regulatory subunit of phosphoinositide-3-kinase. Mediates binding to a subset of tyrosine-phosphorylated proteins through its SH2 domain. Acts as an adapter, mediating the association of the p110 catalytic unit of the alpha, beta and delta enzymes to the plasma membrane, where p110 phosphorylates inositol lipids. May play an additional role in the regulation of the actin cytoskeleton. Necessary for the insulin-stimulated increase in glucose uptake and glycogen synthesis in insulin-sensitive tissues. Its SH2 domains interacts with the YTHM motif of phosphorylated INSR in vitro. Defects in PIK3R1 are a cause of severe insulin resistance. Four alternatively spliced isoforms have been described. Note: This description may include information from UniProtKB.
Protein type: Kinase, lipid; Enzyme, regulatory subunit; Motility/polarity/chemotaxis
Molecular Function: protein C-terminus binding; protein domain specific binding; 1-phosphatidylinositol-3-kinase activity; neurotrophin TRKA receptor binding; platelet-derived growth factor receptor binding; phosphoprotein binding; 1-phosphatidylinositol-3-kinase regulator activity; phosphoinositide 3-kinase regulator activity; receptor tyrosine kinase binding; protein phosphatase binding; protein kinase binding; insulin receptor binding; ATPase binding; insulin binding; calmodulin binding; transferase activity; insulin-like growth factor receptor binding; protein binding; ErbB-3 class receptor binding; insulin receptor substrate binding; ubiquitin protein ligase binding; phosphoinositide 3-kinase binding; estrogen receptor binding; kinase activity; receptor binding
Biological Process: negative regulation of osteoclast differentiation; phosphoinositide 3-kinase cascade; response to cAMP; negative regulation of heart rate; negative regulation of smooth muscle cell proliferation; response to glucocorticoid stimulus; signal transduction; protein amino acid phosphorylation; NFAT protein import into nucleus; regulation of phosphoinositide 3-kinase activity; response to insulin stimulus; negative regulation of blood pressure; negative regulation of proteolysis; glucose metabolic process; positive regulation of tumor necrosis factor production; negative regulation of cell-matrix adhesion; positive regulation of myoblast differentiation; insulin-like growth factor receptor signaling pathway; DNA damage response, signal transduction resulting in induction of apoptosis; induction of apoptosis via death domain receptors; B cell differentiation; insulin receptor signaling pathway; positive regulation of transcription from RNA polymerase II promoter; negative regulation of cell-cell adhesion; positive regulation of protein amino acid phosphorylation; phosphorylation; negative regulation of apoptosis; positive regulation of cell migration
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.