PTEN (Ab-370) Antibody
Description
Epitope Mapping
The PTEN (Ab-370) Antibody targets a specific region in the C-terminal domain of PTEN. While different commercial sources may describe the immunogen slightly differently, the consensus indicates that this antibody recognizes amino acids in the vicinity of residues 368-372, with the sequence D-V-S-D-N .
Research has shown that the C-terminal region of PTEN contains intrinsically disordered protein regions (IDPRs) that play crucial roles in regulating PTEN function through post-translational modifications and protein-protein interactions . The epitope recognized by this antibody falls within this functionally significant region.
Specificity Considerations
Studies on anti-PTEN antibodies targeting the C-terminal region have demonstrated that post-translational modifications or mutations can affect antibody recognition patterns. Research examining the specificity of various anti-PTEN monoclonal antibodies has shown that:
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Phosphorylation at specific residues in the C-terminus can abolish antibody binding
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Tumor-associated mutations may result in loss of antibody reactivity
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Different antibodies targeting the C-terminus exhibit distinct patterns of epitope recognition
This information highlights the importance of understanding the precise epitope recognized by PTEN (Ab-370) Antibody when interpreting experimental results, particularly in contexts where PTEN may be subject to post-translational modifications or mutations.
Validated Experimental Applications
The PTEN (Ab-370) Antibody has been validated for several common research techniques:
Western Blot Analysis
When used for Western blot applications, the antibody successfully detects PTEN protein in cell lysates from PTEN-positive cell lines. The recommended dilution range is 1:500 to 1:1000 . The antibody recognizes the expected 47 kDa band corresponding to the PTEN protein.
Immunohistochemistry
For immunohistochemical applications, the antibody can be used at dilutions ranging from 1:50 to 1:200 to detect PTEN expression in tissue sections . This application is particularly valuable for evaluating PTEN expression in tumor samples, where loss of PTEN is a common feature in various cancer types.
ELISA
The antibody can also be employed in enzyme-linked immunosorbent assays at a recommended dilution of approximately 1:10000 , providing a method for quantitative analysis of PTEN protein levels in biological samples.
Research Relevance
PTEN (Ab-370) Antibody serves as a valuable tool in multiple research contexts:
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Cancer research, particularly in studies involving glioblastomas and other tumors with PTEN alterations
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Cell signaling investigations focusing on the PI3K/AKT pathway
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Studies examining post-translational modifications of PTEN
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Analysis of PTEN expression patterns in normal and pathological tissues
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Investigations of tumor suppressor mechanisms
PTEN Structure and Function
PTEN functions as a key tumor suppressor by antagonizing the phosphatidylinositol 3-kinase (PI3K) signaling pathway. It dephosphorylates phosphatidylinositol-3,4,5-trisphosphate (PIP3), thereby inhibiting AKT activation and downstream signaling events involved in cell proliferation and survival .
The protein contains several functional domains:
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An N-terminal phosphatase domain
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A C2 domain involved in membrane binding
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A C-terminal tail region where the Ab-370 antibody targets
The C-terminal region plays a critical role in regulating PTEN stability, subcellular localization, and catalytic activity. This region undergoes various post-translational modifications, including phosphorylation, acetylation, and caspase-3 cleavage . Deletion of the PTEN C-terminal tail generates a relatively unstable protein with altered membrane and nuclear localization patterns .
PTEN in Disease Pathology
PTEN alterations are implicated in multiple human diseases, particularly cancers. The gene exhibits a high frequency of mutations in human glioblastomas and is also mutated in other cancers . Precise detection of PTEN protein expression using validated antibodies like PTEN (Ab-370) Antibody is essential for:
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Diagnostic evaluation of tumor samples
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Biomarker development
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Patient stratification for targeted therapies
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Understanding disease mechanisms
Comparison with Other Anti-PTEN Antibodies
Research has shown that different anti-PTEN antibodies may recognize distinct epitopes within the PTEN protein, particularly in the C-terminal region. Studies comparing various commercial anti-PTEN monoclonal antibodies have revealed that:
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Antibodies recognizing the C-terminal region may have different sensitivities and specificities
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Some antibodies may be more sensitive to C-terminal deletions than others
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Post-translational modifications can differentially affect the reactivity of distinct antibodies
This variability highlights the importance of selecting the appropriate anti-PTEN antibody for specific experimental applications and understanding the potential limitations of each antibody.
Product Specs
Target Background
- PTEN interacts with the splicing machinery, spliceosome, to regulate its assembly and pre-mRNA splicing. PMID: 29921876
- The expression of PTEN and miR-144 was inversely correlated in metastatic breast cancer cell lines. PMID: 30132256
- Disruption of PTEN protein isoform PTENbeta (PTENbeta) alters rDNA transcription and promotes ribosomal biogenesis. PMID: 28332494
- Ataxin-3 overexpression promoted cell proliferation, while Ataxin-3 knockdown inhibited cell proliferation in testicular cancer cells. Up-regulation of Ataxin-3 inhibited PTEN expression and activated the AKT/mTOR pathway. PMID: 29902454
- There was a certain degree of mitochondrial oxidative activity observed in PTEN-wild type SF767 cells compared to PTEN-deleted A172 and U87MG cells characterized by a loss-of-function point mutation of PTEN. PMID: 29209894
- PTEN and miR-718 expression were significantly correlated in patients with gastric cancer. Low expression of PTEN and high levels of miR-718 were notably associated with a lower 5-year overall survival rate, indicating their prognostic significance in gastric cancer. PMID: 30131483
- Diagnostic or therapeutic chest radiation may predispose patients with decreased stromal PTEN expression to secondary breast cancer, and prophylactic EGFR inhibition may mitigate this risk. PMID: 30018330
- Shikonin inhibits proliferation and promotes apoptosis in human endometrioid endometrial cancer (EEC) cells by modulating the miR-106b/PTEN/AKT/mTOR signaling pathway, suggesting its potential therapeutic role in EEC treatment. PMID: 29449346
- SIRT6 inhibited proliferation, migration, and invasion of colon cancer cells by up-regulating PTEN expression and down-regulating AKT1 expression. PMID: 29957460
- PTEN interacts with death domain associated protein (DAXX) and directly regulates oncogene expression by modulating DAXX-histone H3.3 (H3.3) association on the chromatin. PMID: 28497778
- There may be a regulatory loop between miR21 and PTEN, and miR21 inhibition affected the proliferative, invasive, and apoptotic abilities of oral squamous cell carcinoma (OSCC) cells. miR-21 expression was observed in 80.0% of OSCC tissues and 30.0% of normal tissues, while PTEN expression exhibited an opposite trend in OSCC tissues (37.1%) and normal tissues (80.0%). PMID: 30132571
- MTSS1 is stabilized by the protein phosphatase activity of PTEN. Loss of PTEN in pancreatic ductal adenocarcinoma (PDAC) cells results in both increased metastatic potential and decreased MTSS1 expression, which can be rescued by ectopic MTSS1 expression. PMID: 29175021
- Low PTEN mRNA expression was associated with down-regulation of a group of genes involved in immune responses and B-cell development. PMID: 29734016
- MiR-374b was highly expressed, while PTEN was downregulated in gastrointestinal stromal tumor (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 the PI3K/Akt signaling pathway in GIST-T1 cells. PMID: 29902839
- PTEN loss is associated with castration-resistant prostate cancer. PMID: 29302046
- Low PTEN expression is associated with thyroid cancer progression. PMID: 30015900
- This review provides insights into the regulation of PTEN by non-coding RNAs, which could contribute to the development of novel approaches for treating diseases with abnormal PTEN expression. PMID: 30217221
- The IRIS-driven metastatic mechanism stems from IRIS-dependent suppression of PTEN transcription, which disrupts the PI3K/AKT/GSK-3beta pathway, leading to prolyl hydroxylase-independent HIF-1alpha stabilization and activation in a normoxic environment. PMID: 30254159
- Ion Personal Genome Machine (PGM) and Ion Torrent Ampliseq Cancer panel sequencing of hotspot regions in PIK3CA, AKT, and PTEN genes identified genetic mutations in 39 triple-negative breast cancer (TNBC) samples from Moroccan patients. These results were correlated with clinical-pathologic data. PMID: 30227836
- Data indicate a significant prognostic role for assessing transcriptional regulator ERG (ERG) and PTEN in men with prostate cancer. PMID: 30101374
- Low PTEN expression is associated with multiple myeloma. PMID: 30015974
- The loss of Sirt3 triggered fatal mitochondrial fission by suppressing the Akt/PTEN pathway. PMID: 30021354
- SIX1 was overexpressed in osteosarcoma tissues, blood samples, and cell lines, while PTEN expression was reduced. PMID: 29807230
- miR23b3p and PTEN interfered with the viability and apoptosis of smooth muscle cells. PMID: 29845190
- PDCD4 and PTEN were the functional targets of miR-21. PMID: 30074182
- 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
- In breast cancer, PTEN undergoes 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
- Cases with a PIK3CA mutation and/or low PTEN expression levels showed a lower pathologic complete response (pCR) rate (4%) compared to cases with wild-type PI3KCA and high PTEN expression levels (39%). PMID: 29110152
- This study presents a novel cross-talk between miR-181a and PTEN, which is induced by hepatitis B virus X protein, shedding light on hepatitis B virus-related hepatocarcinogenesis. PMID: 28053323
- Bioinformatics analysis revealed that the 3'UTR of PTEN mRNA is targeted by hsa-miR-142-5p, which regulates its expression, triggering cancer stem cell-like properties in cutaneous squamous cell carcinoma. PMID: 28857248
- PTEN lipid phosphatase inactivation abolished the MOB1-LATS1/2 interaction, decreased YAP phosphorylation, and promoted YAP nuclear translocation, enhancing the synergistic effect of YAP-TEAD, thus inducing cell proliferation and migration. PMID: 30134988
- TERT could induce thyroid carcinoma cell proliferation primarily through the PTEN/AKT signaling pathway. PMID: 29901196
- miR214 mediates vascular inflammation and apoptosis via PTEN expression. PMID: 29916551
- This study provides novel information on the susceptibility of PTEN to the inflammatory oxidant HOCl and its effects on the protein's structure and activity. PMID: 29298524
- This study proposes a new mechanism by which loss of PTEN and consequent activation of the PI3K-AKT-mTORC1-S6K1 signaling pathway impairs DNA repair by downregulation of MRE11. PMID: 28967905
- In prostate tumor tissue microarrays, loss of PTEN correlates with increased tyrosine kinase 6 PTK6 tyrosine 342 (PY342) phosphorylation and poor outcome. PMID: 29142193
- In silico analysis identified PTEN as the downstream target of miR-21, which was further confirmed by expression analysis. PMID: 29807978
- Decreased PTEN was associated with poorer survival outcomes in patients with kidney cancer, highlighting its tumor suppressor role in kidney cancer tumorigenesis and progression. PMID: 29408173
- MiR-221, along 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, with the PTEN/Akt pathway axis identified as a target of drug resistance induced by miR-221. PMID: 29876362
- SPAG6 silencing induces PTEN expression to regulate apoptosis through the PI3K/AKT pathway, suggesting that SPAG6 may be a potential therapeutic target for myelodysplastic syndromes. PMID: 29749435
- MiR-142-5p downregulation inhibits PTEN and reduces the cancer effects of CD4+ T cells on non-small cell lung cancer (NSCLC) cell lines. This study demonstrated that miR-142-5p regulated CD4+ T cells in human NSCLC through PD-L1 expression via the PTEN pathway. PMID: 29767245
- A statistically significant association between PTEN loss and triple-negative breast cancers was found in African American women. PMID: 29653745
- MiR-130b was upregulated in the lupus nephritis group compared to 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
- MiRNA23a expression may regulate acute myocardial infarction (AMI) through targeting PTEN in patients and in vitro, suggesting PTEN/miRNA23a as potential targets for clinical treatment of AMI. PMID: 29488607
- TRPC1 regulated HIF1alpha levels in PTEN-deficient MDA-MB-468 and HCC1569 breast cancer cell lines. This regulation stems from effects on the constitutive translation of HIF1alpha under normoxic conditions via an Akt-dependent pathway. PMID: 28559303
- MiR367 directly binds to PTEN mRNA and regulates PTEN protein expression. PMID: 29512776
- This study confirmed the importance of pAURKA in the development of gastric adenocarcinoma and revealed a novel functional link between PTEN, AURKA, and pAURKA activation. PMID: 29512701
- CKS2 knockdown induced PTEN up-regulation and may associate with P53 pathway activation. PMID: 29487004
- This study demonstrated that the suppression of rheumatoid arthritis fibroblast-like synoviocyte was mediated by PTEN involving survivin silencing. PMID: 28337018
- The overexpression of PTEN concomitant with Livin gene silencing was confirmed as a feasible and effective in vitro and in vivo gene modulation method, representing a potential therapeutic strategy for gastric cancer treatment. PMID: 29436592
