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Of two Jak2 paralogues present in zebrafish, Jak2a but not Jak2b is involved in the intracellular transmission of the Ifn-gamma signal.
JAK2 V617F-positive polycythemia vera is associated with B-cell acute lymphoblastic leukemia.
study confirms the clinical significance of driver mutational status and JAK2(mut) load in MPNs; in addition, unravels a novel clinical association between high CALR(mut) load and a more proliferative phenotype in ET
This study explored the relationship between mutations in the Janus kinase 2 gene ( JAK2), MPL, and the calreticulin gene ( CALR) in Uygur and Han Chinese patients with BCR-ABL fusion gene-negative myeloproliferative neoplasms.
Mutations in the JAK2 V617F with concomitant del(5q) is associated with transformation of Myelodysplastic syndrome to acute myeloid leukemia.
Study demonstrates that GM-CSF stimulates the interaction between JAK2 and Cbl, which promotes JAK2 ubiquitination. The K970 ubiquitination site on JAK2 is found to be important for JAK2 phosphorylation, and for downstream signal transduction.
this study shows that endothelial cells harbouring the JAK2V617F mutation display pro-adherent and pro-thrombotic features
The kinase inhibitory region of SOCS1 targets the substrate binding groove of JAK1 and JAK2 with high specificity and thereby blocks any subsequent phosphorylation.
Clonal analysis shows that the dominant JAK2 V617F-positive clone in Polycythemia Vera harbors EGFR C329R substitution, thus this mutation may contribute to clonal expansion.
Patients with CALR mutation had significantly higher concentration of PDGF-BB and lower concentration of SDF-1alpha than patients with JAK2V617F mutation. High concentration of PDGF-BB and low concentration of SDF-1alpha in patients with CALR(+) ET may indicate a contribution of these chemokines in disturbed Ca2+ metabolism in platelets.
Here, we present two crystal structures of the human JAK2 FERM and SH2 domains bound to Leptin receptor (LEPR) and Erythropoietin receptor (EPOR), which identify a novel dimeric conformation for JAK2.
pathogenesis mechanism of JAK2 F556V mutation in the MPNs
Mir-204 attenuates angiogenesis in lung adenocarcinoma via JAK2-STAT3 pathway.
FEZF1-AS1 acts as an oncogenic lncRNA in human hepatocellular carcinoma by promoting JAK2/STAT3 signaling-mediated epithelial mesenchymal transformation.
Case Reports/Review: JAK2 mutation-associated cerebral arterial infarction and cerebral and systemic venous thromboembolism.
HSP27 is a partner of JAK2-STAT5 and a potential therapeutic target in myelofibrosis.
Our study suggests that JAK2V617F mutation may increase the risk of thrombosis in chronic myeloproliferative neoplasms.
Progression to polythythemia vera from familial thrombocytosis with germline JAK2 R867Q mutation.
JAK2 and STAT3 are activated in Idiopathic pulmonary fibrosis
The expression of Chemokine (C-X-C motif) ligand 12 (CXCL12) and stem cell factor (SCF) were upregulated in JAK2V617F-bearing ECs.
SOCS2 negatively regulates the development of natural killer cells by inhibiting JAK2 activity via direct interaction.
Janus kinase 2 protein (JAK2) and beta-catenin were found to interact with cadherin-22 (Cdh22) and involved in CDH22 signaling in female germ line stem cells (FGSCs).
results suggest that IL-6 gene requires up-regulation of phospho-JAK2/STAT3, PACAP, and PAC1R and down-regulation of the TNF-alpha gene to modulate its anticonvulsive/neuroprotective potential
While expression of mutant Jak2 was necessary for leukemia induction, neither its continued expression nor enzymatic activity was required to maintain leukemia survival and rapid proliferation
High JAK2 expression is associated with graft-versus-host disease.
Results demonstrate that JAK2 deficiency delays tumor formation in GH-transgenic mice, which is linked to insignificant oncogenic STAT3 signaling and reduced reactive oxygen species-induced oxidative damage.
Reg3g acts as an immunosuppressive promoter by activating the JAK2/STAT3 signaling pathway in dendritic cells and triggering the generation of an immunosuppressive tumor microenvironment.
High JAK2 expression is associated with skeletal muscle wasting in cancer cachexia.
Data (including data from studies in knockout mice) suggest that various tissues utilize Jak2 signaling to regulate insulin, glucose, and lipid metabolism; adipocyte Jak2 appears to regulate hepatic insulin resistance in mechanism independent of adiposity (obesity), liver lipid content (non-alcoholic fatty liver disease), and hepatic insulin signaling.
Advanced glycation end products induce apoptosis and inflammation in mouse podocytes through CXCL9-mediated JAK2/STAT3 pathway activation.
Cilostazol protects MIR injury by activating a PPARgamma/JAK2/STAT3 pathway.
These results suggest that JAK2 regulated the microfilaments aggregation during the mouse oocyte maturation.
alpha7nAChR stimulation reduced neuroinflammation via activation of the JAK2-STAT3 pathway, thereby ameliorating the short- and long-term sequelae after intracerebral hemorrhage .
After Dox treatment, the protein expression of p-Jak2 and p-Stat3 levels was significantly increased in MT(+/+) cardiomyocytes, suggesting that the JAK2/STAT3 pathway was partially involved in MT protection against Dox-induced cardiotoxicity
CIS interacted with phosphorylated EpoR at Y401, which was critical for the activation of STAT5 and ERK.
Cell volume homeostasis requiring Na+/H+ exchange signaled by JAK2 first becomes prominent during mouse embryonic development at the late one-cell stage.
a novel signaling axis that regulates JAK2 in normal and malignant HSPCs and suggest new therapeutic strategies for treating CBL(mut) myeloid malignancies.
In summary, JAK2 functions in a homeostatic capacity in podocytes by facilitating autophagy. It does this by regulating the expression of the transcription factor TFEB that is necessary for normal autophagic-lysosomal function
nitration of JAK2 may act as an inhibitory counterpart to phosphorylation activation, reflecting a very localized break on the progression of GH signal transduction processes spanning JAK-STAT-AKT interactions
Janus kinase 2 (JAK2) gene polymorphism is a potential marker for milk production traits in cattle
Results indicate that SNPs in STAT5A and JAK2 genes were associated with somatic cell count and score in milk and cytokines but none of the SNP was associated with milk production traits suggesting an important role in immunity.
Methionine promoted casein synthesis, and this may be mediated by enhanced intracellular substrate availability and by activating JAK2-STAT5 and mTOR signaling pathways.
SNPs in JAK2 and STAT5B are associated with mastitis susceptibility in Chinese Holstein cattle
These applications affect not only EC in the monolayer but also circulating detached cells and involve mechanistic interactions not previously described.
Localized changes in the state of nitration of regulatory phosphorylation domains of JAK2 in caveoLAE during inflammation suggest a unique mechanism through which discrete signal transduction switching might occur in the liver
This gene product is a protein tyrosine kinase involved in a specific subset of cytokine receptor signaling pathways. It has been found to be constituitively associated with the prolactin receptor and is required for responses to gamma interferon. Mice that do not express an active protein for this gene exhibit embryonic lethality associated with the absence of definitive erythropoiesis.
, PTK JAK2b
, protein tyrosine kinase JAK2b
, tyrosine-protein kinase JAK2
, Janus kinase 2 (a protein tyrosine kinase)
, tyrosine kinase