Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chloride Nucleotide-Sensitive Channel 1A (CLNS1A) Regulates Genome Stability and Cell Cycle Progression to Control Pathogenic T Helper 17 Cell Function and Autoimmunity

ABSTRACT: RNA-sequencing of myelin-specific 2D2 CD4+ T cells isolated from the spinal cord and spleen of mice with EAE.

ORGANISM(S): Mus musculus

PROVIDER: GSE263269 | GEO | 2025/04/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Chloride Nucleotide-Sensitive Channel 1A (CLNS1A) Regulates Genome Stability and Cell Cycle Progression to Control Pathogenic T Helper 17 Cell Function and Autoimmunity [RNA-seq]

Project description:RNA-sequencing of in vitro differentiated shRenilla (control) and shClns1a transduced pTh17 cells.

2025-04-01 | GSE263141 | GEO

Chloride Nucleotide-Sensitive Channel 1A (CLNS1A) Regulates Genome Stability and Cell Cycle Progression to Control Pathogenic T Helper 17 Cell Function and Autoimmunity [CUT&RUN]

Project description:CUT&RUN sequencing of CLNS1A and PRMT5 in in vitro differentiated pTh17 cells.

2025-04-01 | GSE263140 | GEO

Chloride Nucleotide-Sensitive Channel 1A (CLNS1A) Regulates Genome Stability and Cell Cycle Progression to Control Pathogenic T Helper 17 Cell Function and Autoimmunity [ATAC-seq]

Project description:Assay for transposase-accessible chromatin with sequencing (ATAC-seq) for shRenilla (control) or shClns1a transduced pTh17 cells restimulated with aCD3/CD28 for 24h.

2025-04-01 | GSE263139 | GEO

The microRNA miR-22 represses T helper 17 cell pathogenicity by targeting PTEN-regulated pathways

Project description:Multiple sclerosis is a chronic autoimmune disease driven by pathogenic Th17 cells. Here, we dissected the role of miR-22 in pathogenic Th17 cells by autoantigen-specific disease models. We first showed that miR-22 was upregulated in peripheral lymphoid organs and spinal cords of mice developed autoimmune encephalomyelitis. Although miR-22 was upregulated in multiple helper T cell subsets, it was dispensable for T helper cell differentiation in vitro. While miR-22-/- mice exhibited milder symptoms of disease in an active EAE model, adoptive transfer of miR-22-/- 2D2 Th17 cells into naive recipient mice promoted higher disease incidence and severity compared to mice transferred with control 2D2 Th17 cells. Global transcriptional analysis of miR-22-deficient pathogenic Th17 cells revealed upregulated genes in phosphatase and tensin homologue (PTEN)-mediated pathways, and Pten was further identified as one of its potential targets. Therefore, we identified that Th17 cell intrinsic-miR-22 could protect mice from autoimmunity by targeting PTEN-regulated pathways.

2020-05-22 | GSE134895 | GEO

Gene expression data from polarized T helper cells isolated from mice with opticospinal (OSE) experimental autoimmune encephalomyelitis (EAE)

Project description:T cells from the spleen of a mixed-gender pool of four double-transgenic 2D2 (TCRMOG) x IgHMOG mice (OSE) mice, which spontaneously develop experimental autoimmune encephalomyelitis (EAE), were used to derive TH1- and TH17-polarized cells, as described in https://doi.org/10.1371/journal.pone.0015531. Here, expression was compared, first, between TH1 and naïve TH0 and, second, between TH17 and naïve TH0 cells.

2020-08-21 | E-MTAB-9133 | biostudies-arrayexpress

Chloride Nucleotide-Sensitive Channel 1A (CLNS1A) Regulates Genome Stability and Cell Cycle Progression to Control Pathogenic T Helper 17 Cell Function and Autoimmunity

Project description:Chloride Nucleotide-Sensitive Channel 1A (CLNS1A) Regulates Genome Stability and Cell Cycle Progression to Control Pathogenic T Helper 17 Cell Function and Autoimmunity

| PRJNA1096376 | ENA

Chloride Nucleotide-Sensitive Channel 1A (CLNS1A) Regulates Genome Stability and Cell Cycle Progression to Control Pathogenic T Helper 17 Cell Function and Autoimmunity [CUT&RUN]

Project description:Chloride Nucleotide-Sensitive Channel 1A (CLNS1A) Regulates Genome Stability and Cell Cycle Progression to Control Pathogenic T Helper 17 Cell Function and Autoimmunity [CUT&RUN]

| PRJNA1095964 | ENA

Chloride Nucleotide-Sensitive Channel 1A (CLNS1A) Regulates Genome Stability and Cell Cycle Progression to Control Pathogenic T Helper 17 Cell Function and Autoimmunity [ATAC-seq]

| PRJNA1095965 | ENA

Chloride Nucleotide-Sensitive Channel 1A (CLNS1A) Regulates Genome Stability and Cell Cycle Progression to Control Pathogenic T Helper 17 Cell Function and Autoimmunity [RNA-seq]

| PRJNA1095967 | ENA

Transcription profiling of chloride channel ClC-2 knock out mice with a Leukoencephalopathy-like phenotype vs.wild type

Project description:ClC-2 is a broadly expressed Cl- channel of the CLC family of Cl- channels and transporters which is abundantly expressed in brain. Here it was proposed to participate in lowering the cytoplasmic Cl- concentration of neurons, a process that establishes an inhibitory response to the neurotransmitters GABA and glycine (Staley et al., 1996). Heterozygous mutations in CLCN2 (the gene encoding ClC-2) were recently reported in a few patients with three clinically distinct forms of epilepsy (Haug et al, 2003). However, the disruption of ClC-2 in mice (ClC-2 KO mouse) did not entail epilepsy (BÃÂ¶sl et al., 2001; Nehrke et al., 2002) but myelin vacuolation in fiber tracts of the central nervous system. We used a gene expression profiling of the ClC-2 KO mouse in brain to identify possible disease mechanism which cause the observed myelin phenotype. As these myelin vacuolation became apparent in the fiber tracts of ClC-2 KO cerebellum at P28 and increased with age, we analysed the cerebellum of ClC-2 KO mice at different postnatal ages, before (P14) and after (P35) the KO cerebellum has been affected by myelin vacuolation.

2008-05-01 | E-MEXP-1028 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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