Phospho-PTEN (S380) Recombinant Monoclonal Antibody

說明書

中文名稱：

磷酸化-PTEN (S380)重組抗體
貨號：

CSB-RA018964A380phHU
規(guī)格：

￥1320
圖片：
Western Blot
Positive WB detected in HepG2 whole cell lysate
All lanes Phospho-PTEN antibody at 1.9μg/ml
Secondary
Goat polyclonal to rabbit IgG at 1/50000 dilution
Predicted band size: 54 KDa
Observed band size: 54 KDa
其他：

產(chǎn)品詳情
產(chǎn)品評價
相關(guān)產(chǎn)品
靶點詳情

產(chǎn)品詳情

產(chǎn)品描述：

CSB-RA018964A380phHU Phospho-PTEN (S380)重組單克隆抗體是針對PTEN蛋白絲氨酸380位點磷酸化修飾研發(fā)的高特異性檢測工具。PTEN作為重要的腫瘤抑制蛋白，通過拮抗PI3K/AKT信號通路調(diào)控細(xì)胞生長與凋亡，其S380位點的磷酸化修飾可影響蛋白穩(wěn)定性及亞細(xì)胞定位，在腫瘤發(fā)生發(fā)展與細(xì)胞信號轉(zhuǎn)導(dǎo)研究中具有重要價值。本抗體經(jīng)ELISA和蛋白質(zhì)印跡（WB）嚴(yán)格驗證，能精準(zhǔn)識別內(nèi)源性磷酸化PTEN蛋白，在WB實驗中可于預(yù)期分子量位置呈現(xiàn)清晰單一條帶，推薦使用稀釋比例為1:500-1:5000。該產(chǎn)品適用于腫瘤生物學(xué)、PTEN翻譯后修飾機制及PI3K/AKT通路相關(guān)研究領(lǐng)域，可應(yīng)用于細(xì)胞模型、組織樣本或體外蛋白體系中磷酸化PTEN的定性及半定量檢測，為探索PTEN功能調(diào)控及癌癥相關(guān)分子機制提供可靠工具。
Uniprot No.：

P60484
基因名：

PTEN
別名：

10q23del antibody; BZS antibody; DEC antibody; GLM2 antibody; MGC11227 antibody; MHAM antibody; MMAC1 antibody; MMAC1 phosphatase and tensin homolog deleted on chromosome 10 antibody; Mutated in multiple advanced cancers 1 antibody; Phosphatase and tensin homolog antibody; Phosphatase and tensin like protein antibody; Phosphatidylinositol 3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN antibody; Pten antibody; PTEN_HUMAN antibody; PTEN1 antibody; TEP1 antibody
反應(yīng)種屬：

Human
免疫原：

A synthesized peptide derived from Human Phospho-PTEN (S380)
免疫原種屬：

Homo sapiens (Human)
標(biāo)記方式：

Non-conjugated
克隆類型：

Monoclonal
抗體亞型：

Rabbit IgG
純化方式：

Affinity-chromatography
克隆號：

4D10
濃度：

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

Rabbit IgG in 10mM phosphate buffered saline , pH 7.4, 150mM sodium chloride, 0.05% BSA, 0.02% sodium azide and 50% glycerol.
產(chǎn)品提供形式：

Liquid
應(yīng)用范圍：

ELISA, WB

推薦稀釋比：

Application	Recommended Dilution
WB	1:500-1:5000

Protocols：

ELISA Protocol
Western Blotting (WB) Protocol
儲存條件：

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)品評價

靶點詳情

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 MAGI2 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. In motile cells, suppresses the formation of lateral pseudopods and thereby promotes cell polarization and directed movement.; Functional kinase, like isoform 1 it antagonizes the PI3K-AKT/PKB signaling pathway. Plays a role in mitochondrial energetic metabolism by promoting COX activity and ATP production, via collaboration with isoform 1 in increasing protein levels of PINK1.
基因功能參考文獻(xiàn)：
1. Nuclear phosphatase and tensin homologue on chromosome ten protein (PTEN) interacts with the splicing machinery, spliceosome, to regulate its assembly and pre-mRNA splicing. PMID: 29921876
2. the expression of PTEN and miR-144 was inversely correlated in metastatic breast cancer cell lines. PMID: 30132256
3. Disruption of PTEN proteinisoform PTENbeta (PTENbeta) alters rDNA transcription and promotes ribosomal biogenesis. PMID: 28332494
4. Functionally, Ataxin-3 overexpression promoted cell proliferation, and Ataxin-3 knockdown inhibited cell proliferation in testicular cancer cell. In addition, up-regulation of Ataxin-3 inhibited the expression of PTEN and activated the AKT/mTOR pathway. PMID: 29902454
5. a certain degree of mitochondrial oxidative activity, with some difference for PTEN-wild type SF767 cells respect to PTEN-deleted A172 and U87MG characterized by a loss-of-function point mutation of PTEN. PMID: 29209894
6. We demonstrated that expression of PTEN and miR-718 were significantly correlated in patients with gastric cancer. Low expression of PTEN and high level of miR-718 were notably associated with a lower 5-year overall survival rate. Both PTEN and miR-718 were identified as prognostic factors of gastric cancer. PMID: 30131483
7. The data indicate that diagnostic or therapeutic chest radiation may predispose patients with decreased stromal PTEN expression to secondary breast cancer, and that prophylactic EGFR inhibition may reduce this risk. PMID: 30018330
8. findings indicated that shikonin inhibits proliferation and promotes apoptosis in human endometrioid endometrial cancer (EEC) cells by modulating the miR-106b/PTEN/AKT/mTOR signaling pathway, suggesting shikonin could act a potential therapeutic agent in the EEC treatment. PMID: 29449346
9. SIRT6 inhibited proliferation, migration, and invasion of colon cancer cells by up-regulating PTEN expression and down-regulating AKT1 expression. PMID: 29957460
10. Data show that phosphatase and tensin homolog (PTEN) interacts with death domain associated protein (DAXX) and, in turn PTEN directly regulates oncogene expression by modulating DAXX-histone H3.3 (H3.3) association on the chromatin. PMID: 28497778
11. Study suggested that there may be a regulatory loop between miR21 and PTEN, and that miR21 inhibition affected the proliferative, invasive and apoptotic abilities of oral squamous cell carcinoma (OSCC) cells. miR-21 expression was observed in 80.0% OSCC tissues and in 30.0% of normal tissues. By contrast, PTEN expression exhibited an opposite trend in OSCC tissues 37.1%, and normal tissues 80.0%. PMID: 30132571
12. MTSS1 is stabilized by the protein phosphatase activity of the tumor suppressor PTEN. Our data show that PTEN loss in PDAC cells results in both increased metastatic potential and decreased MTSS1 expression. Furthermore, we show that ectopic MTSS1 expression rescues this effect. PMID: 29175021
13. Low PTEN mRNA expression was associated with down-regulation of a group of genes involved in immune responses and B-cell development. PMID: 29734016
14. Results showed that MiR-374b was highly expressed, while PTEN was downregulated in the GIST tissues. The levels of miR-374b, PI3K, AKT and PTEN were related to tumor diameter and pathological stage. Additionally, miR-374b increased the mRNA and protein levels of PI3K, Akt, MMP2, MMP9, P53 and cyclinD1, suggesting that miR-374b activates PI3K/Akt signaling pathway in GIST-T1 cells. PMID: 29902839
15. PTEN loss is associated with castration-resistant prostate cancer. PMID: 29302046
16. Low PTEN expression is associated with thyroid cancer progression. PMID: 30015900
17. we provide a review on current understandings of the regulation of PTEN by ncRNAs, which could contribute to the development of novel approaches to the diseases with abnormal expression of PTEN. PMID: 30217221
18. The IRIS-driven metastatic mechanism results from IRIS-dependent suppression of phosphatase and tensin homolog (PTEN) transcription, which in turn perturbs the PI3K/AKT/GSK-3beta pathway leading to prolyl hydroxylase-independent HIF-1alpha stabilization and activation in a normoxic environment. PMID: 30254159
19. In this study, we used the Ion Personal Genome Machine (PGM) and Ion Torrent Ampliseq Cancer panel to sequence hotspot regions from PIK3CA, AKT and PTEN genes to identify genetic mutations in 39 samples of TNBC subtype from Moroccan patients and to correlate the results with clinical-pathologic data PMID: 30227836
20. Data indicate a significant prognostic role for assessing transcriptional regulator ERG (ERG) and phosphatase and tensin homolog protein (PTEN) in men with prostate cancer. PMID: 30101374
21. Low PTEN expression is associated with multiple myeloma. PMID: 30015974
22. The loss of Sirt3 triggered fatal mitochondrial fission by suppressing the Akt/PTEN pathway. PMID: 30021354
23. Results showed that SIX1 was overexpressed in osteosarcoma tissues, blood samples and cell lines, whereas PTEN expression was reduced. PMID: 29807230
24. miR23b3p and PTEN interfered with the viability and apoptosis of smooth muscle cells. PMID: 29845190
25. PDCD4 and PTEN were the functional targets of miR-21. PMID: 30074182
26. miR-205 functions as an oncogenic miRNA by directly binding to SMAD4 and PTEN, providing a novel target for the molecular treatment of ovarian cancer. PMID: 28145479
27. Studies have indicated that in breast cancer, PTEN undergo mutations. There is a functional and mechanistic link between the BMI-1 oncoprotein and tumor suppressor PTEN in the development and progression of breast cancer. [review] PMID: 30096458
28. When considered together (43 cases), 1/25 cases (4%) with a PIK3CA mutation and/or low PTEN expression levels had a pathologic complete response (pCR)compared to 7/18 cases (39%) with wild-type PI3KCA and high PTEN expression levels (p = 0.006). PMID: 29110152
29. Taken together, the authors presented here a novel cross-talk between miR-181a and PTEN which was raised by hepatitis B virus X protein, and this shined a new line in hepatitis B virus-related hepato-carcinogenesis. PMID: 28053323
30. Bioinformatics analysis demonstrated that the 3'UTR of PTEN mRNA was targeted by hsa-miR-142-5p which regulates its expression triggering cancer stem cell-like properties of cutaneous squamous cell carcinoma. PMID: 28857248
31. PTEN lipid phosphatase inactivation abolished the MOB1-LATS1/2 interaction, decreased YAP phosphorylation and finally promoted YAP nuclear translocation, which enhanced the synergistic effect of YAP-TEAD, thus inducing cell proliferation and migration. PMID: 30134988
32. TERT could induce thyroid carcinoma cell proliferation mainly through the PTEN/AKT signaling pathway. PMID: 29901196
33. These results suggest that miR214 mediates vascular inflammation and apoptosis via PTEN expression. PMID: 29916551
34. A novel information on the susceptibility of PTEN to the inflammatory oxidant HOCl and its effects on the structure and activity of the protein is provided. PMID: 29298524
35. Study proposes a new mechanism by which loss of PTEN and consequent activation of the PI3K-AKT-mTORC1-S6K1 signalling pathway impairs DNA repair by downregulation of MRE11. PMID: 28967905
36. In prostate tumor tissue microarrays, loss of PTEN phosphohydrolase (PTEN) correlates with increased tyrosine kinase 6 PTK6 tyrosine 342 (PY342) phosphorylation and poor outcome. PMID: 29142193
37. in silico analysis revealed PTEN to be the downstream target of miR-21, which was further confirmed by expression analysis. PMID: 29807978
38. The decreased PTEN was associated with poorer survival outcomes of patients with kidney cancer and PTEN acts as a tumor suppressor in tumorigeneses and progression in kidney cancer. PMID: 29408173
39. MiR-221 together with proteins MDR1 and ABCG2 was upregulated in Cisplatin-resistant A549 lung cancer cells. Anti-miR-221 inhibits proliferation and induces senescence in lung cancer cells. PTEN/Akt pathway axis was identified as a target of drug resistance induced by miR-221. PMID: 29876362
40. These results demonstrate that SPAG6 silencing induces PTEN expression to regulate apoptosis though the PI3K/AKT pathway, indicating that SPAG6 may be a potential therapeutic target for myelodysplastic syndromes. PMID: 29749435
41. The inhibition of PTEN also reduced the cancer effects of CD4+ T cells on non-small cell lung cancer (NSCLC) cell lines following miR-142-5p downregulation. Therefore, our study demonstrated that miR-142-5p regulated CD4+ T cells in human NSCLC through PD-L1 expression via the PTEN pathway. PMID: 29767245
42. a statistically significant association between PTEN loss and the triple negative breast cancers was found in African American women PMID: 29653745
43. miR-130b was upregulated in the lupus nephritis group, compared with that in the control group. PTEN was identified as a virtual target of miR-130b, and there was a negative regulatory association between miR-130b and PTEN. miR-130b and PTEN interfered with the viability and apoptosis of mesangial cells. PMID: 29620214
44. The results of the present study indicate that the expression of miRNA23a may regulate acute myocardial infarction (AMI) through targeting PTEN in patients and in vitro, and PTEN/miRNA23a may therefore be potential targets for the clinical treatment of AMI. PMID: 29488607
45. TRPC1 regulated HIF1alpha levels in PTEN-deficient MDA-MB-468 and HCC1569 breast cancer cell lines. This regulation arises from effects on the constitutive translation of HIF1alpha under normoxic conditions via an Akt-dependent pathway. PMID: 28559303
46. miR367 was revealed to bind directly to phosphatase and tensin homolog (PTEN) mRNA and regulate the expression of the PTEN protein PMID: 29512776
47. The present study confirmed that pAURKA is important in the development of gastric adenocarcinoma and revealed a novel functional link between PTEN, AURKA and pAURKA activation PMID: 29512701
48. study found that CKS2 knockdown induced PTEN up-regulation and may associate with P53 pathway activation PMID: 29487004
49. Study showed for the first time that the suppression of rheumatiod arthritis fibroblast-like synoviocyte was mediated by phosphatase and tensin homolog involving survivin silencing. PMID: 28337018
50. The overexpression of PTEN concomitant with Livin gene silencing was confirmed as a feasible and effective in vitro and in vivo gene modulation method, which may represent a potential therapeutic strategy for the treatment of Gastric Cancer. PMID: 29436592
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相關(guān)疾病：

Cowden syndrome 1 (CWS1); Lhermitte-Duclos disease (LDD); Bannayan-Riley-Ruvalcaba syndrome (BRRS); Squamous cell carcinoma of the head and neck (HNSCC); Endometrial cancer (ENDMC); Glioma 2 (GLM2); VACTERL association with hydrocephalus (VACTERL-H); Prostate cancer (PC); Macrocephaly/autism syndrome (MCEPHAS)
亞細(xì)胞定位：

Cytoplasm. Nucleus. Nucleus, PML body.; [Isoform alpha]: Secreted. Note=May be secreted via a classical signal peptide and reenter into cells with the help of a poly-Arg motif.
組織特異性：

Expressed at a relatively high level in all adult tissues, including heart, brain, placenta, lung, liver, muscle, kidney and pancreas.
數(shù)據(jù)庫鏈接：

HGNC: 9588

OMIM: 137800

KEGG: hsa:5728

STRING: 9606.ENSP00000361021

UniGene: Hs.500466

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