Final answer:
The statement suggesting Rb acts as a repressor for p53 is false. Both Rb and p53 are separate tumor suppressor proteins involved in cell cycle regulation, and their inactivation may contribute to cancer development.
Step-by-step explanation:
The statement 'Rb is the repressor for p53? If it is inactive it cannot stop the cell cycle if there is a problem, and this leads to cancer.' is False. Retinoblastoma protein (Rb) and p53 are two distinct proteins that play crucial roles in the regulation of the cell cycle. Rb is known as a tumor suppressor protein that, when active, prevents cells from entering the S phase of the cell cycle by binding to E2F transcription factors and stopping the production of proteins necessary for the G1/S transition. As the cell grows, Rb becomes phosphorylated and inactive, releasing E2F to promote the cell cycle transition. On the other hand, p53 is a multifunctional protein that acts primarily at the G1 checkpoint and can halt the cell cycle in the presence of damaged DNA to allow for repair or trigger apoptosis to prevent the propagation of this damage. p53 aids in the accumulation of p21, another cell cycle inhibitor, making it unlikey that the cell will progress to the S phase under stressful conditions. Both Rb and p53 are vital tumor suppressor proteins, and their misfunction due to mutations or inactivation can lead to cancer.