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Mouse Monoclonal Anti-JAK2 antibody (STJ98896)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, ELISA
Recommended dilution: WB 1:500-2000; ELISA 1:10000-20000
Recommended protocols: check protocols
Click or hover above images to see image description for Anti-JAK2 antibody.
Check alternative names for the antibodyExpand
|JAK 2 antibody|JAK-2 antibody|JAK2 antibody|JAK2_HUMAN antibody|Janus Activating Kinase 2 antibody|Janus kinase 2 (a protein tyrosine kinase) antibody|Janus kinase 2 antibody|JTK 10 antibody|JTK10 antibody|kinase Jak2 antibody|OTTHUMP00000043260 antibody|THCYT3 antibody|Tyrosine protein kinase JAK2 antibody|Tyrosine-protein kinase JAK2 antibody|Phospho anti-JAK2 (Y1007 + Y1008) antibody [E132] (ab32101)
SCBT cat No: sc-390539|sc-34479|sc-294|sc-278|sc-7229|sc-34480|sc-71461|sc-56921|sc-6932|sc-34481|
|Catalogue No.|| |
Human, Mouse, Rat
Anti-JAK2 antibody detects endogenous JAK2 protein .
Synthetic Peptide of JAK2.
|Recommended dilution|| |
WB 1:500-2000; ELISA 1:10000-20000
|Molecular weight|| |
Anti-JAK2 antibody was tube-contained in liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Anti-JAK2 antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
JAK 2 antibody, JAK-2 antibody, JAK2 antibody, JAK2_HUMAN antibody, Janus Activating Kinase 2 antibody, Janus kinase 2 (a protein tyrosine kinase) antibody, Janus kinase 2 antibody, JTK 10 antibody, JTK10 antibody, kinase Jak2 antibody, OTTHUMP00000043260 antibody, THCYT3 antibody, Tyrosine protein kinase JAK2 antibody, Tyrosine-protein kinase JAK2 antibody
|Database links|| |
|Protein function|| |
Non-receptor tyrosine kinase involved in various processes such as cell growth, development, differentiation or histone modifications. Mediates essential signaling events in both innate and adaptive immunity. In the cytoplasm, plays a pivotal role in signal transduction via its association with type I receptors such as growth hormone (GHR), prolactin (PRLR), leptin (LEPR), erythropoietin (EPOR), thrombopoietin (THPO); or type II receptors including IFN-alpha, IFN-beta, IFN-gamma and multiple interleukins (PubMed:7615558). Following ligand-binding to cell surface receptors, phosphorylates specific tyrosine residues on the cytoplasmic tails of the receptor, creating docking sites for STATs proteins (PubMed:9618263). Subsequently, phosphorylates the STATs proteins once they are recruited to the receptor. Phosphorylated STATs then form homodimer or heterodimers and translocate to the nucleus to activate gene transcription. For example, cell stimulation with erythropoietin (EPO) during erythropoiesis leads to JAK2 autophosphorylation, activation, and its association with erythropoietin receptor (EPOR) that becomes phosphorylated in its cytoplasmic domain. Then, STAT5 (STAT5A or STAT5B) is recruited, phosphorylated and activated by JAK2. Once activated, dimerized STAT5 translocates into the nucleus and promotes the transcription of several essential genes involved in the modulation of erythropoiesis. In addition, JAK2 mediates angiotensin-2-induced ARHGEF1 phosphorylation (PubMed:20098430). Plays a role in cell cycle by phosphorylating CDKN1B (PubMed:21423214). Cooperates with TEC through reciprocal phosphorylation to mediate cytokine-driven activation of FOS transcription. In the nucleus, plays a key role in chromatin by specifically mediating phosphorylation of ‘Tyr-41’ of histone H3 (H3Y41ph), a specific tag that promotes exclusion of CBX5 (HP1 alpha) from chromatin (PubMed:19783980). .
|Protein tissue specificity|| |
Ubiquitously expressed throughout most tissues. .
|Involvement in disease|| |
Note=Chromosomal aberrations involving JAK2 are found in both chronic and acute forms of eosinophilic, lymphoblastic and myeloid leukemia. Translocation t(8;9)(p22;p24) with PCM1 links the protein kinase domain of JAK2 to the major portion of PCM1. Translocation t(9;12)(p24;p13) with ETV6.; Budd-Chiari syndrome (BDCHS) [MIM:600880]: A syndrome caused by obstruction of hepatic venous outflow involving either the hepatic veins or the terminal segment of the inferior vena cava. Obstructions are generally caused by thrombosis and lead to hepatic congestion and ischemic necrosis. Clinical manifestations observed in the majority of patients include hepatomegaly, right upper quadrant pain and abdominal ascites. Budd-Chiari syndrome is associated with a combination of disease states including primary myeloproliferative syndromes and thrombophilia due to factor V Leiden, protein C deficiency and antithrombin III deficiency. Budd-Chiari syndrome is a rare but typical complication in patients with polycythemia vera. . Note=Disease susceptibility is associated with variations affecting the gene represented in this entry.; Polycythemia vera (PV) [MIM:263300]: A myeloproliferative disorder characterized by abnormal proliferation of all hematopoietic bone marrow elements, erythroid hyperplasia, an absolute increase in total blood volume, but also by myeloid leukocytosis, thrombocytosis and splenomegaly. . Note=The disease is caused by mutations affecting the gene represented in this entry.; Thrombocythemia 3 (THCYT3) [MIM:614521]: A myeloproliferative disorder characterized by excessive platelet production, resulting in increased numbers of circulating platelets. It can be associated with spontaneous hemorrhages and thrombotic episodes. . Note=The disease may be caused by mutations affecting the gene represented in this entry.; Myelofibrosis (MYELOF) [MIM:254450]: A disorder characterized by replacement of the bone marrow by fibrous tissue, occurring in association with a myeloproliferative disorder. Clinical manifestations may include anemia, pallor, splenomegaly, hypermetabolic state, petechiae, ecchymosis, bleeding, lymphadenopathy, hepatomegaly, portal hypertension. Note=The disease is caused by mutations affecting the gene represented in this entry.; Leukemia, acute myelogenous (AML) [MIM:601626]: A subtype of acute leukemia, a cancer of the white blood cells. AML is a malignant disease of bone marrow characterized by maturational arrest of hematopoietic precursors at an early stage of development. Clonal expansion of myeloid blasts occurs in bone marrow, blood, and other tissue. Myelogenous leukemias develop from changes in cells that normally produce neutrophils, basophils, eosinophils and monocytes. . Note=The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
Belongs to the protein kinase superfamily. Tyr protein kinase family. JAK subfamily. ; Contains 1 FERM domain. ; Contains 2 protein kinase domains. ; Contains 1 SH2 domain. Possesses 2 protein kinase domains. The second one probably contains the catalytic domain, while the presence of slight differences suggest a different role for protein kinase 1 (By similarity).
|Protein post-translational modifications|| |
Autophosphorylated, leading to regulate its activity. Leptin promotes phosphorylation on tyrosine residues, including phosphorylation on Tyr-813 (By similarity). Autophosphorylation on Tyr-119 in response to EPO down-regulates its kinase activity (By similarity). Autophosphorylation on Tyr-868, Tyr-966 and Tyr-972 in response to growth hormone (GH) are required for maximal kinase activity (By similarity). Also phosphorylated by TEC (By similarity). Phosphorylated on tyrosine residues in response to interferon gamma signaling (PubMed:7615558, PubMed:7673114). .
|Protein cellular localization|| |
Endomembrane system ; Peripheral membrane protein . Cytoplasm . Nucleus .
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St John’s Laboratory Ltd.
|Product type|| |
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