Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJEB46592 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

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.

2021-08-02 | E-MTAB-10793 | biostudies-arrayexpress

RNA-seq: H3K9ac regulated 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). RNA-seq were conducted to investigate the transcriptional profilings in control, TN and TN+CBZ.

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

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

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

| PRJEB46586 | ENA

RNA sequencing of whole blood cells in patients with trigeminal neuralgia

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.

2021-10-28 | GSE186505 | GEO

In situ tissue profile of rat trigeminal nerve in trigeminal neuralgia using spatial transcriptome sequencing

Project description:Investigation on the transcriptome and intercellular communication of different cells of trigeminal nerve in trigeminal neuralgia rat by spatial transcriptome sequencing

2024-02-29 | GSE233838 | GEO

Genome-wide acetylated histone 3 lysine 9 (H3K9ac) in HDAC3-depleted liver rescued with deacectylase-dead HDAC3 mutants

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.

2013-11-25 | E-GEOD-49365 | biostudies-arrayexpress

Diurnal changes of HDAC3, Rev-erbα, NCoR and Pol II recruitment to the mouse liver genome and of H3K9Ac

Project description:We reported a diurnal changes in the recruitment of HDAC3, Rev-erbα, NCoR and Pol II to the mouse liver genome as well as H3K9 acetylation in vivo at ZT10 and ZT22. ChIP-Seq profiling of HDAC3, Rev-erbα, NCoR and Pol II binding and H3K9Ac in mouse liver harvested at 2 different times (ZT10 and ZT22) of the day

2011-03-11 | E-GEOD-26345 | biostudies-arrayexpress

Changes of H3K9ac and H3K27ac recruitment in pachytene spermatocytes and round spermatids from testes-specific HDAC3-depleted mice and genome-wide maps of HDAC3,NCOR and Sox30 in wild-type and Sox30 KO testes

Project description:We reported changes in the recruitment of H3K9ac and H3K27ac in HDAC3-depleted mouse testes in the late meiotic and early haploid stages. We also investigated genome-wide occupancy of HDAC3, NCOR and Sox30 to the mouse testes from wild-type and Sox30 KO mice.

2021-05-26 | GSE153063 | GEO

Genome-wide acetylated histone 3 lysine 9 (H3K9ac) in HDAC3-depleted liver rescued with deacectylase-dead HDAC3 mutants

2013-11-25 | GSE49365 | GEO

Highly synchronized cortical circuit dynamics revealed by a new mouse model of neuropathic pain

Project description:The cerebral cortex plays a key role in the multi-dimensional human pain experience. However, the neural mechanisms mediating pain-related cortical activity remain largely unknown, particularly in primary somatosensory cortex (S1). We therefore developed a new animal model of trigeminal neuralgia, a prototypical neuropathic pain, which allowed us to evaluate pain-related cortical dynamics with unprecedented translational relevance. Our novel model (FLIT: Foramen Lacerum Impingement of Trigeminal-nerve) displayed robust clinically relevant trigeminal neuralgia-like behaviors, including asymmetric facial grimacing, dental pain-like behaviors, anxiety-like behavior, and sexual dysfunction, capturing many features of the human pain experience. Awake FLIT mice exhibited highly synchronized spontaneous population activity in S1, due to GABAergic interneuron hypoactivity. Remarkably, clinically effective treatments including carbamazepine and trigeminal nerve root decompression abrogated S1 synchronization and alleviated trigeminal neuralgia-like behaviors. These results reveal synchronized S1 activity as a new and important cortical substrate of neuropathic pain, which can be clinically targeted to provide effective therapy.

2023-02-10 | GSE162284 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data