What are the control mechanisms of glycolysis and the Krebs cycle.
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What are the control mechanisms of glycolysis and the Krebs cycle.
What are the control points? What molecules regulate at each checkpoint? How these mechanisms combine to regulate cellular
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- In Xenopus, one of the substrates of mitotic CDKs is the phosphatase Cdc25. When phosphorylated by mitotic CDKs, Cdc25 is activated. What is the substrate of Cdc25? How does this information help to explain the rapid rise in mitotic CDK activity as cells enter mitosis?GLUT4 is a protein channel that facilitates the transport of glucose into the cell. Under nor- mal conditions, some of the GLUT4 proteins that are synthesized by the cell do not become active and are instead stored within the membranes of vesicles. The insulin receptor tyrosine kinase (TRK) is a receptor protein that facilitates the decrease of glucose concentration in the bloodstream by increasing the uptake of glucose by cells. When the insulin hormone binds the insulin TRK receptor, a signal transduction pathway causes the activation and addition of GLUT4 to the cell membrane. A model of this signal transduction pathway is illustrated in the figure below. insulin insulin receptor cytoplasm A model of the insulin TRK receptor signal-transduction pathway. Which of the following best predicts the effect of a loss of function of the insulin TRK2 A B C D The stimulation of the signal transduction pathway will increase. The storage of GLUT4 inside the cell will increase. The concentration…Mutants of cyclin B that are resistant to degradation by the cyclin B protease have been generated. How would the presence of these cyclin B mutants affect the events at the metaphase to anaphase transition?
- Autophagy Is Required for PKA Activation and Cell Viability upon GlucoseStarvation. The functional relationship between PKA and autophagyis largely unclear. Because PKA controls cell metabolism particularly related to glucose status (21–23), we first examined the relationship between autophagy and PKA activity in the control of cellmetabolism with glucose limitation. We found that in addition toactivating autophagy, glucose starvation also induced the phosphorylation of cAMP response element-binding (p-CREB), a wellknown PKA substrate, indicative of elevated PKA activity in bothHEK293T and HCT116 cells. In contrast, disruption of autophagyby deletion of essential autophagy gene Atg7 or Atg14 abolished theincrease of p-CREB levels in the above cells (SI Appendix, Fig.S1 A, B, D, and E), suggesting that inactivation of autophagy suppresses PKA activity in response to energy shortage. Moreover, lossof Atg7 or Atg14 accelerated cell death in response to glucosestarvation (SI Appendix, Fig.…Explain why the structure of the ER, mitochondria, and Golg apparatus assist their respective functions.Cytochrome c is part of the respiratory chain in most cells. How can cytochrome c be a signal to induce (start) apoptosis if it already exists in most cells?
- Which of the following changes to the microtubule binding protein, Tau, commonly occurs in Alzheimerâ s and other neurodegenerative diseases? A Tau is hypo-phosphorylated and does not bind to microtubules to destabilize them. B Tau levels are so low in the cell that they only bind to some microtubules. C Tau is hyper-phosphorylated and does not bind to microtubules to stabilize them. D Microtubules are hyper-phosphorylated and do not bind to Tau.Upon learning about the mechanism of apoptosis, the question asked was; Is cytochrome c being released from mitochondria or is it being expressed by an induced nuclear gene and being produced in the cytosol. Which one of the following observations would provide the best evidence that it was being released from the mitochondria? Bcl2 blocks release of cytochrome c from mitochondria and also inhibits apoptosis Active Fas receptors trigger release of cytochrome c from mitochondria. Extracellular signals that block apoptosis do not produce cytosolic cytochrome c Caspase inhibitors block release of cytochrome c from the mitochondriaWhen the gene encoding a certain cellular kinase is deleted, the resulting mutant cells arrest in the cell cycle and do not divide. These mutants can be rescued when a gene encoding an N-terminal GFP fusion of the protein is expressed, but not when a gene encoding a C-terminal GFP fusion is expressed. Which fusion protein is appropriate to use in studying cellular localization and activity? Explain why.
- What statement about Cdks/Cyclins below is false? A) Cyclins phosphorylate Cdks B) Cdks are kinases C) Cdk expression is constant during the cell cycle D) Cyclin expression fluctuates during the cell cycle E) Cdk activity fluctuates during the cell cycleIn this module, we learned about G protein function as a binary switch. G proteins have an intrinsic enzymatic ability to hydrolyze GTP to GDP + Pi. Why, then, would a cell need additional G protein controls like GEFs or GAPs? What advantages do you see this providing?You are studying the M-cyclin. You treat mitotic cells with an inhibitor of the proteasome and find that M-cyclin is no longer degraded and that this prolongs mitosis. You also find that in the presence of the inhibitor, M-cyclin is now running slower/larger in a Western than you have previously observed. In 1-2 sentences, explain why this might be happening. Edit View Insert Format Tools Table 12pt Paragraph B IU Αν S A C I AT²✓ #tv A MacBook Air X : G
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