84-4012-29　RAC-beta serine/threonine-Protein kinase (FITC) 100ug　331818

特徴

• AKT2 is one of 3 closely related serine/threonine-protein kinases (AKT1, AKT2 and AKT3) called the AKT kinase, and which regulate many processes including metabolism, proliferation, cell survival, growth and angiogenesis.
• This is mediated through serine and/or threonine phosphorylation of a range of downstream substrates.
• Over 100 substrate candidates have been reported so far, but for most of them, no isoform specificityhas been reported.
• AKT is responsible of the regulation of glucose uptake by mediating insulin-induced translocation of the SLC2A4/GLUT4 glucose transporter to the cell surface.
• Phosphorylation of PTPN1 at 'Ser-50' negatively modulates its phosphatase activity preventing dephosphorylation of the insulin receptor and the attenuation of insulin signaling.
• Phosphorylation of TBC1D4 triggers the binding of this effector to inhibitory 14-3-3 proteins, which is required for insulin-stimulated glucose transport.
• AKT regulates also the storage of glucose in the form of glycogen by phosphorylating GSK3A at 'Ser-21' and GSK3B at 'Ser-9', resulting in inhibition of its kinase activity.
• Phosphorylation of GSK3 isoforms by AKT is also thought to be one mechanism by which cell proliferation is driven.
• AKT regulates also cell survival via the phosphorylation of MAP3K5 (apoptosis signal-related kinase).
• Phosphorylation of 'Ser-83' decreases MAP3K5 kinase activity stimulated by oxidative stress and thereby prevents apoptosis.
• AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 at 'Ser-939' and 'Thr-1462', thereby activating mTORC1 signaling and leading to both phosphorylation of 4E-BP1 and in activation of RPS6KB1.
• AKT is involved in the phosphorylation of members of the FOXO factors (Forkhead family of transcription factors), leading to binding of 14-3-3 proteins and cytoplasmic localization.
• In particular, FOXO1 is phosphorylated at 'Thr-24', 'Ser-256' and 'Ser-319'.
• FOXO3 and FOXO4 are phosphorylated on equivalent sites.
• AKT has an important role in the regulation of NF-kappa-B-dependent gene transcription and positively regulates the activity of CREB1 (cyclic AMP (cAMP)-response element binding protein).
• The phosphorylation of CREB1 induces the binding of accessory proteins that are necessary for the transcription of pro-survival genes such as BCL2 and MCL1.
• AKT phosphorylates 'Ser-454' on ATP citrate lyase (ACLY), thereby potentially regulating ACLY activity and fatty acid synthesis.
• Activates the 3B isoform ofcyclic nucleotide phosphodiesterase (PDE3B) via phosphorylation of 'Ser-273', resulting in reduced cyclic AMP levels and inhibition of lipolysis.
• Phosphorylates PIKFYVE on 'Ser-318', which results in increased PI3P-5 activity.
• The Rho GTPase-activating protein DLC1 is another substrate and its phosphorylation is implicated in the regulation cell proliferation and cell growth.
• AKT plays a role as 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.
• Signals downstream of phosphatidylinositol 3-kinase (PI3K) to mediate the effects of various growth factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I).
• AKT mediates the antiapoptotic effects of IGF-I.
• Essential for the SPATA13-mediated regulation of cell migration and adhesion assembly and disassembly.
• May be involved in the regulation of the placental development.
• Ref.10 Ref.20 One of the few specific substrates of AKT2 identified recently is PITX2.
• Phosphorylation of PITX2 impairs its association with the CCND1 mRNA-stabilizing complex thus shortening the half-life of CCND1.
• AKT2 seems also to be the principal isoform responsibleof the regulation of glucose uptake.
• Phosphorylates C2CD5 on 'Ser-197' during insulin-stimulated adipocytes.
• AKT2 is also specifically involved in skeletal muscle differentiation, one of its substrates in this process being ANKRD2.
• Down-regulation by RNA interference reduces the expression of the phosphorylated form of BAD, resulting in the induction of caspase-dependent apoptosis.
• Phosphorylates CLK2 on 'Thr-343'.
• Applications:Suitable for use in ELISA and Western Blot.
• Other applications not tested.
• Recommended Dilution:Optimal dilutions to be determined by the researcher.
• Storage and StabilityStore product at 4°C if to be used immediately within two weeks.
• For long-term storage, aliquot to avoid repeated freezing and thawing and store at -20°C.
• Aliquots are stable at -20°C for 12 months after receipt.
• Dilute required amount only prior to immediate use.
• Further dilutions can be made in assay buffer.
• Caution: FITC conjugates are sensitive to light.
• For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.