RVQ3 17. What are \"pocket proteins?\" how are they regulated? 18. What are the
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Question
RVQ317. What are "pocket proteins?" how are they regulated? 18. What are the two major groups of CKIs that regulate the cell cycle, and what are their targets? 19. When during the cell cycle does the "restriction point" occur? 20. In humans, what are the specific names for the M cyclin/CDKs? 21. In humans, what are the specific names for the G1 cyclin/CDKs? 22. In humans, what is the specific name for S-phase cyclin/CDK? 23. Describe in general the activities of cyclin-dependent kinases (cdk’s). How are they regulated? 24. The common feature of all cancers is uncontrolled cell growth. However, there are several mechanisms by which uncontrolled growth is achieved in a cell. Experimental evidence indicates that retinoblastoma, a cancer, is caused by a mutation in the RB gene. However, loss of one retinoblastoma (Rb) gene does not lead to cancer. How can you explain this? Based on this evidence, is Rb a proto-oncogene or a tumor suppressor gene?
RVQ3
17. What are "pocket proteins?" how are they regulated? 18. What are the two major groups of CKIs that regulate the cell cycle, and what are their targets? 19. When during the cell cycle does the "restriction point" occur? 20. In humans, what are the specific names for the M cyclin/CDKs? 21. In humans, what are the specific names for the G1 cyclin/CDKs? 22. In humans, what is the specific name for S-phase cyclin/CDK? 23. Describe in general the activities of cyclin-dependent kinases (cdk’s). How are they regulated? 24. The common feature of all cancers is uncontrolled cell growth. However, there are several mechanisms by which uncontrolled growth is achieved in a cell. Experimental evidence indicates that retinoblastoma, a cancer, is caused by a mutation in the RB gene. However, loss of one retinoblastoma (Rb) gene does not lead to cancer. How can you explain this? Based on this evidence, is Rb a proto-oncogene or a tumor suppressor gene?
17. What are "pocket proteins?" how are they regulated? 18. What are the two major groups of CKIs that regulate the cell cycle, and what are their targets? 19. When during the cell cycle does the "restriction point" occur? 20. In humans, what are the specific names for the M cyclin/CDKs? 21. In humans, what are the specific names for the G1 cyclin/CDKs? 22. In humans, what is the specific name for S-phase cyclin/CDK? 23. Describe in general the activities of cyclin-dependent kinases (cdk’s). How are they regulated? 24. The common feature of all cancers is uncontrolled cell growth. However, there are several mechanisms by which uncontrolled growth is achieved in a cell. Experimental evidence indicates that retinoblastoma, a cancer, is caused by a mutation in the RB gene. However, loss of one retinoblastoma (Rb) gene does not lead to cancer. How can you explain this? Based on this evidence, is Rb a proto-oncogene or a tumor suppressor gene? 17. What are "pocket proteins?" how are they regulated? 18. What are the two major groups of CKIs that regulate the cell cycle, and what are their targets? 19. When during the cell cycle does the "restriction point" occur? 20. In humans, what are the specific names for the M cyclin/CDKs? 21. In humans, what are the specific names for the G1 cyclin/CDKs? 22. In humans, what is the specific name for S-phase cyclin/CDK? 23. Describe in general the activities of cyclin-dependent kinases (cdk’s). How are they regulated? 24. The common feature of all cancers is uncontrolled cell growth. However, there are several mechanisms by which uncontrolled growth is achieved in a cell. Experimental evidence indicates that retinoblastoma, a cancer, is caused by a mutation in the RB gene. However, loss of one retinoblastoma (Rb) gene does not lead to cancer. How can you explain this? Based on this evidence, is Rb a proto-oncogene or a tumor suppressor gene?
Explanation / Answer
17. The retinoblastoma proteins pRB, p107 and p130 are known as the 'pocket protein' family. These regulate the cell cycle at the G1-S transition phase by targeting the E2F-transcription factors. They also inhibit the Cdk2, or activate p27 (Kip1) proteins to control the G1-S transition. They also arrest G0/G1 progression.
Pocket proteins are regulated by Phosphorylation by CycD and Cdk4 and Cdk6, which releases the E2F transcription factor, resulting in activation of genes for the G1-S progression or G0-exit.
18. CKIs, or the cyclin-dependent kinase inhibitors, inhibit kinase activities during G1 phase in response to DNA damage.
The two major groups of CKIs are INK4 and CIP/KIP. The INK4 inhibitors target Cdk proteins, whereas CIP/KIP inhibitors target cyclin D and CDK4 or CDK6.
19. The G1-S progression requires growth factors. But at a certain point, after the cell commits to the S-phase, the cell no longer needs any growth factor. This point is called restriction point. It occurs at the late G1 phase, just before the DNA synthesis of the S-phase.
20. The M cyclin in vertebrates is called cyclin-B. Its Cdk partner is Cdk-1 in humans. The Cyclin-B/Cdk1 complex is called Maturation Promoting Factor.
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