2. (8pts each) Short response (max 2 sentences each IN YOUR OWN WORDs) A. How ar
ID: 272031 • Letter: 2
Question
2. (8pts each) Short response (max 2 sentences each IN YOUR OWN WORDs) A. How are caspases prevented from signaling the cell for apoptosis until the appropriate time? B. Please provide a specific mechanism that TURNS OFF the following signaling molecules that are commonly found in RTK pathways. Also, please circle which one(s) need to be turmed off for the signaling response to be stopped Receptor Tyrosine Kinase: Ras-GTPase: MAP Kinase Kinase: Calcium (Ca2): C. Please circle whether the following proteins are proto-oncogenes or tumor suppressors: i. Caspases ii. DNA damage checkpoint protein (ex. p53) proto-oncogene I tumor suppressor ii. G1/S-phase cyclin (ex. Cyclin D) proto-oncogene I tumor suppressor proto-oncogene I tumor suppressor iv. Wee1 proto-oncogenetumor suppressor D. Please state whether you agree or disagree with the following, and provide your reasoning: Treating cells with cholera toxin (which activates Gs proteins) or with pertussis toxin (which inhibits Gi proteins) leads to similar relative changes in CAMP levels in the cell. Circle: AGREE or DISAGREE ReasoningExplanation / Answer
A. anti-apoptotic proteins like BCL-X, BCL-2 bind to procaspases and prevent their activation by transformation into the caspases
B. RTK is turned off by a phosphatase that removed the activating phosphate from the receptor
Ras-GTPase:
MAP kinase kinase
calcium: calmodulin
caspases induce apoptosis and thus are tumor suprressor
DNA damage check point are also tumor suppressor
Cyclin D is a proto oncogene
Wee1 inhibits mitosis and thus is a tumor suppressor gene
D Agreed. Gs activated adenylate cyclase to produce cAMP and Gi inhibits it and decreases level of cAMP. If you activate Gs it will increase cAMP and if you inhibit Gi it will also increase cAMP levels.
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