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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 (show IFNG Proteins) signal.
ANGPTL1 (show ANGPTL1 Proteins) inhibited angiogenesis by interacting with integrin alpha1beta1 receptor to suppress the downstreamJAK2-STAT3 (show STAT3 Proteins) signaling pathway.
Therefore, JAK2V617F influences target binding in both pSTAT3 and EZH2 (show EZH2 Proteins). Without mutations in epigenetic regulators, JAK2V617F can induce downstream epigenomic modifications. Thus, epigenetic changes in JAK2 downstream targets might be trackable in vivo.
Subjects with JAK2V617F mutation and an allele burden>/=50% had an age-independent higher incidence of elevated hs-CRP (show CRP Proteins) level (OR=1.97; 95% CI,1.21-3.22; P=0.006) compared with a combined cohort of subjects with JAK2V617F <50% allele burden
High JAK2 expression is associated with neuroblastoma (show ARHGEF16 Proteins).
Study provides evidence that JAK1 (show JAK1 Proteins)/2 loss-of-function mutations are a genetic mechanism of lack of reactive PD-L1 (show CD274 Proteins) expression and response to interferon gamma (show IFNG Proteins), leading to primary resistance to PD-1 (show PDCD1 Proteins) blockade therapy.
Single-nucleotide polymorphism in JAK2 gene is associated with breast cancers.
When transduced into rad chimera mice, 3 human activating JAK2 mutants can differentially couple to selective cytokine receptors EpoR (show EPOR Proteins) and GCSFR (show CSF3R Proteins) and change the signaling repertoire, revealing the molecular basis for phenotypic differences elicited by JAK2 (V617F) or mutations in exon 12.
inhibition of the H3K27 demethylase (show MBD2 Proteins) JMJD3 in naive CD4 (show CD4 Proteins) T cells demonstrates how critically important molecules required for T cell differentiation, such as JAK2 and IL12RB2 (show IL12RB2 Proteins), are regulated by H3K27me3.
Testing for JAK2 mutations is now included in the World Health Organization (WHO) criteria for the diagnosis of MPN, and in 2011 the oral JAK2 kinase inhibitor ruxolitinib became the first Food and Drug Administration (FDA)-approved drug for the treatment of myelofibrosis.
In our study, there was no genotypic or phenotypic association between the JAK2 rs10758669 variant and UC. Only the (C) allele was identified to increase the risk of a more severe disease progression.
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 (show CBL Proteins)(mut (show MUT Proteins)) 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 (show TFEB Proteins) that is necessary for normal autophagic-lysosomal function
these findings demonstrate that expression of Hmga2 cooperates with Jak2(V617F) in the pathogenesis of Mmyelofibrosis.
Study shows that Jak2 with V617F mutation induces murine model for myeloproliferative neoplasm.
results suggest that loss of Ezh2 (show EZH2 Proteins) cooperates with Jak2V617F in the development of myelofibrosis in Jak2V617F
JAK2-V617F-expressing mice treated with an Ezh2 (show EZH2 Proteins) inhibitor showed higher platelet counts than vehicle controls. Our data support the proposed tumor suppressor function of EZH2 (show EZH2 Proteins)
findings demonstrate that clinically relevant doses of the JAK1 (show JAK1 Proteins)/2 inhibitor ruxolitinib suppresses the harmful consequences of macrophage overactivation characterizing Hemophagocytic lymphohistiocytosis in 2 murine models.
JAK2 has a role in hepatocarcinogenesis through regulating critical inflammatory pathways
Data show that CUZD1 (show CUZD1 Proteins) interacts with a complex containing JAK1 (show JAK1 Proteins)/JAK2 and STAT5 (show STAT5A Proteins), downstream transducers of prolactin (show PRL Proteins) signaling in the mammary gland.
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 (show JAK3 Proteins)-STAT (show STAT1 Proteins)-AKT (show AKT1 Proteins) interactions
Janus kinase 2 (JAK2) gene polymorphism is a potential marker for milk production traits in cattle
Results indicate that SNPs in STAT5A (show STAT5A Proteins) 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 (show STAT5A Proteins) and mTOR (show FRAP1 Proteins) signaling pathways.
SNPs in JAK2 and STAT5B (show STAT5B Proteins) are associated with mastitis susceptibility in Chinese Holstein cattle
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