Insulin receptor tyrosine kinase phosphorylates IRS-1, which then activates PI3K. The lipid product of PI3K that recruits PDK1 to the membrane is:
- A Phosphatidylinositol-4,5-bisphosphate (PIP2)
- B Phosphatidylinositol-3,4,5-trisphosphate (PIP3) ✓
- C Diacylglycerol (DAG)
- D Inositol-1,4,5-trisphosphate (IP3)
Explanation
PI3K phosphorylates PIP2 to produce PIP3 at the plasma membrane. PIP3 serves as a docking site for the PH domains of PDK1 and AKT (PKB), bringing them to the membrane where PDK1 phosphorylates and activates AKT. PTEN phosphatase degrades PIP3 and functions as a tumour suppressor opposing this pathway. DAG and IP3 are products of PLC-mediated PIP2 hydrolysis, not PI3K.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.