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ChIP-seq to investigate H3K9ac regulation by HDAC3 in trigeminal ganglion of SD rat trigeminal neuralgia model

ABSTRACT: ChIP-seq to investigate H3K9ac regulation by HDAC3 in trigeminal ganglion of SD rat trigeminal neuralgia model

PROVIDER: PRJEB46586 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR6356090_1.fastq.gz	Fastqsanger.gz
	ERR6356090_2.fastq.gz	Fastqsanger.gz
	ERR6356100_1.fastq.gz	Fastqsanger.gz
	ERR6356100_2.fastq.gz	Fastqsanger.gz

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ChIP-seq to investigate H3K9ac regulation by HDAC3 in trigeminal ganglion of SD rat trigeminal neuralgia model

Project description:The epigenetic roles in trigeminal neuralgia (TN) still remain unclear. H3K9ac alteration in neuralgia is obscure and controversy. In this study, we established TN rat model via chronic compression, and further treated with 100 mg/kg/d carbamazepine (CBZ). ChIP-seq were conducted to investigate the genome-wide distribution of H3K9ac and HDAC3 in control, TN and TN+CBZ.

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RNA-seq: H3K9ac regulated by HDAC3 in trigeminal ganglion of SD rat trigeminal neuralgia model

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2021-08-02 | E-MTAB-10792 | biostudies-arrayexpress

RNA-seq: H3K9ac regulated by HDAC3 in trigeminal ganglion of SD rat trigeminal neuralgia model

Project description:RNA-seq: H3K9ac regulated by HDAC3 in trigeminal ganglion of SD rat trigeminal neuralgia model

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Project description:Trigeminal neuralgia (TN) is a type of neuropathic pain caused by injury to sensory nerves, manifesting as severe paroxysmal pain of the head and face. Trigeminal neuralgia brings a huge burden to patients, without long-term effective treatment. Changes in the expression of pain-related genes in the whole blood samples of patients play an important role in the pathogenesis, diagnosis, and evaluation of treatment effects of trigeminal neuralgia. To better understand the mechanism of trigeminal neuralgia, we collect the whole blood samples from the trigeminal neuralgia patients and the pain-free healthy comparisons. RNA-seq was conducted between the two groups to find the transcriptome changes in patients with trigeminal neuralgia.

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Project description:We found that several deacetylase-dead HDAC3 mutants were able to rescue the metabolic phenotype of HDAC3-depleted livers. Here we profile the histone acetylation in the presence of different HDAC3 mutants in mouse liver. Deacetylase-dead HDAC3 mutants, including HAHA, KA, YF and HEBI, were introduced into HDAC3-depleted (Cre) mouse livers by virus along with wild-type (WT) HDAC3 as a control. Livers were harvested at 5 pm (ZT 10) and subjected to ChIP with anti-H3K9ac antibodies followed by deep sequencing.

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