Anatomy and Cell Biology 4429A Lecture 13: Lecture 13. Viruses and Oncogenes notes

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coffeecicada91

22 Jan 2012

School

Western University

Department

Anatomy and Cell Biology

Course

Anatomy and Cell Biology 4429A

Professor

Paul Walton

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Document Summary

Multiple mutations (not just one because that would be lethal), turn off some genes and turn on others to change the cell. Viruses can express oncogenes or down-regulate tumor suppressor genes v-src=viral src phosphorylates proteins on tyrosine residues. Rous sarcoma virus has the additional proteins v-src (as well as its rna polymerase, envelope proteins in the gene) Form of src in every cell of your body = c-src. Viral form is truncated at the end by a little bit, c-src is a bit longer = regulated by phosphorylating the 527tyr = nt present on the viral form. This means v-src is always on because it is missing the tyr that can be regulated. Why would rna viruses want to get away from their simple lifestyle and incorporate pieces of our genes we had this kinase first and the virus took it from us. They can only infect cells that are dividing and growing.

Related Questions

1. When a growth factor binds to a receptor tyrosine kinase, the receptor becomes phosphorylated on tyrosine residues.

a. How does this occur?

b. Why is this phosphorylation important in initiating an intracellular signaling cascade?

c. Why does phosphorylation change the activity of proteins? (What happens to the protein physically when it is phosphorylated?)

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Cyclin B1, a key cell cycle regulatory protein in vertebrates, is mostly cytosolic before mitosis. Early in mitosis, however, the protein is phosphorylated by certain protein kinases and consequently accumulates in the nucleus. How can phosphorylation bring about nuclear accumulation of this protein?

A. Phosphorylation within the nuclear localization signal inhibits the function of the signal.

B. Phosphorylation within the nuclear export signal enhances the function of the signal.

C. Phosphorylation within the nuclear export signal interferes with the function of the signal.

D. Phosphorylation elsewhere on the protein enhances binding to cytosolic proteins

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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

Anatomy and Cell Biology 4429A Lecture 13: Lecture 13. Viruses and Oncogenes notes

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