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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.
In patients with myelofibrosis, 1.5% coincidence of CALR and JAK2 V617F confirmed a different phenotype of the disease in CALR-mutated patients as compared with CALR-unmutated individuals. Those with CALR mutation were significantly younger and had borderline higher platelet counts, less pronounced splenomegaly and less frequent B symptoms at diagnosis.
de novo acute myeloid leukaemia with JAK2 V617F mutation has lower VAF, fewer complex karyotypes, more frequent mutations in genes encoding mediators of DNA methylation and less frequent splenomegaly.
Modest contribution of JAK2 V617F allele burden to the occurrence of major thrombosis in polycthemia vera and essential thrombocythemia
High JAK2 expression is associated with erythroblastic leukemia.
JAK2 Mutations are associated with Polycythaemia Vera.
Hyperprolactinemia-inducing antipsychotics instigate precancerous cells to progress to cancer via JAK/STAT5 to suppress the apoptosis anticancer barrier, and these cancer-promoting effects can be prevented by prophylactic anti-JAK/STAT5 treatment.
Heat shock protein 90 inhibitor (HSP90i)-resistant triple-negative breast cancer (TNBC) clones show selective sensitivity to Janus kinase 2 (JAK2) inhibition. Inhibition of JAK and HSP90 causes higher induction of apoptosis, despite prior acquired resistance to HSP90i. A combined inhibition of the JAK-STAT signalling pathway and HSP90 could overcome this resistance.
MPL, CALR and JAK2 are considered driver mutations in myeloproliferative neoplasms.The occurrence of two driver mutations in the same patient was determined and the clinical presentation and disease progression were compared with those in patients with only one driver mutation. Co-occurrence of 2 driver mutations affects the presentation or evolution of MPN, especially essential thrombocythemia.
Although driver mutations in JAK2, CALR, and MPL are generally considered mutually exclusive,15 patients with concomitant JAK2 V617F and CALR mutations were identified, of whom 10 had essential thrombocytosis. This supports the possibility of coexisting JAK2 V617F and CALR mutations.
JAK2 mRNA expression is associated with CpG island methylator phenotype (CIMP) status in human colorectal cancer.
JAK2 K607N and mutations disrupted this interaction enhanced JAK2-STAT5 pathway activation and the proliferation of Ba/F3 cells. Thus our studies provide clues in understanding the leukemogenesis of JAK2 K607N mutation in AML.
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.
Low-burden TP53 mutations in chronic phase of myeloproliferative neoplasms: association with age, hydroxyurea administration, disease type and JAK2 mutational status.
Fibrotic progression in Polycythemia vera is associated with early concomitant driver-mutations besides JAK2.
Efficacy of the Janus kinase 1/2 inhibitor ruxolitinib in the treatment of vasculopathy associated with TMEM173-activating mutations in 3 children.
Data found that the L884P mutation in JAK2 enhances the flexibility of the allosteric pocket and alters their conformations, which amplify the conformational entropy change (-TDeltaS) and weaken the interactions between the inhibitors and JAK2. It seems that both of the changes of the conformational entropies and enthalpies contribute to the L884P-induced resistance in the binding of JAK2 Type-II inhibitors.
Five patients had cytogenetic abnormalities (62.5%), with abnormalities in chromosomes -5, +8 and -7 being common. Eight patients underwent the JAK2 V617F gene test when diagnosed with MPN. The prognosis of patients with LT was poor, and the average survival time was 6.7 months
This gene product is a protein tyrosine kinase involved in a specific subset of cytokine receptor signaling pathways.
LncRNA TUG1 interacting with miR-144 contributes to proliferation, migration and tumorigenesis through activating the JAK2/STAT3 pathway in hepatocellular carcinoma.
321 and 86 patients were randomized in JANUS 1 (ruxolitinib: n = 161; placebo: n = 160) and JANUS 2 (ruxolitinib: n = 43; placebo: n = 43).
study identifies Plek2 as an effector of the JAK2/STAT5 pathway and a key factor in the pathogenesis of JAK2V617F-induced myeloproliferative neoplasms (MPNs), pointing to Plek2 as a viable target for the treatment of MPNs.
JAK2 activation regulates cPLA2 gene expression.
Aberrant expression of circular RNA circScd1 affects the extent of hepatocellular lipidosis in NAFLD and promotes fatty liver disease via the JAK2/STAT5 pathway.
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.
HSP27 is a partner of JAK2-STAT5 and a potential therapeutic target in myelofibrosis.
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.
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