Dataset Information

Possible Contribution of Inflammation-Associated Hypoxia to Increased K_2P5.1 K⁺ Channel Expression in CD4⁺ T cells of the Mouse Model for Inflammatory Bowel Disease.

ABSTRACT: Previous studies have reported the up-regulation of the two-pore domain K⁺ channel K_2P5.1 in the CD4⁺ T cells of patients with multiple sclerosis (MS) and rheumatoid arthritis (RA), as well as in a mouse model of inflammatory bowel disease (IBD). However, the mechanisms underlying this up-regulation remain unclear. Inflammation-associated hypoxia is involved in the pathogenesis of autoimmune diseases, such as IBD, MS, and RA, and T cells are exposed to a hypoxic environment during their recruitment from inflamed tissues to secondary lymphoid tissues. We herein investigated whether inflammation-associated hypoxia is attributable to the increased expression and activity of K_2P5.1 in the splenic CD4⁺ T cells of chemically-induced IBD mode

SUBMITTER: Endo K

PROVIDER: S-EPMC6981474 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Dataset Information

Possible Contribution of Inflammation-Associated Hypoxia to Increased K_2P5.1 K⁺ Channel Expression in CD4⁺ T cells of the Mouse Model for Inflammatory Bowel Disease.

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Possible Contribution of Inflammation-Associated Hypoxia to Increased K2P5.1 K+ Channel Expression in CD4+ T cells of the Mouse Model for Inflammatory Bowel Disease.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Possible Contribution of Inflammation-Associated Hypoxia to Increased K_2P5.1 K⁺ Channel Expression in CD4⁺ T cells of the Mouse Model for Inflammatory Bowel Disease.