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磷酸化蛋白酪氨酸激酶JAK-2抗体

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  • ¥2200
  • Biorigin
  • BN40820R
  • 2025年08月02日
  • WB,IHC-P,ICC,
  • Human,Mouse,Rat,Chicken,Pig,Rabbit,Daniorerio,
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    • 详细信息
    • 文献和实验
    • 技术资料
    • 适应物种

      Human,Mouse,Rat,Chicken,Pig,Rabbit,Daniorerio,

    • 应用范围

      WB,IHC-P,ICC,

    • 抗体英文名

      phospho-JAK2 (Tyr1007+Tyr1008)

    • 规格

      100ul

    英文名称 phospho-JAK2 (Tyr1007+Tyr1008)
    中文名称 磷酸化蛋白酪氨酸激酶JAK-2抗体
    别    名 JAK2 (phospho Y1007); p-JAK2 (phospho Y1007); JAK2 (phospho Y1007 + Y1008); p-JAK2 (phospho Y1007 + Y1008); JAK2(Phospho-Tyr1007/1008); Tyrosine protein kinase JAK2; JAK 2; JAK-2; JAK2; JAK2_HUMAN; Janus Activating Kinase 2; Janus Kinase 2; JTK 10; JTK10; OTTHUMP00000043260; Tyrosine-protein kinase JAK2; Tyrosine protein kinase JAK2.  

     

     

    产品类型 磷酸化抗体 
    研究领域 肿瘤  细胞生物  染色质和核信号  信号转导  激酶和磷酸酶  表观遗传学  
    抗体来源 Rabbit
    克隆类型 Polyclonal
    交叉反应 Human, Mouse, Rat,  (predicted: Chicken, Pig, Rabbit, Daniorerio,)
    产品应用 ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=1μg/Test ICC=1:100-500 IF=1:100-500 (石蜡切片需做抗原修复)
    not yet tested in other applications.
    optimal dilutions/concentrations should be determined by the end user.
    分 子 量 131kDa
    细胞定位 细胞核 细胞浆 细胞膜 
    性    状 Liquid
    浓    度 1mg/ml
    免 疫 原 KLH conjugated Synthesised phosphopeptide derived from human JAK2 around the phosphorylation site of Tyr1007/1008:KE(p-Y)(p-Y)KV 
    亚    型 IgG
    纯化方法 affinity purified by Protein A
    储 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
    保存条件 Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
    PubMed PubMed
    产品介绍 JAK2 (Janus Activating Kinase 2) is a tyrosine kinase of the non-receptor type, that associates with the intracellular domains of cytokine receptors; JAK2 is the predominant JAK kinase activated in response to several growth factors and cytokines such as IL-3, GM-CSF and erythropoietin; it has been found to be constitutively associated with the prolactin receptor and is required for responses to gamma interferon. Ligand binding to a variety of cell surface receptors (e.g., cytokine, growth factor, GPCRs) leads to an association of those receptors with JAK proteins, which are then activated via phosphorylation on tyrosines 1007 and 1008 in the kinase activation loop. Activated JAK proteins phosphorylate and activate STAT (signal transducers and activators of transcription) proteins, which then dimerize and translocate to the nucleus. Once in the nucleus, STAT proteins bind to DNA and modify the transcription of various genes.

    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. 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.

    Subunit:
    Interacts with EPOR, LYN, SIRPA, SH2B1 and TEC. Interacts with IL23R, SKB1 and STAM2.

    Subcellular Location:
    Endomembrane system; Peripheral membrane protein. Cytoplasm. Nucleus.

    Tissue Specificity:
    Ubiquitously expressed throughout most tissues.

    Post-translational modifications:
    Autophosphorylated, 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. Also phosphorylated by TEC.

    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.
    Defects in JAK2 are a cause of susceptibility to 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.

    Similarity:
    Belongs to the protein kinase superfamily. Tyr protein kinase family. JAK subfamily.
    Contains 1 FERM domain.
    Contains 1 protein kinase domain.
    Contains 1 SH2 domain.

    SWISS:
    O60674

    Gene ID:
    3717

    Database links:

    Entrez Gene: 3717 Human

    Entrez Gene: 16452 Mouse

    Entrez Gene: 24514 Rat

    GenBank: NP_004963 Human

    Omim: 147796 Human

    SwissProt: O60674 Human

    SwissProt: Q62120 Mouse

    SwissProt: Q62689 Rat

    Unigene: 656213 Human

    Unigene: 275839 Mouse

    Unigene: 18909 Rat



    Important Note:
    This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

    激酶和磷酸酶(Kinases and Phosphatases)

     

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    图标文献和实验
    相关实验
    • 常见 8 大信号通路总结!

      介素、生长因子或其它化学信使的信号可以激活此受体;这激活了 JAK 的激酶功能,导致对其自身的磷酸化(磷酸基团作为蛋白质上的开关);接下来 STAT 蛋白结合到被磷酸化的受体上,在此 STAT 被 JAK 磷酸化;被磷酸化的 STAT 蛋白结合到另一个被磷酸化的 STAT 蛋白上(二聚化)并易位到细胞核中;在细胞核中,它结合到 DNA 上并启动转录那些响应 STAT 的基因。5. TGFβ/SMAD signaling pathwayTGFβ/SMAD 通路调控机制:TGF-β 双聚体会结合到 type

    • 受体相关性蛋白酪氨酸激酶介导的信号途径

      的。链与Tyk2连接。 细胞因子受体信号转导中JaklSTAT家族成员的分布 细胞因子和受体结合后受体分子即发生聚合,造成与之相连的Jak蛋白酪氨酸激酶相互靠拢,彼此发生磷酸化而激活。激活的Jak启动多条信号转导途径。最短的也是最重要的一条途径是先使得受体分子胞内区上的酪氨酸残基发生磷酸化,通过转录因子STAT基因激活。表5-4表明,STAT也是一个家族,不同的Jak激活不同的STAT家族成员,进而活化不同的细胞因子基因。例如STAT 5和STAT 6 分别参与ⅡJ―2R

    • Mol Cell:浙大王青青团队等合作揭示乳酸化调控 RNA m⁶A 修饰促进肿瘤浸润髓系细胞的免疫抑制功能

      削弱其促进肿瘤的能力。RNA-seq 分析提示 JAK-STAT 可能是 METLL3 调控的下游通路,TIMs 的 JAK-STAT 通路对其促肿瘤作用具有枢纽性作用(2022 年是 JAK-STAT 通路发现 30 周年 [6])。作者利用 m6A 甲基化免疫共沉淀测序分析,证实 TIMs 中 Jak1 的 mRNA 上 m6A 修饰增加,以 m6A-YTHDF1 依赖形式提高其在多聚核糖体的翻译效率。JAK1 促进转录因子 STAT3 的磷酸化,启动 STAT3 下游免疫抑制效应分子 IL

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