Review cont\'d 16. Describe how cyclin D interacts with E2F to regulate the cell

Question

Review cont'd
16. Describe how cyclin D interacts with E2F to regulate the cell cycle 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? 25. In what ways does Myc oncoprotein deregulate cell proliferation and differentiation. 26. How might loss of CDK inhibitor’s function affect cell cycle advance? 27. What is the function of p53 . 28. How does the domain structure of p53 regulate its functions? 29. What evidence supports the involvement of EMT in human tumor pathogenesis? 30. What are the keys teps in the spread of a primary tumor? 31. What kind of proteins are involved in invasive ness. Specify the extracellular protease.
Review cont'd
16. Describe how cyclin D interacts with E2F to regulate the cell cycle 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? 25. In what ways does Myc oncoprotein deregulate cell proliferation and differentiation. 26. How might loss of CDK inhibitor’s function affect cell cycle advance? 27. What is the function of p53 . 28. How does the domain structure of p53 regulate its functions? 29. What evidence supports the involvement of EMT in human tumor pathogenesis? 30. What are the keys teps in the spread of a primary tumor? 31. What kind of proteins are involved in invasive ness. Specify the extracellular protease.
Review cont'd
16. Describe how cyclin D interacts with E2F to regulate the cell cycle 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? 25. In what ways does Myc oncoprotein deregulate cell proliferation and differentiation. 26. How might loss of CDK inhibitor’s function affect cell cycle advance? 27. What is the function of p53 . 28. How does the domain structure of p53 regulate its functions? 29. What evidence supports the involvement of EMT in human tumor pathogenesis? 30. What are the keys teps in the spread of a primary tumor? 31. What kind of proteins are involved in invasive ness. Specify the extracellular protease.

Explanation / Answer

A) Cyclin D is the cell regulating cyclin protein in which it produced by stimulation of growth factors like Ras/Raf, ERK ,MAPL,MEK,MYc which alters the transcription rate and controlls the gene expression. This cyclin is very essential in key regulation of cell cycle, eg Rb gene which is TSG for progreesion of cellcycle.

It is binded to the to the E2F family member of transcription factors and control transcription by phosphorylation,when it is inative state, if it is active it inhibits the Rb by phosphorylation and doesnt binds to the E2F. Thus cyclin D plays important role in cell regulation and proliferation.

B) Pocket proteins are family of cell cycle regulators which induces and regulates cell cycle e3vents by controlling G1-S transistion, by inactivating and activating by phosphorylation of Tumour supressor genes and otehr factors like E2F, Rb2.

It is very hard to answer all the questions at a time, i answered first two among.

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