Define Explain the role of CDK inhibitors. If cyclin-CDK com-plexes are necessary to allow regulated progression through the eukaryotic cell cycle, what would be the physiologicalrationale for CDK inhibitors?
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Define
Explain the role of CDK inhibitors. If cyclin-CDK com-
plexes are necessary to allow regulated progression through
the eukaryotic cell cycle, what would be the physiological
rationale for CDK inhibitors?
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Solved in 3 steps
- Explain the role of CDK inhibitors. If cyclin-CDK complexes are necessary to allow regulated progression through the eukaryotic cell cycle, what would be the physiological rationale for CDK inhibitors?Briefly describe how the cyclin D-cdk4/6 and cyclin E-cdk2 complexes regulate Retinoblastoma protein (pRb) functions?The destruction of the various cyclins is commonly used to inactivate the Cdk/cyclin complexes. Why is it advantageous to inactivate these complexes via protein destruction instead of some other method that does not require the re-synthesis of a cyclin protein the next time the cell divides?
- Changes in the activity of a variety of Cdks are essential for accurate progression through the cell cycle, and yet the levels of Cdk expression are fairly constant during the cell cycle. Briefly describe three mechanisms by which the activity of Cdks is regulated.Drug A323 inhibits the activity of the cyclin-dependent kinase (CDK) - G1 cyclin complex. Consider possible effects of the drug on the cell cycle of normal and malignant cells. Predict what is likely to happen if the drug is added to the cell types described in A). Motivate your answers and describe the role of cycle-regulatory pathways that are relevant with respect to the action. of drug A323. A) Carcinoma cells in which both allels of the Rb gene carries loss of function mutation.Describe at least two Cdk regulation check points during the cell cycle, Describe how that Step is regulate moluculary and what would happen if that step did not happen correctly
- (46) A mutated form of protein p5x is found in patients with squamous cell carcinoma. In vitro studies show that the normal p5x molecule binds to DNA, and neoplastic cells accumulate in the G0 phase of the cell cycle. In contrast, the mutated form of p5x does not bin d to DNA. These finding are most characteristics of which of the following? (A) Growht factor receptors (B) GTP-binding protein (C) Nonreceptor tyrosine kinases (D) Oncogene proteins (E) Tumor suppressor gene proteinsThe PYK gene codes for the expression of pyruvate kinase, which is one of the enzymestargeted for anti-cancer drug design. You have identified an RNAi that targets the mRNAof PYK gene. To study the effect of the RNAi towards pyruvate kinase, the respected RNAiis expressed in Saccharomyces cerevisiae. The level of pyruvate kinase can be detectedwith a fluorescent antibody.(a). Predict the result that you will obtain in recombinant S. cerevisiae that expresses therespected RNAi.(b). Compare the result in Q3a(i) with the wild-type S. cerevisiae.What inhibit CDK activity by bindingdirectly to the cyclin-CDK complex.
- Discuss the relationship of the Bcl-2 family, caspase family, and mitochondrion in apoptosis.After a cell "clears" the G₁ restriction checkpoint, it can proceed into S phase. This S phase entry is achieved by a cyclin dependent kinase (Cdk2) and its cyclin (Cyclin E), but additionally requires the action of a protein kinase (CDC2) as well as a phosphatase (CDC25) enzyme. Explain how these 4 proteins work together to orchestrate S phase entry.Progression through the cell cycledepends on the phosphorylationof hundreds of different proteins bycyclin–Cdk complexes. What are themolecular mechanisms ensuring thatthese proteins are phosphorylated atprecisely the right time and place?