Assume that the substrate cycle that exists as shown undergoes reciprocal regulation such that the production of B is upregulated by 50% and the production of A is downregulated by 50%, What will the next flux of B in this situation be?
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- When the Na+/K+ ATPase is in the E1 confirmation, why is it essential to maintain the K+ binding sites in a low affinity state?Tumor necrosis factor (TNF) signaling Discuss the nature of the TNF ligand and the receptor for that ligand, and explain the general steps in the pathway (use figure 8.53 and explain in your own words). Make sure to include an explanation of the proteolytic and phosphorylation cascades. What advantage is there in having a cascade part of these pathways? What purpose does it serve?How is cigarette smoking related to elastase function? Methionine sulfoxide is formed by cigarette smoke in the antitrypsin protein, which leads to the full manifestation of the disease in individuals heterozygous for emphysema. Oxidation of methionine 358 by cigarette smoke of the elastase inhibitor active site leads to an increased inhibition of elastase and subsequent overaccumulation of mucus in the lungs. The inhibitor of elastase is axidized by cigarette smoke so elastase doesn't function properly in healthy individuals. Cigarette smoke modifies the elastase methionine residues such that the enzyme activity is blocked.
- A strain of mice has been developed that lack the enzyme phosphorylase kinase. Yet, after strenuous exercise, the glycogen stores of a mouse of this strain are depleted. Explain how this depletion is possible.Is the regulation shown (denoted by?) positive or negative regulation? Explain why the type of regulation shown here is advantageous for the cellIf intracellular [ATP] = 5 mM, [ADP] = 0.5 mM, and [Pi] = 1.0 mM, calculate the concentration of AMP at pH 7 and 25°C under the condition that the adenylate kinase reaction is at equilibrium.
- a gain-of-expression of MCT1 transporters in pancreatic b-cells wreaks havoc on the cell’s function. To consider this point further, determine the number of ATP that result from complete catabolism of a) 5 lactate and b) 5 b-hydroxybutyrate in aerobic conditions in humans. Assume TCA intermediates are NOT limiting. Use the exact number of c-subunits and the details of the electron transport chain in humans to determine the number of ATP from NADH and FADH2 (not 2.5ATP per NADH and 1.5ATP per FADH2Mutations in adenylate kinase have led to a hyperactive enzyme that ultimately ends up elevating ADP levels in a cell.Calculate the EC (energy charge) given the following atypical adenylate concentrations for the cell containing the mutant adenylate kinase: ATP = 0.5 ??��, ADP = 12.2 ??��, AMP = 80 ??��.Explain how the addition of a phosphate group to certain amino acids of kinase D can result in the activation of D. Explain how the activation of the pathway shown in Figure 1 can lead to increased production of A.
- signal amplification of cells relies on which of hte following increased activity of protein phosphatases sequential increase in the different components, wherein a single, activated component can activate many copies of the next component in the pathway increasing numbers of cell-surface receptors as the signal is transduced increasing amounts of ligand aas signal transdutciton proceedsAutophagy 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.…Phosphorylase kinase integrates signals from thecyclic-AMP-dependent and Ca2+-dependent signalingpathways that control glycogen breakdown in liver andmuscle cells (Figure Q15–4). Phosphorylase kinase is com-posed of four subunits. One is the protein kinase that cata-lyzes the addition of phosphate to glycogen phosphorylaseto activate it for glycogen breakdown. The other three sub-units are regulatory proteins that control the activity of thecatalytic subunit. Two contain sites for phosphorylation byPKA, which is activated by cyclic AMP. The remaining sub-unit is calmodulin, which binds Ca2+ when the cytosolicCa2+ concentration rises. The regulatory subunits controlthe equilibrium between the active and inactive confor-mations of the catalytic subunit, with each phosphate andCa2+ nudging the equilibrium toward the active confor-mation. How does this arrangement allow phosphorylasekinase to serve its role as an integrator protein for the mul-tiple pathways that stimulate glycogen…