货号：14-488

品牌：Merck Millipore

规格：

目录价：￥4200.00

市场价格：￥3570.00

会员价格：￥3360.00

金山科研平台，产品价格货期咨询微信：jinshanbio Description: PTEN, active View All» Trade Name: Upstate (Millipore) View All» Qty/Pk: 10 µg View All» Product Overview: N-terminal His-tagged, recombinant human PTEN View All» Background Information: PTEN hydrolyzes phosphate at the 3 position on the inositol ring of PtdIns(3,4,5)P₃, and Ins(1,3,4,5)P₄. Although PTEN has the consensus sequence of a protein tyrosine phosphatase, it dephosphorylates p-nitrophenylphosphate and other synthetic and protein substrates poorly. The greatest catalytic activity has been observed with the highly negatively charged, multiply phosphorylated polymer of (Glu-Tyr)n. View All» Key Applications: Phosphatase Assay View All» Usage Statement: Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals. View All» Entrez Gene Summary: This gene was identified as a tumor suppressor that is mutated in a large number of cancers at high frequency. The protein encoded this gene is a phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase. It contains a tensin like domain as well as a catalytic domain similar to that of the dual specificity protein tyrosine phosphatases. Unlike most of the protein tyrosine phosphatases, this protein preferentially dephosphorylates phosphoinositide substrates. It negatively regulates intracellular levels of phosphatidylinositol-3,4,5-trisphosphate in cells and functions as a tumor suppressor by negatively regulating AKT/PKB signaling pathway. View All» UniProt Summary: FUNCTION: SwissProt: P60484 # 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. May be a negative regulator of insulin signaling and glucose metabolism in adipose tissue.COFACTOR: Magnesium.SIZE: 403 amino acids; 47166 Da SUBUNIT: Monomer. The unphosphorylated form interacts with the second PDZ domain of AIP1 and with DLG1 and MAST2 in vitro.SUBCELLULAR LOCATION: Cytoplasm.TISSUE SPECIFICITY: Expressed at a relatively high level in all adult tissues, including heart, brain, placenta, lung, liver, muscle, kidney and pancreas.DOMAIN: SwissProt: P60484 The C2 domain binds phospholipid membranes in vitro in a Ca(2+)-independent manner; this binding is important for its tumor suppressor function.PTM: Phosphorylation results in an inhibited activity towards PIP3. Phosphorylation can both inhibit and promote PDZ-binding.DISEASE: SwissProt: P60484 # Mutations of PTEN are found in a large number of cancers. & Defects in PTEN are a cause of Cowden disease (CD) [MIM:158350]; also known as Cowden syndrome (CS). CD is an autosomal dominant cancer predisposition syndrome associated with elevated risk for tumors of the breast, thyroid and skin. The predominant phenotype for CD is multiple hamartoma syndrome, in many organ systems including the breast (70% of CD patients), thyroid (40-60%), skin, CNS (40%), gastrointestinal tract. Affected individuals are at an increased risk of both breast and thyroid cancers. Trichilemmomas (benign tumors of the hair follicle infundibulum), and mucocutaneous papillomatosis (99%) are hallmarks of CD. & Defects in PTEN are the cause of Lhermitte-Duclos disease (LDD) [MIM:158350]; also known as cerebelloparenchymal disorder VI. LDD is characterized by dysplastic gangliocytoma of the cerebellum which often results in cerebellar signs and seizures. LDD and CD seem to be the same entity, and are considered as hamartoma-neoplasia syndromes. & Defects in PTEN are a cause of Bannayan-Zonana syndrome (BZS) [MIM:153480]; also known as Ruvalcaba-Riley-Smith or Bannayan-Riley-Ruvalcaba syndrome (BRRS). In BZS there seems not to be an increased risk of malignancy. It has a partial clinical overlap with CD. BZS is characterized by the classic triad of macrocephaly, lipomatosis and pigmented macules of the gland penis. & Defects in PTEN are a cause of squamous cell carcinoma of the head and neck (HNSCC) [MIM:275355]. & Defects in PTEN are a cause of susceptibility to endometrial cancer [MIM:608089]. & Defects in PTEN are a cause of Proteus syndrome [MIM:176920]. Proteus syndrome is a hamartomatous disorder characterized by overgrowth of multiple tissues, connective tissue and epidermal naevi, and vascular malformations. These presentations are usually apparent at birth or soon after and continue to develop as the patient ages. It is named after the Greek god Proteus who, legend has it, could change his shape at will to avoid capture. Tumors, mostly benign but some malignant, have also been reported in Proteus syndrome, generally presenting by the age of 20 years and including papillary adenocarcinoma of the testis, meningioma, and cystadenoma of the ovaries. & Defects in PTEN are a cause of oligodendroglioma [MIM:137800]; also called oligodendroblastoma or familial glioma of brain. Oligodendroglioma is a usually benign neoplasm derived from and composed of oligodendrogliocytes in varying stages of differentiation. The majority are seen in adults in the white matter of the brain. & Defects in PTEN are a cause of VACTERL association with hydrocephalus [MIM:276950]; which includes also VATER association with hydrocephalus. VACTERL is an acronym for vertebral anomalies, anal atresia, congenital cardiac disease, tracheoesophageal fistula, renal anomalies, radial dysplasia, and other limb defects. & Defects in PTEN are involved in prostate cancer [MIM:176807]. & Defects in PTEN are a cause of macrocephaly/autism syndrome [MIM:605309]. Patients have autism spectrum disorders and macrocephaly, with head circumferences ranging from +2.5 to +8 SD for age and sex (average head circumference +4.0 SD).SIMILARITY: Contains 1 C2 tensin-type domain. & Contains 1 phosphatase tensin-type domain. View All» Species: Human View All» Molecular Weight: 50 kDa View All» Brand Family: Upstate View All» Source: Human PTEN expressed in Sf9 cells. View All» Protein Target: PTEN View All» Presentation: 50mM Tris-HCl, pH 8.0, 150mM NaCl, 81mM imidazole, 1mM EDTA, 5mM glutathione, 2mM DTT, 267mM sucrose, and 10% glycerol. The presence of glutathione, dithiothreitol or β-mercaptoethanol is absolutely required for stability. View All» Storage Conditions: 1 year at -70°C. View All» Target Sub-Family: Lipid phosphatase View All» Gene Symbol:

• PTEN

• TEP1

• PTEN1

• MMAC1

• MHAM

• BZS

• MGC11227
  View All» Product Name: PTEN, active View All» Quality Assurance: Routinely evaluated by dephosphorylation of PtdIns(3,4,5)P₃. View All» UniProt Number: P60484 View All» Specific Activity: For Specific Activity data, refer to the Certificate of Analysis for individual lots of this enzyme. View All» Entrez Gene Number: NM_000314.4 View All» Purification Method: Ni-NTA agarose chromatography View All»
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