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JAK3 up-regulates SGLT1 (show SLC5A1 ELISA Kits) activity by increasing the carrier protein abundance in the cell membrane, an effect enforcing cellular glucose uptake into activated lymphocytes and thus contributing to the immune response.
JAK3 and MCL-1 (show MCL1 ELISA Kits) were down-regulated in patient CD8 (show CD8A ELISA Kits)(+) T cells versus their normal counterparts, likely due to defective suppressor activity of miR (show MLXIP ELISA Kits)-29b and miR (show MLXIP ELISA Kits)-198 in RCC (show XRCC1 ELISA Kits) CD8 (show CD8A ELISA Kits)(+) T cells.
N225K and A550V PTPN6 (show PTPN6 ELISA Kits) mutations cause loss-of-function leading to JAK3 mediated deregulation of STAT3 (show STAT3 ELISA Kits) pathway and uncover a mechanism that tumor cells can use to control PTPN6 (show PTPN6 ELISA Kits) substrate specificity.
Study shows JAK3 mutations in 16% of patients with T-cell prolymphocytic leukemia which might be an important prognostic marker.
This study showed that JAK3 is a powerful negative regulator of the creatine transporter SLC6A8 (show SLC6A8 ELISA Kits).
Letter/Case Report: ersistent rotavirus diarrhea post-transplant in a novel JAK3-SCID (show PRKDC ELISA Kits) patient after vaccination.
interleukin-4 (show IL4 ELISA Kits) regulates hematopoietic lineage choice by activating the JAK3-STAT6 (show STAT6 ELISA Kits) pathway, which causes dendritic-cell-specific DNA demethylation.
Foxp3 (show FOXP3 ELISA Kits) has a rapid turn over in Treg partly controlled at the transcriptional level by the JAK/STAT (show STAT1 ELISA Kits) 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 ELISA Kits)/STAT5 (show STAT5A ELISA Kits) signalling in CTCL (show TSPYL2 ELISA Kits) cells represses the expression of the gene encoding miR (show MLXIP ELISA Kits)-22, a novel tumor suppressor miRNA.
JAK1 (show JAK1 ELISA Kits), JAK2 (show JAK2 ELISA Kits), and JAK3 are involved in stimulation of functional activity of mesenchymal progenitor cells by fibroblast growth factor.
JAK mediated signaling is involved in the differentiation and proliferation of mesenchymal progenitor cells.
This study evaluated a chemical genetic toolkit that evaluated a biphasic requirement for JAK3 kinase activity in IL-2 (show IL2 ELISA Kits)-driven T cell proliferation.
Experiments implicate JAK1 (show JAK1 ELISA Kits)/3 signaling in cancer- and myocardial infarction-mediated diaphragm weakness in mice.
JAK3 contributes to the regulation of membrane Kv1.5 (show KCNA5 ELISA Kits) protein abundance and activity, an effect sensitive to ouabain and thus possibly involving Na(+)/K(+) ATPase (show ATP1A1 ELISA Kits) activity.
JAK3 deficiency is followed by down-regulation of cytosolic Ca(2 (show CA2 ELISA Kits)+) release, receptor and store operated Ca(2 (show CA2 ELISA Kits)+) entry and Na(+)/Ca(2 (show CA2 ELISA Kits)+) exchanger activity in dendritic cells.
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 (show MARS ELISA Kits)
Our results demonstrate that JAK3/STAT6 (show STAT6 ELISA Kits) has an important role in bone marrow-derived fibroblast activation, extracellular matrix production, and interstitial fibrosis development.
Data show that IL-4 (show IL4 ELISA Kits) induces upregulation of the junction protein claudin-5 (show CLDN5 ELISA Kits) in endothelial cells (ECs) through activation of Jak/STAT6 (show STAT6 ELISA Kits) and phosphorylation and translocation of FoxO1 (show FOXO1 ELISA Kits) 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