Phospho-PTEN(Ser385)抗体特异性结合抗原：抗体本身不能直接溶解或杀伤带有特异抗原的靶细胞，通常需要补体或吞噬细胞等共同发挥效应以**病原微生物或导致病理损伤。然而，抗体可通过与病毒或**的特异性结合，直接发挥中和病毒的作用。
产品编号xy- 5567R
英文名称Phospho-PTEN(Ser385)
中文名称磷酸化肿瘤抑制基因PTEN抗体
别 名PTEN(phospho S385); 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.
说 明 书100ul
产品类型磷酸化抗体
研究领域肿瘤 **学 信号转导 转录调节因子 激酶和磷酸酶
抗体来源Rabbit
克隆类型Polyclonal
Phospho-PTEN(Ser385)抗体交叉反应 Human, Mouse, Rat,
产品应用WB=1:500-2000 ELISA=1:500-1000 IHC-P=1:400-800 IHC-F=1:400-800 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44kDa
细胞定位细胞核 细胞浆
性 状Lyophilized or Liquid
浓 度1mg/1ml
免 疫 原KLH conjugated Synthesised phosphopeptide derived from human PTEN around the phosphorylation site of Ser385:TD(p-S)DP
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.
Phospho-PTEN(Ser385)抗体保存条件Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
PubMedPubMed
产品介绍background:
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.
Function:
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 ***** 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.
Subunit:
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.
Subcellular Location:
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.
Tissue Specificity:
Expressed at a relatively high level in all ***** tissues, including heart, brain, placenta, lung, liver, muscle, kidney and pancreas.
Post-translational modifications:
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.
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.
DISEASE:
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-Myhre-Smith syndrome (RMSS) 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 head and neck squamous cell carcinomas (HNSCC) [MIM:275355]; also known as squamous cell carcinoma of the head and neck.
Defects in PTEN are a cause of susceptibility to endometrial cancer (ENDMC) [MIM:608089].
Note=PTEN mutations are found in a subset of patients with Proteus syndrome, a genetically heterogeneous condition. The molecular diagnosis of PTEN mutation positive cases classifies Proteus syndrome patients as part of the PTEN hamartoma syndrome spectrum. As such, patients surviving the early years of Proteus syndrome are likely at a greater risk of developing malignancies.
Defects in PTEN are a cause of susceptibility to glioma type 2 (GLM2) [MIM:613028]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas.
[DISEASE] Defects in PTEN are a cause of VACTERL association with hydrocephalus (VACTERL-H) [MIM:276950]. 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 may be a cause of susceptibility to prostate cancer (PC) [MIM:176807]. It is a malignancy originating in tissues of the prostate. Most prostate cancers are adenocarcinomas that develop in the acini of the prostatic ducts. Other rare histopathologic types of prostate cancer that occur in approximately 5% of patients include small cell carcinoma, mucinous carcinoma, prostatic ductal carcinoma, transitional cell carcinoma, squamous cell carcinoma, basal cell carcinoma, adenoid cystic carcinoma (basaloid), signet-ring cell carcinoma and neuroendocrine carcinoma.
Defects in PTEN are a cause of macrocephaly/autism syndrome (MCEPHAS) [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).
Note=A microdeletion of chromosome 10q23 involving BMPR1A and PTEN is a cause of chromosome 10q23 deletion syndrome, which shows overlapping features of the following three disorders: Bannayan-Zonana syndrome, Cowden disease and juvenile polyposis syndrome.
Similarity:
Contains 1 C2 tensin-type domain.
Contains 1 phosphatase tensin-type domain.
SWISS:
P60484
Gene ID:
5728
Phospho-PTEN(Ser385)抗体（antibody,
Ab）是由效应B细胞（效应**B细胞）分泌，机体用于抵御外来物质，如病毒，**等抗原，结构呈“Y”字型的球状蛋白质，仅仅存在于脊椎动物的血液和B**细胞膜表面。凡是能够跟抗体结合的物质，均被称作抗原，因此对于抗抗体（能够结合抗体的抗体）来说，抗体本身也是一种抗原物质。
Phospho-PTEN(Ser385)抗体普通抗体重链和轻链的结构
重链结构：普通的**球蛋白具有2条重链（H链），分子量约为50kD,有μ、δ、γ、ε和α五种重链亚型，对应的**球蛋白名称分别为IgM、IgG、IgA、IgD和IgE。
轻链结构： 普通**球蛋白具有2条轻链（L链），分子质量约25kDa，有κ链和λ链两种亚型，这两种轻链决定了Ig的亚型类别（IgG1，IgG2，IgG3，IgG4）。一个天然的Ig分子两条轻链总是相同的，但在同一个体内可存在分别带有κ或λ链的抗体分子。不同种属生物体内两型轻链的比例不同，正常人血清**球蛋白κ链：λ链约为2：1，而在小鼠的比例为20：1。
2.2抗体Fab段和Fc段
IgG经木瓜蛋白酶酶切后裂解为2个完全相同的Fab段和1个Fc段,每个Fab段都为单价,可与抗原结合但不会再发生凝集反应；经胃蛋白酶酶切后裂解为1个完整F(ab)2片段和碎片化的Fc片段,F(ab’)2片段为双价,可同时结合两个抗原表位。Fab段为抗原结合片段（fragment of antigen binding，Fab），相当于抗体分子的两个臂，由一个完整的轻链和重链的VH和CH1结构域组成。Fc段为可结晶段（fragment crystallizable，Fc）相当于Ig的CH2和CH3结构域，是Ig与效应分子或者细胞相互作用的部位。Fab段包含完整的可变区，以及恒定区的CH1区域。Fc段仅指Ig恒定区CH2和CH3的区域，相当于Y字结构下面那一部分。
合格 SLC25A38 溶质载体家族蛋白25成员38抗体
合格 SLC26A3 溶质载体家族蛋白26成员3抗体
合格 SLC2A13 溶质载体家族蛋白2成员A13抗体
合格 SLC30A10 溶质载体家族蛋白30成员A10抗体
合格 SLC30A9 溶质载体家族蛋白30成员A9抗体
合格 SLC35D2 溶质载体家族蛋白35成员D2抗体
合格 合格 SLC38A1 溶质载体家族蛋白38成员1抗体
合格 SLC38A9 溶质载体家族蛋白38成员A8抗体
合格 SLC39A14 溶质载体家族蛋白39成员A14抗体
合格 SLC39A2 溶质载体家族蛋白39成员A2抗体
合格 合格 SLC39A4 溶质载体家族蛋白39成员A4抗体
合格 SLC39A5 溶质载体家族蛋白39成员A5抗体
合格 SLC22A1 溶质载体家族蛋白22成员A1/有机阳离子转运蛋白1抗体
合格 RGS13 G蛋白信号转导调节因子13抗体
合格 RGS17 G蛋白信号转导调节因子17抗体
合格 RGS18 G蛋白信号转导调节因子18抗体
合格 RGS3 G蛋白信号转导调节因子3抗体
合格 RGS6 G蛋白信号转导调节因子6抗体
合格 RHBG RH家族B型糖蛋白RHBG抗体
合格 MCP-3 单核细胞趋化蛋白3抗体
合格 合格 Rho guanine exchange factor 16 鸟嘌呤交换因子16抗体
合格 RhoF RhoF蛋白抗体
合格 phospho-Parkin (Ser131) 磷酸化帕金森病蛋白2抗体
合格 PARN 多聚腺苷酸特异性核糖核酸抗体
合格 PARP14 多腺苷二磷酸多聚酶PARP14抗体
合格 PARP8 多腺苷二磷酸多聚酶PARP8抗体
合格 PARVB 小细胞蛋白PARVβ抗体
合格 PARVA 基质重塑相关蛋白PARVA抗体