Product nameAnti-JAK2 (phospho Y1007) antibody
See all JAK2 primary antibodies
DescriptionRabbit polyclonal to JAK2 (phospho Y1007)
Tested applicationsSuitable for: IHC-P, WBmore details
Species reactivityReacts with: Mouse, Rat, Human
Synthetic peptide within Human JAK2 (phospho Y1007). The exact sequence is proprietary.
Database link: O60674
- HT29 cell extract treated with IL-4, Human breast carcinoma tissue.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.3
Preservative: 0.02% Sodium azide
Constituents: 50% Glycerol, 49% PBS
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab195055 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||1/50 - 1/100.|
|WB||1/500 - 1/2000. Predicted molecular weight: 131 kDa.|
FunctionNon-receptor tyrosine kinase involved in various processes such as cell cycle progression, apoptosis, mitotic recombination, genetic instability and histone modifications. In the cytoplasm, plays a pivotal role in signal transduction via its association with cytokine receptors, which constitutes an initiating step in signaling for many members of the cytokine receptor superfamily including the receptors for growth hormone (GHR), prolactin (PRLR), leptin (LEPR), erythropoietin (EPOR), granulocyte-macrophage colony-stimulating factor (CSF2), thrombopoietin (THPO) and multiple interleukins. Following stimulation with erythropoietin (EPO) during erythropoiesis, it is autophosphorylated and activated, leading to its association with erythropoietin receptor (EPOR) and tyrosine phosphorylation of residues in the EPOR cytoplasmic domain. Also involved in promoting the localization of EPOR to the plasma membrane. Also acts downstream of some G-protein coupled receptors. Plays a role in the control of body weight (By similarity). Mediates angiotensin-2-induced ARHGEF1 phosphorylation. 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.
Tissue specificityExpressed in blood, bone marrow and lymph node.
Involvement in diseaseNote=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.
Defects in JAK2 are a cause of susceptibility to Budd-Chiari syndrome (BCS) [MIM:600880]. It is 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.
Defects in JAK2 are a cause of 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.
Defects in JAK2 gene may be a cause of essential thrombocythemia (ET) [MIM:187950]. ET is characterized by elevated platelet levels due to sustained proliferation of megakaryocytes, and frequently lead to thrombotic and haemorrhagic complications.
Defects in JAK2 are a cause of myelofibrosis (MYELOF) [MIM:254450]. Myelofibrosis is 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.
Defects in JAK2 are a cause of acute myelogenous leukemia (AML) [MIM:601626]. AML is a malignant disease in which hematopoietic precursors are arrested in an early stage of development.
Sequence similaritiesBelongs to the protein kinase superfamily. Tyr protein kinase family. JAK subfamily.
Contains 1 FERM domain.
Contains 1 protein kinase domain.
Contains 1 SH2 domain.
DomainPossesses 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.
modificationsAutophosphorylated, leading to regulate its activity. Leptin promotes phosphorylation on tyrosine residues, including phosphorylation on Tyr-813. Autophosphorylation on Tyr-119 in response to EPO down-regulates its kinase activity. Autophosphorylation on Tyr-868, Tyr-966 and Tyr-972 in response to growth hormone (GH) are required for maximal kinase activity.
Cellular localizationEndomembrane system. Nucleus.
- Information by UniProt
- JAK 2 antibody
- JAK-2 antibody
- JAK2 antibody
All lanes : Anti-JAK2 (phospho Y1007) antibody (ab195055) at 1/500 dilution
Lane 1 : HT29 cell extract untreated
Lane 2 : HT29 cell extract treated with IL-4
Predicted band size: 131 kDa
Immunohistochemical analysis of paraffin-embedded human breast carcinoma tissue labeling JAK2 with ab195055 at a 1/50 dilution.
This product has been referenced in:
- Geng Z et al. FNDC5 attenuates obesity-induced cardiac hypertrophy by inactivating JAK2/STAT3-associated inflammation and oxidative stress. J Transl Med 17:107 (2019). Read more (PubMed: 30940158) »
- Chen PJ et al. microRNA-874 inhibition targeting STAT3 protects the heart from ischemia-reperfusion injury by attenuating cardiomyocyte apoptosis in a mouse model. J Cell Physiol 234:6182-6193 (2019). Read more (PubMed: 30370578) »