The retinoblastoma (RB) protein controls the G1 to S transition. The state of RB that enforces this cell cycle arrest, and the event that abolishes it, are respectively:
- A Hypophosphorylated RB binds E2F transcription factors; phosphorylation by cyclin D-CDK4/6 releases E2F ✓
- B Hyperphosphorylated RB binds E2F; dephosphorylation by PP2A releases E2F
- C Hypophosphorylated RB binds p53; acetylation of RB releases p53
- D Ubiquitinated RB binds E2F; deubiquitination by USP28 releases E2F
Explanation
In its active growth-suppressive form RB is hypophosphorylated and sequesters E2F, preventing transcription of S-phase genes such as cyclin E. Mitogenic signalling activates cyclin D-CDK4/6, which phosphorylates RB; hyperphosphorylated RB releases E2F and the cell enters S phase. Option B reverses the phosphorylation states, and options C and D incorrectly substitute p53 or ubiquitination as the binding partner.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.