Human PTEN Antibody Summary
Thr2-Val403
Accession # P60484
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Scientific Data
PTEN Specificity is Shown by Immunocytochemistry in Knockout Cell Line. PTEN was detected in immersion fixed HeLa cells (positive) HeLa KO (negative) using Mouse Anti-Human PTEN Monoclonal Antibody (Catalog # MAB66551) at 8 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Mouse IgG Secondary Antibody (red; Catalog # NL007) and counterstained with DAPI (blue). Specific staining was localized to cytoplasm. View our protocol for Fluorescent ICC Staining of Cells on Coverslips.
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: PTEN
The tumor suppressor gene PTEN (phosphatase and tensin homolog deleted on chromosome 10), also known as MMAC1 (mutated in multiple advanced cancers 1), encodes a phosphatase that contains the catalytic signature motif (HCxxGxxRS/T) found in all members of the protein tyrosine phosphatase family. In vitro, the recombinant PTEN has both lipid phosphatase and protein phosphatase activities (1, 2). Interestingly, accumulating evidence has shown that the tumor suppressor activity of PTEN relies on its ability to dephosphorylate phosphatidylinositol (3,4,5)-triphosphate specifically at position 3 of the inositol ring (3). This activity reduces the levels of phosphatidylinositol (3,4,5)-triphosphate which is specifically produced from phosphatidylinositol (4,5)-diphosphate by PI 3-kinase upon activation by a variety of stimuli. Therefore, PTEN antagonizes PI 3-kinase-induced downstream signaling events and cellular processes including cell growth, apoptosis and cell motility. In vivo, the importance of PTEN catalytic activity in its tumor suppressor functions is underscored by the fact that the majority of PTEN missense mutations detected in tumor specimens target the phosphatase domain and cause a loss in PTEN phosphatase activity (4).
- Maehama, T. and J. Dixon (1998) J. Biol. Chem. 273:13375.
- Das, S. et al. (2003) Proc. Natl. Acad. Sci. USA 100:7491.
- Myers, M. et al. (1998) Proc. Natl. Acad. Sci. USA 95:13513.
- Waite, K. and C. Eng (2002) Am. J. Hum. Genet. 70:829.
Product Datasheets
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