BIOCH410 Lecture Notes - Lecture 2: Tumor Suppressor Gene, Cyclin-Dependent Kinase 4, E2F

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crimsonpanda122

12 Feb 2020

School

University of Alberta

Department

Biochemistry

Course

BIOCH410

Professor

Carlos Patron

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Document Summary

Retina blastoma (rb) protein is highly controlled by phosphorylation. Complex of rb and e2f is very stable. If rb protein is hyper phosphorylated, it will dissociate from e2f. Activates regions in the nuclear dna that are responsible for allowing gene transcription. Growth factors are major regulators of this process. Cdk4 linked to e2f activity and cell cycle entry. Growth factors block a blocker of cdk4. There are mutations in rb that prevent it from interacting with e2f. When those mutations occur, you can have early onset cancer. The a ected cells tend to divide quickly and tumor develops. Growth factors also, interacts with gf receptors. When p53 is active, the cells make a lot of proteins that lead to growth arrest. Can also have adopts the p53 is active. A stimuli like uv, stress, can cause activation of p53. So, good because it causes adopts of damaged cells. But if p53 has mutation, growth arrest will not occur.

Related Questions

B__1) Driver mutations provide a growth advantage to a tumor cell. Which type of mutation is known to accumulate in cancer cells but has no direct contribution to the cancer phenotype?

A) alteration mutations B) passenger mutations C) carrier mutations

D) indirect mutations E) insignificant mutations

_A__2) Which of the following general mechanisms appear to be involved in the formation of cancer cells?

A) genomic instability, DNA repair failure, chromatin modifications

B) inversions, operon formation, methylation

C) RNA failure, DNA phosphorylation, phosphorylation of adenyl cyclase

D) transdetermination, mutation, allosteric interactions

E) suppression, tabulation, projection

_A__3) What is the name of the protein that combines with cyclins to exert local control of the cell cycle?

A) cyclin-dependent kinase B) phosphatase C) ATPase D) integrase E) hexokinase

_D__4) A protein functions as a cell-cycle regulator that causes cell death (apoptosis) to a damaged cell. What is the symbol given to this protein?

A) p34 B) p102 C) cyclin D) p53 E) phosphokinase

_A__5) The retinoblastoma protein (pRB), like p53, serves as a(n) ________ in regulating the cell cycle.

A) tumor suppressor B) tumor enhancer C) up regulator D) oncogene E) pseudooncogene

_C__6) Mutant versions of genes that are normally involved in promoting the cell cycle are known as ________.

A) tumor suppressors B) proto-oncogenes C) oncogenes D) malignant genes E) attenuators

_B__7) In sporadic cases of retinoblastoma, how many gene mutations are thought to be necessary in the same cell for a tumor to develop?

A) one B) two C) four D) six

__D_8) What is the name of the protein that appears to regulate the entry of cells into an S phase? This protein is also known as the "guardian of the genome."

A) p34 B) p102 C) cyclin D) p53 E) phosphokinase

The Myc gene is a very important proto-oncogene that encodes the Myc transcription factor. The Myc gene is normally only expressed in response to the presence of growth factors, and once expressed the Myc protein promotes passage through the restriction point by activating the transcription of early cell cycle genes. As an indication of the importance of Myc, overexpression of the Myc protein is sufficient to cause tumorigenesis in many cell types. For example, Burkittâs lymphoma is the result of a chromosomal translocation that leads to increased myc expression in B-lymphocytes.

(A) (3 pts) What is the restriction point, and which CDK complex is most directly activated by passage through the restriction point?

(B) (10 pts) Describe how activation of the CDK complex from part (A) leads to entry of cells into S-phase. Your answer must indicate the protein(s) that this CDK directly acts on, the proteins that directly stimulate S-phase entry, and the mechanism that prevents premature entry into S-phase.

(C) (8 pts) Indicate whether each protein you mention in part (B) is a proto-oncoprotein (e.g. a protein encoded by a proto-oncogene) or a tumor suppressor. You can incorporate this into your answer to part (B) if you choose.

(D) (4 pts) Why does the overexpression of Myc lead to cancer, for example Burkittâs lymphoma?

BIOCH410 Lecture Notes - Lecture 2: Tumor Suppressor Gene, Cyclin-Dependent Kinase 4, E2F

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