The PI3Kb isoform can be activated by insulin via the insulin receptor to initiate a cascade of events that control cell growth and metabolism. The activation of PI3Kb is mediated by the p85 regulatory subunit binding to tyrosine phosphorylated insulin receptor substrate (IRS) proteins (e.g. IRS-1 and IRS-2). It was also shown that PI3Kb is involved in apoptosis in human colon carcinoma cells. Injection of neutralizing antibodies specific to p110b in WiDr, HCT116 and CO 115 adenocarcinoma cells inhibited de novo DNA synthesis. PI3Kb is the major PI3K isoform required for apoptotic cell and Fc-g receptor mediated phagocytosis shown for primary mouse macrophages and the Jurkat human leukemia T cell line. It was shown by several research groups that the catalytic subunit of PI3Kb can be activated by Gbg subunits of G-protein coupled receptors.
Source:Complex of N-terminal His- tagged recombinant full-length human p110 beta, and untagged, recombinant full length, human p85 alpha. Coexpressed in a Baculovirus infected Sf9 cell expression system.
Molecular Weight: p110b: 124kD, p85a: 83.7kD
Specific Activity:7.9pmol/min/mg
Application:Useful for the study of enzyme kinetics, screening inhibitors, and selectivity profiling. Other applications not tested.
Recommended Dilution:A 50ul kinase reaction is conducted in a buffer containing 10mM Tris-HCl, pH 7.5, 50mM NaCl, 5mM MgCl2, 5uM ATP, 17ug Phosphoinositol-4,5-Bisphosphate, and 150ng enzyme for 90 minutes at room temperature. ATP reduction is detected using Kinase-Glo® Luminescent Kinase Assay Platform.
Storage and Stability:Aliquot to avoid repeated freezing and thawing and store at -70°C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquots are stable for at least 6 months.
