Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Murine K2P5.1 Deficiency Has No Impact on Autoimmune Neuroinflammation due to Compensatory K2P3.1- and KV1.3-Dependent Mechanisms.

International journal of molecular sciences - 24 Jul 2015

Bittner Stefan, Bobak Nicole, Hofmann Majella-Sophie, Schuhmann Michael K, Ruck Tobias, Göbel Kerstin, Brück Wolfgang, Wiendl Heinz, Meuth Sven G

Abstract excerpt

Lymphocytes express potassium channels that regulate physiological cell functions, such as activation, proliferation and migration. Expression levels of K2P5.1 (TASK2; KCNK5) channels belonging to the family of two-pore domain potassium channels have previously been correlated to the activity of autoreactive T lymphocytes in patients with multiple sclerosis and rheumatoid arthritis. In humans, K2P5.1 channels are...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Callithrix
Share to Encephalomyelitis, Autoimmune, Experimental

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Deletion

Share to Immune System

Share to Potassium Channels, Tandem Pore Domain

Share to Receptors, Antigen, T-Cell

Share to T-Lymphocytes

Share to Up-Regulation

Source

Open in PubMed Open full text

Identifiers

PMID: 26213925
DOI: 10.3390/ijms160816880
PMCID: PMC4581175

Genes

KCNK5

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Murine K2P5.1 Deficiency Has No Impact on Autoimmune Neuroinflammation due to Compensatory K2P3.1- and KV1.3-Dependent Mechanisms.PMID 26213925Read ↗

Kv1.3 deletion biases T cells toward an immunoregulatory phenotype and renders mice resistant to autoimmune encephalomyelitis.Semantic proximity Read ↗

Antigenic Stimulation of Kv1.3-Deficient Th Cells Gives Rise to a Population of Foxp3-Independent T Cells with Suppressive Properties.Semantic proximity Read ↗

Potassium channels as therapeutic targets for autoimmune disorders.Semantic proximity Read ↗

Kv1.3 in the spotlight for treating immune diseasesSemantic proximity Read ↗

Mutation of the Polyproline Sequence in CD3ε Evidences TCR Signaling Requirements for Differentiation and Function of Pro-Inflammatory Tγδ17 Cells.Semantic proximity Read ↗

K2P18.1 translates T cell receptor signals into thymic regulatory T cell developmentSemantic proximity Read ↗

Cocktails of KLK5 Protease Inhibitors and Anti-TNFα Therapeutics: an Effective Treatment for Netherton Syndrome.Semantic proximity Read ↗

TRPV1 gates tissue access and sustains pathogenicity in autoimmune encephalitis.Semantic proximity Read ↗

IKK2 controls the inflammatory potential of tissue-resident regulatory T cellsSemantic proximity Read ↗

Tyro3 worsens the clinical course of experimental autoimmune encephalomyelitis in mice and is associated with suppression of interleukin-4.Semantic proximity Read ↗

Regulatory role of KCa3.1 in immune cell function and its emerging association with rheumatoid arthritisSemantic proximity Read ↗

Emerging role for the voltage-dependent K+ channel Kv1.5 in B-lymphocyte physiology: expression associated with human lymphoma malignancy.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.