Recombinant Human Tyrosine-protein kinase JAK2 (JAK2), partial

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Code CSB-EP011931HU
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Size $224
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
  • Based on the SEQUEST from database of E.coli host and target protein, the LC-MS/MS Analysis result of CSB-EP011931HU could indicate that this peptide derived from E.coli-expressed Homo sapiens (Human) JAK2.
  • Based on the SEQUEST from database of E.coli host and target protein, the LC-MS/MS Analysis result of CSB-EP011931HU could indicate that this peptide derived from E.coli-expressed Homo sapiens (Human) JAK2.
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Product Details

Purity
Greater than 90% as determined by SDS-PAGE.
Target Names
JAK2
Uniprot No.
Research Area
Immunology
Alternative Names
JAK 2; JAK-2; JAK2; JAK2_HUMAN; Janus Activating Kinase 2; Janus kinase 2 (a protein tyrosine kinase); Janus kinase 2; JTK 10; JTK10; kinase Jak2; OTTHUMP00000043260; THCYT3; Tyrosine protein kinase JAK2; Tyrosine-protein kinase JAK2
Species
Homo sapiens (Human)
Source
E.coli
Expression Region
752-1132aa
Target Protein Sequence
KPLSALDSQRKLQFYEDRHQLPAPKWAELANLINNCMDYEPDFRPSFRAIIRDLNSLFTPDYELLTENDMLPNMRIGALGFSGAFEDRDPTQFEERHLKFLQQLGKGNFGSVEMCRYDPLQDNTGEVVAVKKLQHSTEEHLRDFEREIEILKSLQHDNIVKYKGVCYSAGRRNLKLIMEYLPYGSLRDYLQKHKERIDHIKLLQYTSQICKGMEYLGTKRYIHRDLATRNILVENENRVKIGDFGLTKVLPQDKEYYKVKEPGESPIFWYAPESLTESKFSVASDVWSFGVVLYELFTYIEKSKSPPAEFMRMIGNDKQGQMIVFHLIELLKNNGRLPRPDGCPDEIYMIMTECWNNNVNQRPSFRDLALRVDQIRDNMAG
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
48.6kDa
Protein Length
Partial
Tag Info
N-terminal 6xHis-tagged
Form
Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer
If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
3-7 business days
Notes
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA
Please contact us to get it.
Description

The region for expressing recombinant Human JAK2 contains amino acids 752-1132. This JAK2 protein is expected to have a theoretical molecular weight of 48.6 kDa. This JAK2 protein is produced using e.coli expression system. The JAK2 gene fragment has been modified by fusing the N-terminal 6xHis tag, providing convenience in detecting and purifying the recombinant JAK2 protein during the following stages.

Human tyrosine-protein kinase JAK2 is a pivotal enzyme involved in signal transduction pathways triggered by a variety of cytokines and growth factors. As a member of the JAK family, JAK2 plays a crucial role in mediating signals from cell surface receptors, particularly those associated with hematopoietic factors. Upon ligand binding to its respective receptor, JAK2 becomes activated, leading to the phosphorylation of downstream signaling molecules, such as signal transducers and activators of transcription (STATs). This activation cascade regulates diverse cellular processes, including immune responses, hematopoiesis, and cell proliferation. Dysregulation of JAK2 has been implicated in various diseases, including myeloproliferative neoplasms, making it an important target for therapeutic interventions.

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Target Background

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. Following ligand-binding to cell surface receptors, phosphorylates specific tyrosine residues on the cytoplasmic tails of the receptor, creating docking sites for STATs proteins. 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. Part of a signaling cascade that is activated by increased cellular retinol and that leads to the activation of STAT5 (STAT5A or STAT5B). In addition, JAK2 mediates angiotensin-2-induced ARHGEF1 phosphorylation. Plays a role in cell cycle by phosphorylating CDKN1B. 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.
Gene References into Functions
  1. Clonal analysis shows that the dominant JAK2 V617F-positive clone in Polycythemia Vera harbors EGFR C329R substitution, thus this mutation may contribute to clonal expansion. PMID: 28550306
  2. Patients with CALR mutation had significantly higher concentration of PDGF-BB and lower concentration of SDF-1alpha than patients with JAK2V617F mutation. High concentration of PDGF-BB and low concentration of SDF-1alpha in patients with CALR(+) ET may indicate a contribution of these chemokines in disturbed Ca2+ metabolism in platelets. PMID: 29390868
  3. Here, we present two crystal structures of the human JAK2 FERM and SH2 domains bound to Leptin receptor (LEPR) and Erythropoietin receptor (EPOR), which identify a novel dimeric conformation for JAK2. PMID: 30044226
  4. pathogenesis mechanism of JAK2 F556V mutation in the MPNs PMID: 29842959
  5. Mir-204 attenuates angiogenesis in lung adenocarcinoma via JAK2-STAT3 pathway. PMID: 29281186
  6. FEZF1-AS1 acts as an oncogenic lncRNA in human hepatocellular carcinoma by promoting JAK2/STAT3 signaling-mediated epithelial mesenchymal transformation. PMID: 29957463
  7. Case Reports/Review: JAK2 mutation-associated cerebral arterial infarction and cerebral and systemic venous thromboembolism. PMID: 30056970
  8. HSP27 is a partner of JAK2-STAT5 and a potential therapeutic target in myelofibrosis. PMID: 29650953
  9. Our study suggests that JAK2V617F mutation may increase the risk of thrombosis in chronic myeloproliferative neoplasms. PMID: 30004057
  10. Progression to polythythemia vera from familial thrombocytosis with germline JAK2 R867Q mutation. PMID: 29368262
  11. JAK2 and STAT3 are activated in Idiopathic pulmonary fibrosis PMID: 29409529
  12. The prevalence of CALR mutation in JAK2V617F-negative essential thrombocythemia in this study is 35.7%. HRM is an effective method of detecting CALR mutation and is a more advantageous method of screening for CALR mutation. PMID: 29521158
  13. Comprehensive genomic characterization identified distinct genetic subgroups and provided a classification of myeloproliferative neoplasms on the basis of causal biologic mechanisms. Mutations in JAK2, CALR, or MPL being the sole abnormality in 45% of the patients. PMID: 30304655
  14. Findings outlined in the current study demonstrated that the inhibition of P16 decreased the growth and metastasis potential of BC cells by inhibiting IL-6/JAK2/STAT3 signaling. PMID: 29388151
  15. MPL-mutated and CALR-mutated essential thrombocythaemia share clinical and histological characteristics, with both genotypes showing higher platelet counts and a marked megakaryocytic proliferation in comparison with JAK2V617F-mutated ET. PMID: 29934356
  16. results herein provide clues to understand the mechanism JAK2 V625F mutation caused myeloproliferative neoplasms and give information for the development of JAK2 mutation specific inhibitors. PMID: 29782975
  17. Concomitant presence of JAK2V617F mutation and BCRABL translocation in two patients: A new entity or a variant of myeloproliferative neoplasms. PMID: 29845291
  18. The JAK2 V617F mutation and thrombocytopenia. PMID: 27614229
  19. PBX1 plays an oncogenic role in clear cell renal carcinoma via JAK2/STAT3 pathway PMID: 29678569
  20. Our study shows that JAK2V617F leads to abnormal expression of numerous proteins at the membrane of circulating PV red blood cells, with overexpression of CALR and persistence of CANX PMID: 28385780
  21. In 94.9% of PV, 85.5% ET and 85.2% PMF, authors found mutations in JAK2, MPL or CALR. 74.9% carried JAK2V617F, 12.3% CALR mutations, 2.1% MPL mutations and 10.7% were triple negative. PMID: 28990497
  22. tyrphostin B42 induced the apoptosis of pancreatic cancer cells (PCCs) by regulating the expression of mitochondrialrelated genes. Therefore, these findings demonstrated that tyrphostin B42 attenuated trichostatin A resistance in PCCs by antagonizing the IL6/JAK2/STAT3 signaling PMID: 29393444
  23. MiR-375 inhibits fetal ASM cell proliferation and migration by targeting JAK2/STAT3 signaling. PMID: 29245068
  24. data show that HIT is more frequent, during heparin treatment, in patients with ET carrying V617F mutation, as compared with patients without mutations PMID: 29022213
  25. Overexpression of ALK4 suppressed glioma cell proliferation, migration and invasion through the inactivation of JAK/STAT3 signaling pathway. PMID: 29278854
  26. We describe a subset of non-small-cell lung cancer patients who had JAK2 amplifications resulting in high expression of PD-L1 PMID: 28795418
  27. High JAK2 expression is associated with hepatocellular carcinoma. PMID: 28677802
  28. JAK2 haplotype 46/1 and JAK2 V617F allele burden in MPN PMID: 29134760
  29. Low JAK2 expression is associated with gastric cancer. PMID: 28656307
  30. The authors discovered tyrosine 78 of Atoh1 is phosphorylated by a Jak2-mediated pathway only in tumor-initiating cells and in human Sonic Hedgehog-type medulloblastoma. PMID: 29168692
  31. conclude that the activating JAK2 V617F mutation does not play a decisive role in the pathogenesis of progressive CKD PMID: 27889755
  32. Our findings revealed that B7-H3 affect ovarian cancer progression through the Jak2/Stat3 pathway, indicating that B7-H3 has the potential to be a useful prognostic marker. PMID: 28765941
  33. In 136 patients with myelofibrosis and a median age of 58 years who underwent allogeneic stem cell transplantation (AHSCT) for molecular residual disease, the percentage of molecular clearance on day 100 was higher in CALR-mutated patients (92%) in comparison with MPL- (75%) and JAKV617F-mutated patients (67%). PMID: 28714945
  34. Mutational subtypes of JAK2 correlate with different clinical features in Japanese patients with myeloproliferative neoplasms. PMID: 29464483
  35. identification of activating somatic mutations in JAK2 and germline mutations in JAK3 with clinical implications PMID: 29082853
  36. Screening for the JAK2 V617F mutation in cerebral venous thrombosis patients seems to be useful because of its relatively high prevalence and the risk of thrombosis recurrence. PMID: 28609766
  37. Ascochlorin significantly decreased phosphorylation of JAK2/STAT3, cancer cell migration and nuclear translocation of STAT3. PMID: 28569433
  38. TLR7, TLR9, and JAK2 genes are potential biomarkers for systemic sclerosis. High TLR7 expression positively correlated with the late form of disease. Decreased levels of TLR9 and JAK2 mRNA were found in the patient's cohort in comparison to non-SSc individuals. PMID: 29147913
  39. This study demonstrated that the JAK2V617F mutation was detectable in Patients with Stroke. PMID: 28625126
  40. Curcumin attenuated neuropathic pain and down-regulated the production of spinal mature IL-1beta by inhibiting the aggregation of NALP1 inflammasome and the activation of the JAK2-STAT3 cascade in astrocytes. PMID: 27381056
  41. High level of phosphorylated JAK2, and STAT3 are associated with systemic lupus erythematosus. PMID: 28177455
  42. this study shows that Nrf2 activation induces lipocyte phenotype in hepatic stellate cells via enhancing SOCS3-dependent feedback inhibition on JAK2/STAT3 cascade PMID: 28601022
  43. bladder cancer cell may inhibit maturation and function of dendritic cells involving of Jak2/STAT3 pathway, and there may be different mechanisms by which adriamycin-resistant BCC restrains DC function in antitumor immune response PMID: 27556503
  44. Multivariate analysis adjusted for age, sex, follow-up period and hematological parameters confirmed that increased activated B cells were universally present in JAK2-mutated, CALR-mutated and triple-negative ET patients when compared to healthy adults. PMID: 28415571
  45. In multivariable analysis, younger age, platelet count, hemoglobin level and JAK2 V617F mutation independently predicted the development of acquired von Willebrand syndrome (AVWS) among essential thrombocythemia (ET)patients; whereas only platelet count predicted its development among polycythemia vera (PV) patients. Among ET patients, JAK2 V617F was a main driver for the development of AVWS. PMID: 27919526
  46. CXCR4 induced VEGF production and JAK2/STAT3 activation and enhanced STAT3 binding to VEGF promoter in gastric cancer cells. PMID: 28544312
  47. these results reveal proteome alterations in MPN granulocytes depending on the phenotype and genotype of patients, highlighting new oncogenic mechanisms associated with JAK2 mutations and overexpression of calreticulin PMID: 28314843
  48. JAK2 mutation is associated with Essential thrombocythemia. PMID: 28205126
  49. Considering JAK2(V617F) -positive disease, a higher (>50%) JAK2(V617F) burden and histological classification are independent prognostic risk factors for disease progression. PMID: 28509339
  50. Taken together, we found that silibinin inhibits the Jak2/STAT3/MMP2 signaling pathway, and inhibits the proliferation, migration, and invasion of triple-negative breast cancer cells. PMID: 28440514

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Involvement in disease
Budd-Chiari syndrome (BDCHS); Polycythemia vera (PV); Thrombocythemia 3 (THCYT3); Myelofibrosis (MYELOF); Leukemia, acute myelogenous (AML)
Subcellular Location
Endomembrane system; Peripheral membrane protein. Cytoplasm. Nucleus.
Protein Families
Protein kinase superfamily, Tyr protein kinase family, JAK subfamily
Tissue Specificity
Ubiquitously expressed throughout most tissues.
Database Links

HGNC: 6192

OMIM: 147796

KEGG: hsa:3717

STRING: 9606.ENSP00000371067

UniGene: Hs.656213

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