JAK2 Monoclonal Antibody

中文名稱(chēng)：

JAK2鼠單克隆抗體
貨號(hào)：

CSB-MA181103
規(guī)格：

￥1090
圖片：
Immunohistochemical analysis of paraffin-embedded Human Lung Carcinoma Tissue using JAK2 Mouse mAb diluted at 1:200

Immunohistochemical analysis of paraffin-embedded Human Breast Carcinoma Tissue using JAK2 Mouse mAb diluted at 1:200
其他：

產(chǎn)品詳情
產(chǎn)品評(píng)價(jià)
相關(guān)產(chǎn)品
靶點(diǎn)詳情

產(chǎn)品詳情

產(chǎn)品描述：

CUSABIO貨號(hào)：CSB-MA181103 JAK2單克隆抗體是針對(duì)Janus激酶2（JAK2）靶點(diǎn)研發(fā)的高特異性科研試劑，適用于探索JAK-STAT信號(hào)通路調(diào)控機(jī)制及疾病相關(guān)性研究。JAK2作為酪氨酸激酶家族核心成員，在造血調(diào)控、免疫應(yīng)答及細(xì)胞增殖中發(fā)揮關(guān)鍵作用，其異常激活與骨髓增殖性腫瘤、白血病及自身免疫性疾病密切相關(guān)。本產(chǎn)品采用雜交瘤技術(shù)制備，經(jīng)嚴(yán)格驗(yàn)證可同時(shí)識(shí)別人、小鼠、大鼠來(lái)源的JAK2抗原，支持ELISA和免疫組化（IHC）雙重檢測(cè)平臺(tái)，滿足細(xì)胞定位分析及蛋白表達(dá)定量需求。其廣譜物種交叉反應(yīng)性為跨物種比較研究提供便利，特別適用于構(gòu)建血液系統(tǒng)疾病動(dòng)物模型、藥物靶點(diǎn)篩選及信號(hào)轉(zhuǎn)導(dǎo)通路機(jī)制解析等科研場(chǎng)景?？贵w批次穩(wěn)定性強(qiáng)，可重復(fù)性高，為JAK2相關(guān)轉(zhuǎn)錄調(diào)控、腫瘤微環(huán)境分析及分子互作研究提供可靠工具。該產(chǎn)品已成功應(yīng)用于多種腫瘤細(xì)胞系及組織樣本檢測(cè)，助力科研人員精準(zhǔn)解析JAK2在病理生理過(guò)程中的功能網(wǎng)絡(luò)。CUSABIO貨號(hào)：CSB-MA181103可通過(guò)各大生物試劑平臺(tái)快速檢索，適用于基礎(chǔ)研究、藥物開(kāi)發(fā)及生物標(biāo)志物探索等非診斷用途的JAK2單抗需求。
Uniprot No.：

O60674
基因名：

JAK2
別名：

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
宿主：

Mouse
反應(yīng)種屬：

Human,Mouse,Rat
免疫原：

Synthetic Peptide
免疫原種屬：

Homo sapiens (Human)
標(biāo)記方式：

Non-conjugated
純化方式：

The antibody was affinity-purified from mouse ascites by affinity-chromatography using specific immunogen.
克隆號(hào)：

27G9
濃度：

It differs from different batches. Please contact us to confirm it.
保存緩沖液：

Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
產(chǎn)品提供形式：

Liquid
應(yīng)用范圍：

ELISA,IHC

推薦稀釋比：

Application	Recommended Dilution
IHC	1:50-1:200

Protocols：

ELISA Protocol
Immunohistochemistry (IHC) Protocol
儲(chǔ)存條件：

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
貨期：

Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
用途：

For Research Use Only. Not for use in diagnostic or therapeutic procedures.

產(chǎn)品評(píng)價(jià)

靶點(diǎn)詳情

功能：

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.
基因功能參考文獻(xiàn)：
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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相關(guān)疾?。?/div>
Budd-Chiari syndrome (BDCHS); Polycythemia vera (PV); Thrombocythemia 3 (THCYT3); Myelofibrosis (MYELOF); Leukemia, acute myelogenous (AML)
亞細(xì)胞定位：

Endomembrane system; Peripheral membrane protein. Cytoplasm. Nucleus.
蛋白家族：

Protein kinase superfamily, Tyr protein kinase family, JAK subfamily
組織特異性：

Ubiquitously expressed throughout most tissues.
數(shù)據(jù)庫(kù)鏈接：

HGNC: 6192

OMIM: 147796

KEGG: hsa:3717

STRING: 9606.ENSP00000371067

UniGene: Hs.656213

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