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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- Tunicamycin can stimulate the UPR pathway in cells. What is the mechanism underlying how tunicamycin works in this manner?Identify and list the functions of the three general classes of proteins that control cell death.What regulatory mechanisms will ensure that end-products and/or products of alternative pathways will not accumulate in cells? Elaborate two
- Does the Tom complex take/require energy? What kind of proteins do the Tom complex bring into the mitochondria?What Ca2+-dependent events occur after Ca2+ is released into the cytosol?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.…
- What is the duration of G2 checkpoint?In a rare inherited disorder, called Wilson’s disease, excessive amounts of copper accumulate in liver and brain tissue. A prominent symptom of the disease is the deposition of copper in greenishbrown layers surrounding the cornea, called Kayser–Fleischer rings. A defective ATP-dependent protein that transports copper across cell membranes causes Wilson’s disease. Apparently, the copper transport protein is required to incorporate copper into ceruloplasmin and to excrete excess copper. In addition to a diet low in copper, Wilson’s disease is treated with zinc sulfate and the chelating agent penicillamine (p. 148). Describe how these treatments work. [Hint: Metallothionein has a greater affinity for copper than for zinc.]What are negative regulation?
- Autophagy is an évolutionary conserved catabolic process devoted to the degradation of intracellular components. Which of the following would you observe during autophagy? Select all that apply MTOR inhibition through phosphorylation and activation of TSC proteins MTOR activation and phosphorylation of downstream target proteins Increased expression of Rab7 which mediates lysosomal fusion Acute inflammatory responseYou are studying the function of Bax as a positive regulator of apoptosis. You've engineered a version of the Bax protein that is functional, but is mislocalized to the plasma membrane rather than the mitochondria. You expect that this will block the intrinsic pathway of apoptosis. When you activate the intrinsic pathway of apoptosis, you are surprised to find that the cells still die. You then do a cell fractionation experiment and verify that Bax is. indeed being sent to the plasma membrane, rather than the mitochondria. In one sentence, what is the most likely hypothesis for what is happening?How did you know that Paclitaxel was inhibiting cell division? What method of observation was used and how did you interpret the images to come to your conclusion that Paclitaxel was inhibiting cell division?