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Jak3-mediated phosphorylation of beta-catenin (show CTNNB1 ELISA Kits) suppressed EGF (show EGF ELISA Kits)-mediated epithelial-mesenchymal transition and facilitated epithelial barrier functions by AJ localization of phosphorylated beta-catenin (show CTNNB1 ELISA Kits) through its interactions with alpha-catenin (show CTNNA1 ELISA Kits).
frequency of JAK3 mutations in the JH2 domain was relatively low in extranodal natural killer/T-cell lymphoma, nasal type (NTCL) in contrast to a previous report; study identified novel JAK3H583Y- and JAK3G589D-activating mutations that were oncogenic and sensitive to a JAK3 inhibitor
In natural killer/T-cell lymphoma (NKTL) as a disease model, phosphorylation of EZH2 (show EZH2 ELISA Kits) by JAK3 promotes the dissociation of the PRC2 complex leading to decreased global histone H3 (show HIST3H3 ELISA Kits) lysine 27 methylation levels.
a causal relationship between MLH1 (show MLH1 ELISA Kits)-deficiency and incidence of oncogenic point mutations in tyrosine kinases driving cell transformation and acquired resistance to kinase-targeted cancer therapies, is reported.
JAK3 mediates smooth muscle cell proliferation and survival during injury-induced vascular remodeling.
Data indicate that phosphorylation of Janus kinase 3 (JAK3) and STAT3 (show STAT3 ELISA Kits) transcription factor (STAT3 (show STAT3 ELISA Kits)) was inhibited by latent membrane protein 1 (LMP1 (show PDLIM7 ELISA Kits))-IgG.
analysis of JAK3 kinetic mechanism and inhibition by tofacitinib
patient had a homozygote of the JAK3 mutation, and her parents were heterozygous carriers.
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.
Small-scale in vivo screening identified several genes, including Cd109 (show CD109 ELISA Kits), that encode novel pro-metastatic factors. We uncovered signaling mediated by Janus kinases (Jaks) and the transcription factor Stat3 (show STAT3 ELISA Kits) as a critical, pharmacologically targetable effector of CD109 (show CD109 ELISA Kits)-driven lung cancer metastasis
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.
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
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.
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