PTEN Mouse mAb, BF647 conjugated(bsm-33319M-BF647)-100ul

PTEN Mouse mAb, BF647 conjugat

ed(bsm-33319M-BF647)-100ul
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  • ¥2980
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  • bsm-33319M-BF647
  • 2025年09月30日
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      100ul

    产品编号bsm-33319M-BF647
    英文名称PTEN Mouse mAb, BF647 conjugated
    中文名称BF647标记的肿瘤抑制基因PTEN单克隆抗体
    英文别名ITGA 2; MGC11227; MHAM; MMAC 1; MMAC1; Bannayan Zonana; BZS a; Multiple hamartoma(Cowden syndrome); Mutated in Mutiple Advanced Cancers 1; Phosphatase and Tensin Homolog; Phosphatidylinositol 345 trisphosphate 3 phosphatase and dual specificity protein phosphatase PTEN; Phosphatidylinositol 345 trisphosphate 3 phosphatase; Platelet antigen BR; PTEN 1; PTEN1; Tensin homolog; TEP 1; TEP1; VLA 2 Receptor alpha Subunit.
    产品应用ICC/IF=1:100-500, IF=1:100-500

    Not yet tested in other applications.
    Optimal working dilutions must be determined by the end user.

    抗体来源Mouse
    免疫原KLH conjugated synthetic peptide derived from human PTEN
    亚型IgG
    纯化方法affinity purified by Protein G
    克隆类型Monoclonal
    浓度1mg/ml
    储存液0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
    研究领域

    Cancer > Cell cycle > Kinases/phosphatases > Phosphatases

    Cancer > Oncoproteins/suppressors > Tumor suppressors > PTEN pathway

    Cell Biology > Cell Cycle > Kinases/Phosphatases > Phosphatases

    Epigenetics and Nuclear Signaling > Transcription > Cancer susceptibility > Tumor Suppressors

    Metabolism > Types of disease > Diabetes

    Metabolism > Types of disease > Metabolic disorders

    Metabolism > Types of disease > Obesity

    Signal Transduction > Signaling Pathway > Lipid Signaling > Lipid Phosphatases

    亚基Monomer. The unphosphorylated form interacts with the second PDZ domain of AIP1 and with DLG1 and MAST2 in vitro. Interacts with MAGI2, MAGI3, MAST1 and MAST3, but neither with MAST4 nor with DLG5. Interaction with MAGI2 increases protein stability. Interacts with NEDD4. Interacts with NDFIP1 and NDFIP2; in the presence of NEDD4 or ITCH, this interaction promotes PTEN ubiquitination. Interacts (via C2 domain) with FRK. Interacts with USP7; the interaction is direct. Interacts with ROCK1. Interacts with XIAP/BIRC4.
    亚细胞定位Cytoplasm. Nucleus. Nucleus, PML body. Note=Monoubiquitinated form is nuclear. Nonubiquitinated form is cytoplasmic. Colocalized with PML and USP7 in PML nuclear bodies. XIAP/BIRC4 promotes its nuclear localization.
    组织特异性Expressed at a relatively high level in all adult tissues, including heart, brain, placenta, lung, liver, muscle, kidney and pancreas.
    翻译后修饰Constitutively phosphorylated by CK2 under normal conditions. Phosphorylated in vitro by MAST1, MAST2 and MAST3. Phosphorylation results in an inhibited activity towards PIP3. Phosphorylation can both inhibit or promote PDZ-binding. Phosphorylation at Tyr-336 by FRK/PTK5 protects this protein from ubiquitin-mediated degradation probably by inhibiting its binding to NEDD4. Phosphorylation by ROCK1 is essential for its stability and activity. Phosphorylation by PLK3 promotes its stability and prevents its degradation by the proteasome.
    _x000D_ Monoubiquitinated; monoubiquitination is increased in presence of retinoic acid. Deubiquitinated by USP7; leading to its nuclear exclusion. Monoubiquitination of one of either Lys-13 and Lys-289 amino acid is sufficient to modulate PTEN compartmentalization. Ubiquitinated by XIAP/BIRC4.
    相似性Contains 1 C2 tensin-type domain.
    Contains 1 phosphatase tensin-type domain.
    功能Tumor suppressor. Acts as a dual-specificity protein phosphatase, dephosphorylating tyrosine-, serine- and threonine-phosphorylated proteins. Also acts as a lipid phosphatase, removing the phosphate in the D3 position of the inositol ring from phosphatidylinositol 3,4,5-trisphosphate, phosphatidylinositol 3,4-diphosphate, phosphatidylinositol 3-phosphate and inositol 1,3,4,5-tetrakisphosphate with order of substrate preference in vitro PtdIns(3,4,5)P3 > PtdIns(3,4)P2 > PtdIns3P > Ins(1,3,4,5)P4. The lipid phosphatase activity is critical for its tumor suppressor function. Antagonizes the PI3K-AKT/PKB signaling pathway by dephosphorylating phosphoinositides and thereby modulating cell cycle progression and cell survival. The unphosphorylated form cooperates with AIP1 to suppress AKT1 activation. Dephosphorylates tyrosine-phosphorylated focal adhesion kinase and inhibits cell migration and integrin-mediated cell spreading and focal adhesion formation. Plays a role as a key modulator of the AKT-mTOR signaling pathway controlling the tempo of the process of newborn neurons integration during adult neurogenesis, including correct neuron positioning, dendritic development and synapse formation. May be a negative regulator of insulin signaling and glucose metabolism in adipose tissue. The nuclear monoubiquitinated form possesses greater apoptotic potential, whereas the cytoplasmic nonubiquitinated form induces less tumor suppressive ability.
    保存条件Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.
    背景资料Potential tumor suppressor. Acts as a phosphoinositide3-phosphatase by regulating PtdIns (3,4,5)P3 levels. Involved in regulation of the AKT1 signaling pathway. The unphosphorylated form cooperates with AIP1 to suppress AKT1 activation.The PTEN/MMAC1 discovers the first to have the suppress of the phosphoric acid enzyme activity cancer gene currently.The gene of PTEN locates the chromosome10q23 area, sending forth sex tumor and a few households cancers with the variety to suffer from the comprehensive disease easilyrelevant.The activity that passes to repress the Akt regulates the cell period, the cell ground rule decease and glues to connect.This text discussed PTEN structure, function and its correlationses, the PTEN is in tumor repress function mechanism.

     

    应用推荐稀释比例
    {ICC/IF}{1:100-500}
    {IF}{1:100-500}

     

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