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Janus kinase 2

JAK2, Janus Kinase 2
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: STAT3, HAD, MPN, CAN, V1a
Papers using JAK2 antibodies
Jak2 FERM Domain Interaction with the Erythropoietin Receptor Regulates Jak2 Kinase Activity.
Lau Andy T. Y., In PLoS ONE, 2007
... Antibodies were from the following sources: anti-pTyr1007/1008 JAK2 antibodies, Cell Signaling Technology; anti-His antibody, Sigma-Aldrich; ...
Invasion activating caveolin-1 mutation in human scirrhous breast cancers
Watson Christine J. et al., In Cell Death and Differentiation, 2000
... MIG-, JAK2 wt- or JAK2 V617F-MCF-7 cells resuspended in 25% Matrigel (BD Biosciences, San Jose, California, USA) ...
Papers on JAK2
Scutellarin protects cardiomyocyte ischemia-reperfusion injury by reducing apoptosis and oxidative stress.
Xu et al., Jinan, China. In Life Sci, Feb 2016
Activation of JAK2/STAT3 signaling and expression of pro- or anti-survival molecules were detected by Western blot.
PD-L1 Is Upregulated by Simultaneous Amplification of the PD-L1 and JAK2 Genes in Non-Small Cell Lung Cancer.
Maehara et al., Fukuoka, Japan. In J Thorac Oncol, Jan 2016
Janus kinase 2 gene (JAK2) CNA and its influence on the PD-L1/PD-1 pathway were also assessed.
Myelodysplastic syndromes: Contemporary review and how we treat.
Tefferi et al., Rochester, United States. In Am J Hematol, Jan 2016
With the advent of next generation sequencing, recurrent somatic mutations in genes involved in epigenetic regulation (TET2, ASXL1, EZH2, DNMT3A, IDH1/2), RNA splicing (SF3B1, SRSF2, U2AF1, ZRSR2), DNA damage response (TP53), transcriptional regulation (RUNX1, BCOR, ETV6) and signal transduction (CBL, NRAS, JAK2) have been identified in MDS.
Hyperactivated mTOR and JAK2/STAT3 Pathways: Molecular Drivers and Potential Therapeutic Targets of Inflammatory and Invasive Ductal Breast Cancers After Neoadjuvant Chemotherapy.
Schneider et al., New Haven, United States. In Clin Breast Cancer, Jan 2016
PATIENTS AND METHODS: Archival tumor tissue from 3 disease types (IBC treated with neoadjuvant chemotherapy [NAC], n = 45; invasive ductal carcinoma [IDC] treated with NAC [n = 24; 'treated IDC'; and untreated IDC [n = 27; 'untreated IDC']) was analyzed for the expression of biomarkers phospho-S6 (pS6) (mTOR), phospho-JAK2 (pJAK2), pSTAT3, interleukin (IL)-6, CD68 (monocytes, macrophages), and CD163 (TAMs).
Randomized, Double-Blind, Phase II Study of Ruxolitinib or Placebo in Combination With Capecitabine in Patients With Metastatic Pancreatic Cancer for Whom Therapy With Gemcitabine Has Failed.
Levy et al., Durham, United States. In J Clin Oncol, Jan 2016
PATIENTS AND METHODS: In this double-blind, phase II study, patients with metastatic pancreatic cancer who had experienced treatment failure with gemcitabine were randomly assigned 1:1 to the JAK1/JAK2 inhibitor ruxolitinib (15 mg twice daily) plus capecitabine (1,000 mg/m(2) twice daily) or placebo plus capecitabine.
The significance of microRNA-184 on JAK2/STAT3 signaling pathway in the formation mechanism of glioblastoma.
Zhai et al., Linyi, China. In Oncol Lett, Dec 2015
The aim of the present study was to examine the expression of microRNA (miR)-184 in Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway in the mechanism of glioblastoma formation, thus providing a new basis for the mechanism of glioblastoma induction.
Acquired uniparental disomy of chromosome 9p in hematological malignancies.
Prchal et al., Houston, United States. In Exp Hematol, Dec 2015
Since then, systematic application of genome-wide single nucleotide polymorphism arrays has demonstrated that 9p aUPD is the most common chromosomal aberration in myeloproliferative neoplasms (MPN) contributing to discovery of PV-defining mutation JAK2(V617F).
Myeloproliferative neoplasms: Current molecular biology and genetics.
Saeidi, Kermān, Iran. In Crit Rev Oncol Hematol, Dec 2015
These findings showed that JAK2V617F, as a diagnostic marker involving JAK2 exon 14 with a high frequency, is the best molecular characterization of Ph-MPNs.
Polycythemia Vera: An Appraisal of the Biology and Management 10 Years After the Discovery of JAK2 V617F.
Hoffman et al., Chicago, United States. In J Clin Oncol, Dec 2015
A decade after the seminal discovery of an activating mutation in the tyrosine kinase JAK2 in nearly all patients with PV, new treatment options are finally beginning to emerge, necessitating a critical reappraisal of the underlying pathogenesis and therapeutic modalities available for PV.
Guidelines for the management of myeloproliferative neoplasms.
Won et al., Seoul, South Korea. In Korean J Intern Med, Nov 2015
The discovery of new genetic aberrations such as Janus kinase 2 (JAK2) have enhanced our understanding of the pathophysiology of MPNs.
Cardiotrophin-1 promotes cardiomyocyte differentiation from mouse induced pluripotent stem cells via JAK2/STAT3/Pim-1 signaling pathway.
Cao et al., Xi'an, China. In J Geriatr Cardiol, Nov 2015
Western blot demonstrated that CT-1 promotes cardiomyocyte differentiation from miPSCs partly via JAK2/STAT3/Pim-1 pathway as compared with control group.
A Pilot Study of the Telomerase Inhibitor Imetelstat for Myelofibrosis.
Pardanani et al., Rochester, United States. In N Engl J Med, Oct 2015
Response rates were 27% among patients with a JAK2 mutation versus 0% among those without a JAK2 mutation (P=0.30) and 32% among patients without an ASXL1 mutation versus 0% among those with an ASXL1 mutation (P=0.07).
Telomerase Inhibitor Imetelstat in Patients with Essential Thrombocythemia.
Snyder et al., Bern, Switzerland. In N Engl J Med, Oct 2015
Molecular responses were seen in 7 of 8 patients who were positive for the JAK2 V617F mutation (88%; 95% confidence interval, 47 to 100).
Effect of methotrexate on JAK/STAT pathway activation in myeloproliferative neoplasms.
Zeidler et al., Sheffield, United Kingdom. In Lancet, Mar 2015
50-95% of patients have an acquired mutation (JAK2V617F) causing constitutive activation of JAK2.
HSP90 and HSP70: Implication in Inflammation Processes and Therapeutic Approaches for Myeloproliferative Neoplasms.
de Thonel et al., Dijon, France. In Mediators Inflamm, 2014
Through their chaperone activity, HSP90, a stabilizer of many oncogenes (e.g., JAK2), and HSP70, a powerful antiapoptotic chaperone, tightly regulate Nuclear Factor-kappa B signalling, a critical pathway in mediating inflammatory responses.
Clinical significance of clonality assessment in JAK2V617F-negative essential thrombocythemia.
Bellosillo et al., Barcelona, Spain. In Ann Hematol, 2012
Disease transformation is associated with clonality in JAK2V617F-negative essential thrombocythemia.
Negative regulation of JAK2 by H3K9 methyltransferase G9a in leukemia.
Seo et al., Seoul, South Korea. In Mol Cell Biol, 2012
data show that HMTase G9a negatively regulates JAK2 transcription and H3Y41 phosphorylation on the lmo2 promoter; and study provides new insights into G9a function in the regulation of hematopoiesis and leukemogenesis
Crystal structures of the JAK2 pseudokinase domain and the pathogenic mutant V617F.
Hubbard et al., New York City, United States. In Nat Struct Mol Biol, 2012
The structural and biochemical data indicate that the V617F mutation rigidifies alpha-helix C in the N lobe of pseudokinase domain JH2, facilitating trans-phosphorylation of tyrosine kinase domain JH1.
Tyrosine kinase pathways modulate tumor susceptibility to natural killer cells.
Ritz et al., Boston, United States. In J Clin Invest, 2012
Gene silencing of two members of the JAK family, JAK1 and JAK2, increased the susceptibility of a variety of tumor cell types to natural killer-mediated lysis
Prevalence of JAK29V617F) mutation in intra-abdominal venous thrombosis.
Shah et al., Mumbai, India. In Trop Gastroenterol, 2011
idiopathic IAVT patients must be screened for JAK2(V617F) mutation to detect latent MPD
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