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16 Cards in this Set

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Match the following: A)Hepatocytes, cardiac muscle cells, digestive epithelial cells, neurons… B) G0 (quiescent cells), permanent cells, daughter cells (enter cell cycle)
1. G0 (quiescent cells): hepatocytes (go in-&-out of the cell cycle)… 2. Permanent cells (don't re-enter the cell cycle): neurons/cardiac muscle cells… 3. Daughter cells (enter the cell cycle): digestive epithelial cells
At which cell cycle stage is p53 most active?
G1 check point before entering the S-phase
What effect does Cdk have on the Rb protein? And which would be an oncogene and which would be a tumor suppressor?
Cdk phosphorylates the Rb protein (where the Rb protein has been sequestering the transcription factor E2F)… 2) Cdk is an oncogene AND the Rb gene would be a tumor suppressor
Describe Cdk's suppression of the Rb protein mechanism.
Mitogen activate cyclin --> leads to cyclin binding to the G1/S-Cdk (kinase) --> The G1/S-Cdk is phosphorylated by two kinases (CAK-activating and Wee1-inactivating) --> Cdc25 phosphatase removes the inactivating phosphate) --> active G1/S-Cdk can then phosphorylate the Rb protein (causing it to release EF2)
In the M-Cdk activation pathway, where is the site of positive feedback?
Active G1/S-Cdk activate the Cdc25 phosphatase, which leads to the dephosphorylation of the inactive G1/S-Cdk
What type of cancer is the Rb protein (tumor suppressor) associated with?
Retinoblastoma (childhood eye-tumor)
What associates with the active Rb-E2F complex? What is its effect?
HDAC… HDAC makes the histones more compact and less accessible to transcription factors
What causes the release of HDAC?
1. What is APC's role?... 2. what activates it?… 3. What cancer is the truncation of APC associated with?
APC (anaphase promoting-complex) is a ubiquitin ligase, which ligases the ubiquitin to the Cdk and leads to the degradation of activated the cyclin… 2. Cdc20… 3. FAP
1. Describe the mechanism that controls activated Cdk by degradation... 2. Describe the mechanism that controls activated Cdk by sequestration
1. Active APC, Cdc-20 (APC activating subunit, ubiquitin and ubiquitin enzymes (E1 and E2) --> leading the degradation by proteosomes... 2. DNA damage --> release of Mdm2 from p53 and p53 is phosphorylated(transcription factor)--> p53 transcribes p21 --> p21 protein inhibits Cdk-cyclin activity
1. What is inactive p53 bound to that inhibits its activity?… 2. What activates p53?
1. Mdm2… 2. X-rays (other DNA damage)
1. What is the role of p21?… 2. Describe the mechanism of p21.
Prevents gene transcription by binding activated Cdk… 2. X-rays damage DNA --> Mdm2 is released from p53 as p53 is phosphylated --> p53 is a transcription factor for p21 --> p21 is transcribed --> translated p21 --> p21 binds Cdk and inhibits its activity
What is CPT-11 (Irinotecan)?
a DNA damaging agent (drug)
What is the effect of CPT-11?
DNA damage --> p53 induction --> p21 expression --> cell arrest
What is added to CPT-11 to cause apoptosis?
Flavopiridol (Flavopiridol + CPT-11 --> apoptosis)
What effect will a p53 mutation have on the use of CPT-11 + flavopiridol?
mutations make this chemotherapeutic combination less effective