Phospho-PTEN-P1 (Ser29, Thr32)Rabbit anti-Bovine, Canine, Chimpanzee, Human, Mouse, Rat, Rhesus Monkey, Polyclonal, Rockland™

Description

• Store vial at -20°C prior to opening
• Aliquot contents and freeze at -20°C or below for extended storage
• Avoid cycles of freezing and thawing
• Centrifuge product if not completely clear after standing at room temperature
• This product is stable for several weeks at 4°C as an undiluted liquid
• Dilute only prior to immediate use
• This affinity-purified antibody is directed against the phosphorylated form of human PTEN protein at the pS29 and pT32 residues
• Reactivity occurs against human PTEN pS29/pT32 protein and the antibody is specific for the phosphorylated form of the proteins
• Approximately 3% reactivity is observed against the non-phosphorylated form of the immunizing peptide
• A BLAST analysis was used to suggest cross reactivity with PTEN proteins from mouse and dog sources based on 100% homology with the immunizing sequence
• Reactivity against homologues from other sources is not known
• PTEN was identified as a tumor suppressor that is mutated in a large number of cancers at high frequency
• The PTEN 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
• PTEN 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
• PTEN 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
• Also, PTEN 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 of PTEN induces less tumor suppressive ability.