through TFAP2C Binding to the Chromatin and Recruitment of HDAC Complex

Project description:Enhancers are fundamental to gene regulation. Post-translational modifications by the small ubiquitin-like modifiers (SUMO) modify chromatin regulation enzymes, including histone acetylases and deacetylases. However, it remains unclear whether SUMOylation regulates enhancer marks, acetylation at the 27th lysine residue of the histone H3 protein (H3K27Ac). We hypothesize that SUMOylation regulates H3K27Ac. To test this hypothesis, we performed genome-wide ChIP-seq analyses. We discovered that knockdown (KD) of the SUMO activating enzyme catalytic subunit UBA2 reduced H3K27Ac at most enhancers. Bioinformatic analysis revealed that TFAP2C-binding sites are enriched in enhancers whose H3K27Ac was reduced by UBA2 KD. ChIP-seq analysis in combination with molecular biological methods showed that TFAP2C binding to enhancers increased upon UBA2 KD or inhibition of SUMOylation by a small molecule SUMOylation inhibitor. However, this is not due to the SUMOylation of TFAP2C itself. Proteomics analysis of TFAP2C interactome on the chromatin identified histone deacetylation (HDAC) machinery. TFAP2C KD reduced HDAC binding to chromatin and increased H3K27Ac marks at enhancer regions, suggesting that TFAP2C is involved in recruiting HDAC. Taken together, our findings provide important insights into regulation of enhancer marks by SUMOylation.

2024-04-13 | PXD045644 | Pride

Global examination of LncMyoD binding sites using ChIRP-seq

Project description:Global examination of LncMyoD binding sites using ChIRP-seq

| PRJNA667739 | ENA