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Foxp3 (show FOXP3 Proteins) has a rapid turn over in Treg partly controlled at the transcriptional level by the JAK/STAT (show STAT1 Proteins) pathway
Results confirm that JAK3 is mutated in T-PLL and underscore the potential therapeutical relevance of epigenetic regulator.
Data provide the first evidence that de-regulated Jak3/STAT3 (show STAT3 Proteins)/STAT5 (show STAT5A Proteins) signalling in CTCL (show TSPYL2 Proteins) cells represses the expression of the gene encoding miR (show MLXIP Proteins)-22, a novel tumor suppressor miRNA.
Study describes three patients with a novel deep intronic mis (show AMH Proteins)-splicing mutation in JAK3 as a cause of T-B+NK- severe combined immunodeficiency (show PRKDC Proteins).
Jak3 has a role in promoting mucosal tolerance through suppressed expression and limiting activation of TLRs thereby preventing intestinal and systemic chronic low-grade inflammation and associated obesity and MetS
that JAK3 may contribute to the pathogenesis of pediatric ALL and serve as an important therapeutic target which can be leveraged to improve outcomes for pediatric patients with ALL.
These results do not confirm association between JAK3 polymorphisms and cardiovascular disease in rheumatoid arthritis.
Activating Janus kinase 3 mutation is associated with mycosis fungoides.
The study reports the first patient with relapsed pediatric Early T-cell precursor acute lymphoblastic leukemia to exhibit a homozygous JAK3 activating mutation, V674A, caused by acquired uniparental disomy.
JAK inhibitor ruxolitinib (that inhibits mainly the JAK3/STAT5 (show STAT5A Proteins) pathway) affects key characteristics of human NK cells, such as cytokine-induced expansion and killing via an impaired cytokine-mediated NK cell activation
This study evaluated a chemical genetic toolkit that evaluated a biphasic requirement for JAK3 kinase activity in IL-2 (show IL2 Proteins)-driven T cell proliferation.
Experiments implicate JAK1 (show JAK1 Proteins)/3 signaling in cancer- and myocardial infarction-mediated diaphragm weakness in mice.
JAK3 contributes to the regulation of membrane Kv1.5 (show KCNA5 Proteins) protein abundance and activity, an effect sensitive to ouabain and thus possibly involving Na(+)/K(+) ATPase (show ATP1A1 Proteins) activity.
JAK3 deficiency is followed by down-regulation of cytosolic Ca(2 (show CA2 Proteins)+) release, receptor and store operated Ca(2 (show CA2 Proteins)+) entry and Na(+)/Ca(2 (show CA2 Proteins)+) exchanger activity in dendritic cells.
Our results demonstrate that JAK3/STAT6 (show STAT6 Proteins) has an important role in bone marrow-derived fibroblast activation, extracellular matrix production, and interstitial fibrosis development.
results showed that different JAK3 mutations induce constitutive activation through distinct mechanisms, pointing to specific therapeutic perspectives
JAK3 down-regulates Na(+)/K(+)-ATPase (show ATP1A1 Proteins) activity, an effect involving gene expression and profoundly curtailing ATP consumption.
In conclusion, JAK3 deficiency leads to increased formation of calcitriol, which contributes to or even accounts for increased release of FGF23 (show FGF23 Proteins) and enhanced intestinal phosphate absorption.
Data show that IL-4 (show IL4 Proteins) induces upregulation of the junction protein claudin-5 (show CLDN5 Proteins) in endothelial cells (ECs) through activation of Jak/STAT6 (show STAT6 Proteins) and phosphorylation and translocation of FoxO1 (show FOXO1 Proteins) from the nucleus to the cytoplasm.
The protein encoded by this gene is a member of the Janus kinase (JAK) family of tyrosine kinases involved in cytokine receptor-mediated intracellular signal transduction. It is predominantly expressed in immune cells and transduces a signal in response to its activation via tyrosine phosphorylation by interleukin receptors. Mutations in this gene are associated with autosomal SCID (severe combined immunodeficiency disease).
Janus kinase 3 (a protein tyrosine kinase, leukocyte)
, leukocyte Janus kinase
, tyrosine-protein kinase JAK3
, Janus kinase 3 protein-tyrosine kinase
, Janus kinase 3, protein-tyrosine kinase
, Janus tyrosine kinase