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Transcriptome analysis of satellite cells with a genetic deletion of HDAC4 to identify the gene modulated by HDAC4

ABSTRACT: Transcriptome analysis of satellite cells with a genetic deletion of HDAC4 to identify the gene modulated by HDAC4

PROVIDER: PRJNA416903 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6246162.fastq.gz	Fastqsanger.gz
	SRR6246163.fastq.gz	Fastqsanger.gz
	SRR6246164.fastq.gz	Fastqsanger.gz
	SRR6246165.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcriptome analysis of satellite cells with a genetic deletion of HDAC4 to identify the gene modulated by HDAC4

Project description:Transcriptome analysis of satellite cells with a genetic deletion of HDAC4 to identify the gene modulated by HDAC4

| PRJNA416903 | ENA

Transcriptome analysis of satellite cells with a genetic deletion of HDAC4 to identify the gene modulated by HDAC4

Project description:NGS technology was used for high-throughput profiling of the transcriptome by comparing satellite cells lacking or not HDAC4.

2018-02-28 | GSE106445 | GEO

Study of the signaling modulated by HDAC4 in skeletal muscle in ALS

Project description:BACKGROUND: Histone deacetylase 4 (HDAC4) has been proposed as a target for the treatment of Amyotrophic Lateral Sclerosis (ALS) because it mediates nerve-skeletal muscle interaction and since its expression in skeletal muscle correlates with the severity of the disease. However, our recent studies on the skeletal muscle response upon long-term denervation highlighted the importance of HDAC4 in maintaining muscle integrity. METHODS: To fully identify the yet uncharacterized HDAC4 functions in ALS, we genetically deleted HDAC4 in skeletal muscles of a mouse model of ALS. Body weight, skeletal muscle, innervation and spinal cord were analyzed over time by morphological and molecular analyses. A transcriptome analysis was also performed to delineate the signaling modulated by HDAC4 in skeletal muscle of a mouse model of ALS. FINDINGS: HDAC4 deletion in skeletal muscle caused earlier ALS onset, characterized by body weight loss, muscle denervation and atrophy, and compromised muscle performance in ALS mice, although the main catabolic pathways were not activated. A transcriptome analysis identified the gene networks modulated by HDAC4 in ALS, revealing UCP1 as a top regulator that may be implicated in worsening ALS features. INTERPRETATION: HDAC4 plays an important role in preserving innervations and skeletal muscle in ALS, likely by modulating the UCP1 gene network. Our study highlights a possible risk in considering HDAC inhibitors for the treatment of ALS.

2019-01-31 | GSE121789 | GEO

Study of the signaling modulated by HDAC4 in skeletal muscle in ALS

Project description:Study of the signaling modulated by HDAC4 in skeletal muscle in ALS

| PRJNA498450 | ENA

ChIP-seq analysis about Hdac4/5 samples

Project description:To identify whether Hdac4/5 were enriched in MuERVL directly, we performed Hdac4/5 ChIP-seq with anti-Hdac4/5 antibody in wildtype ESCs. we conclude that Hdac4/5 binding were enriched on MuERVL-int region and weakly enriched on MT2, suggesting a direct regulatory role of Hdac4/5 on MuERVL expression.

2022-09-05 | GSE178130 | GEO

HDAC4 regulates satellite cell proliferation and differentiation by targeting P21 and Sharp1 genes

Project description:HDAC4 regulates satellite cell proliferation and differentiation by targeting P21 and Sharp1 genes

| PRJNA417021 | ENA

HDAC4 interactors identified by MS/MS

Project description:Access to DNA is the first level of control in regulating gene transcription, a control that is also critical for maintaining DNA integrity. Cellular senescence is characterized by profound transcriptional rearrangements and accumulation of DNA lesions. Here, we discovered an epigenetic complex between HDAC4 and HDAC1/HDAC2 that is involved in the erase of H2BK120 acetylation. The HDAC4/HDAC1/HDAC2 complex modulates the efficiency of DNA repair by homologous recombination, through dynamic deacetylation of H2BK120. Deficiency of HDAC4 leads to accumulation of H2BK120ac, impaired recruitment of BRCA1 and CtIP to the site of lesions, accumulation of damaged DNA and senescence. In senescent cells this complex is disassembled because of increased proteasomal degradation of HDAC4. Forced expression of HDAC4 during RAS-induced senescence reduces the genomic spread of γH2AX and affects H2BK120ac levels, which are increased in DNA-damaged regions accumulated during RAS-induced senescence. In summary, degradation of HDAC4 during senescence causes the accumulation of damaged DNA and contributes to the activation of the transcriptional program controlled by super-enhancers that maintains senescence.

2024-10-17 | PXD051316 | Pride

Hdac4 interactome in Huntington's Disease

Project description:Hdac4 has been found to modulate symptoms in Huntington's Disease (HD) mouse models through an uknown mechanism unrelated to any enzymatic activity. We investigated the protein-protein interactions to gain insight into the role of Hdac4 in HD.

2019-05-01 | PXD011845 | Pride

Satellite cell – specific deletion of CIPC alleviates myopathy in mdx mice.

Project description:The regeneration of skeletal muscle relies on satellite cells which can proliferate, differentiate and form new myofibers upon injury. Emerging evidence suggests that misregulations of satellite cell fate and function influence the severity of Duchenne Muscular Dystrophy (DMD). The myogenic identity and maintenance of the pool of satellite cells is determined by the transcription factor PAX7. Satellite cell proliferation and self-renewal is regulated by the circadian clock. Here, we show that the CLOCK-interacting protein, Circadian (CIPC), a negative-feedback regulator of the circadian clock, is up-regulated during myoblast differentiation. Specific deletion of CIPC in satellite cells alleviated myopathy, improved muscle function and reduced fibrosis in mdx mice. CIPC deficiency led to activation of the ERK1/2 and JNK1/2 signaling pathways, which in turn activated the transcription factor SP1 to trigger the transcription of PAX7. Therefore, CIPC is a negative regulator of satellite cell function and loss of CIPC in satellite cells promotes muscle regeneration.

2022-01-27 | GSE195468 | GEO

Nociceptor HDAC4 regulates inflammatory pain

Project description:Transcriptional alterations are characteristic of persistent pain states but the key regulators remain elusive. Using a conditional knockout (cKO) strategy in mice we sought to determine whether loss of the transcriptional co-repressor histone deacetylase four (HDAC4) would have implications for sensory neuron transcription and nociception. HDAC4 was found to be largely dispensable for transcriptional regulation of naïve sensory neurons but was required for transcriptional responses after injury, with Calca and Trpv1 expression consistently downregulated in HDAC4 cKO compared to littermate controls (0.2-0.44 fold). This downregulation corresponded to reduced sensitivity to capsaicin in vitro (76% +/- 4.4% wildtype capsaicin responders vs 56.9% +/- 4.7% cKO responders) and to reduced thermal hypersensitivity in the complete Freund’s adjuvant model of inflammatory pain (1.3-1.4 fold improvement). These data indicate that HDAC4 is a novel inflammatory pain mediator and may be a good therapeutic target, capable of orchestrating the regulation of multiple downstream effectors. Total RNA was extracted from HDAC4 cKO and HDAC4 fl/fl naïve adult lumbar dorsal root ganglia (n=3/group). mRNA expression was compared using Affymetrix Mouse Gene Arrays (Mouse Gene 2.0ST) run on a GeneChip Fluidics Station 450. Chips were scanned on an Affymetrix GeneChip Scanner.

2015-04-23 | E-GEOD-62405 | biostudies-arrayexpress

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