Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
20 Cards in this Set
- Front
- Back
|
What are the two most important cell cycle regulatory pathways altered in cancer?
|
1. RetinoBlastoma Pathway
2. P53 Pathway |
|
|
How does E2F get activated?
|
When RB protein is phosphorylated.
|
|
|
Where does the E2F bind on the RB protein?
|
The pocket region, which is between domain A & B
|
|
|
What happens when the RB protein is not functional?
|
The E2F protein is always functional
|
|
|
What are the 3 most important mechanisms of RB inactivation?
|
1. Gene deletion and generation of truncated protein (Mutation of RB)
2. Amplification of cyclin D1 3. Deletion of the cyclin D-Cdk inhibitor p16 gene |
|
|
Expression of the E7 papillomavirus protein is responsible for _________.
|
Uterine cervix carcinoma
|
|
|
What does E7 do?
|
Its a viral protein that interacts with RB and prevents its activity. It competitively inhibits RB by preventing its binding with E2F.
|
|
|
Tumors cannot develop unless the RB is not functional. T/F?
|
True
|
|
|
What is the purpose of p53?
|
To ensure damaged DNA is not replicated. Maintains integrity of DNA (aka guardian of DNA)
|
|
|
Which protein is a mediator of Apoptosis?
|
p53 when the damage is too extensive to repair
|
|
|
what happens when p53 is mutated?
|
accumulation of cells with mutated DNA
|
|
|
p53 can activate the expression of two types of genes. discuss.
|
P53 can activate genes which cause cell arrest such as p21 to correct any necessary damage to the DNA. However if the damage is too extensive p53 can activate genes which promote apoptosis.
|
|
|
In cancer cells can undergo apoptosis.
|
False, b/c p53 is not functional
|
|
|
whats the most common method of inactivation of p53.
|
mutation in the DNA binding domain 95% of cases with mutation
|
|
|
What is the difference between the mutation of p53 and RB.
|
Missense mutation which doesn't result in a truncated protein as in RB.
|
|
|
what is E6 and what does it do?
|
its a virally produced protein that interacts with p53 and degrades it.
|
|
|
The control pathway between G1 and S-phase transition?
|
RB control pathway
|
|
|
The control pathway that activates G1/S transition after DNA damage?
|
P53 pathway
|
|
|
How is RB phosphorylated (inactivated)? and what inhibits this process?
|
D/CDK4 complex phosphorylates RB which in turn activates E2F. P16 inhibits D/CDK4 from phosphorylating RB, therefore RB is active when p16 is active/present.
|
|
|
Cyclin D1 amplification is seen in breast and GI cancers. What is the consequence of amplification of Cyclin D1 or any other cyclins/CDK genes ?
|
This will lead to the Cyclin/CDK complex which in turn leads to phosphorylation of RB.
|
