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

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

PROVIDER: PRJNA667737 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR12782000.fastq.gz	Fastqsanger.gz
	SRR12782002.fastq.gz	Fastqsanger.gz
	SRR12781987.fastq.gz	Fastqsanger.gz
	SRR12781989.fastq.gz	Fastqsanger.gz

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

Project description: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.

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

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Histone proteomic associated with epigenetic studies revealed a Ghost proteome in PC1/3 KD macrophages involved in anti - tumoral resistance under IL - 10 stimulation

Project description:In our previous work, our investigation on macrophages has allowed us to show that the inhibition of the enzyme proprotein convertase (PC1/3) controls the activation of macrophages. We demonstrated that PC1/3 knockdown (KD) in macrophages would exhibit an increased secretion of pro-inflammatory and anti-tumoral factors. In this biological context, we assessed for histone modifications and for the presence and contribution of a “Ghost proteome” in these macrophages. In addition, we have identified a set of alternative proteins (AltProts) that have a key role in regulating various signaling pathways. In this study, to further investigate the underlying mechanisms involved in resistance of PC1/3 KD macrophages to anti-inflammatory stimuli, we have conducted a proteomics-systems biology study to assess the epigenome variation focusing on histone modifications and to investigate for the potential contribution of AltProts in regulating PC1/3 KD macrophages resistance. Results from our study have indicated the presence of significant variations in histone modifications along with the identification of 28 AltProts with in part involved in anti-tumoral resistance under IL-10 stimulation. These findings highlight that key role of altered epigenome histone modifications in driving resistance and indicates that, like the reference proteins, AltProts have major impact in the field of epigenetics and regulation of gene expression as shown in our results

2021-02-12 | PXD020610 | Pride

Multiple Histone modifications ChIP-seq in MCF7 cells corresponding to Ctr9 KD (paper title: Ctr9, the scaffold subunit of PAFc, govens PRC2-mediated H3K27me3 domains in breast cancer cells)

Project description:We want to examine the alternation of histone modification spectrum on chormatin in corresponding to Ctr9 loss either in an inducible KD or stable KD fashion in MCF7 breast cancer cells.

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Project description:Time makes histone H3 modifications drift

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ChIP-seq of enhancer-associated transcription factors and histone modifications

Project description:The datasets presented here are transcription factors, transcriptional co-factors or histone modifications associated with active enhancers in a variety of mouse and human cell types. ChIP-seq of enhancer-associated transcription factors and histone modifications

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Histone H3 modifications ChIP on chip

Project description:Chromatin modification through the covalent modifications of histones play crucial role on establishment and propagation of gene expression pattern. Here we sought a global view of histone H3 modifications (tri-M-K4/27 and di-M-K27/36) and occupancy in Arabidopsis thaliana using ChIP combined with high-density tiling microarrays. In these analyses, we included vip3 mutant plants as well to gain an insight into role of Paf1C in plants. Keywords: ChIP on chip

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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).

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