The PDH mechanism coenzyme that plays a direct role in the generation of acetyl CoA is NADH Lipoamide FADH2 TPP
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The PDH mechanism coenzyme that plays a direct role in the generation of acetyl CoA is
NADH
Lipoamide
FADH2
TPP
Step by step
Solved in 3 steps
- Complete oxidation of a 16-carbon fatty acid can yield 129 molecules of ATP Study Figure 19.2 and determine how many ATP molecules would be generated if a 16-carbon fatly acid were metabolized solely by the TCA cycle, in the form of S acetyl-CoA molecules.AsapWhich enzyme is used for both the synthesis and breakdown of acetoacetate? thiolase O HMG-CoA synthase OB-hydroxybutyrate dehydrogenase O B-Ketoacyl-CoA transferase
- Which one of the following statements about coenzyme A is correct? The biosynthesis of coenzyme A requires vitamin B12 O The thioester of acetyl-coenzyme A raises the pka value of the alpha-proton O Hydrolysis of acetyl-coenzyme A is thermodynamically favourable O Acetyl-coenzyme A is involved in the biosynthesis of S-adenosylmethoinineBelow is an image of the Krebs cycle: acetyl-CoA oxaloacetate COASH H20 NADH NAD* H20 malate citrate fumarate isocitrate FADH2 NAD* CO2 FAD АТР NADH + ADP succinate GTP NAD+ a-ketoglutarate H20 GDP NADH + CO2 COASH succinyl CoA COASH Consider the conversion of succinate to fumarate, which is coupled with the production the electron carrier FADH2. If this reaction was NOT coupled with the production of FADH2 (and only catalyzed the conversion of succinate to fumarate), how would this impact ATP production through cell respiration? OATP production would stop because no high energy electron carriers would be produced ATP production would still occur, but there would be a much lower ATP yield because a large number of electron carriers are no longer being made ATP production would stop because without FADH2 we will no longer have electrons moving through the electron transport chain ATP production would still occur, but there would be a slightly lower ATP yield because a small number of…Succinyl-CoA Synthetase mechanism Succinyl-CoA synthetase enzyme active site O Substrates bind to the active site COO of succinyl-CoA synthetase CH2 OH His CH2 . Succinyl-CoA COA- Guanosine Phosphoryl group transfer to GDP to form GTP, which is released from the 2 Formation of succinyl-phosphate COA GTP enzyme Formation of phosphohistidine Guanosine COO Phosphohistidine CH2 GDP GDP CH2 COO CH2 | "Succinate CH, Succinyl-phosphate ČOO a) Which catalytic mechanism occurs in step 2? b) Why must phosphate first bind to succinyl-CoA before interacting with the His site and GDP?
- Identify the Krebs cycle enzyme that consumes a 3-carbon substrate molecule, producing a 2- carbon product molecule (attached to acetyl-CoA), along with NADH, and one molecule of CO2. succinyl CoA synthetase a-ketoglutarate dehydrogenase pyruvate dehydrogenase isocitrate dehydrogenase malate dehydrogenaseThe Citric Acid Cycle results in (Choose all that apply) net oxidation of acetyl CoA carbons to two CO2 O three NAD to NADH reductions involving 6 electrons one FADH2 to FAD oxidation involving 2 electrons three NADH to NAD oxidations involving 6 electrons O one FAD to FADH, reduction involving 2 electrons O a substrate level phosphorylationIn beta-oxidation, which cofactor is required the for second oxidation reaction (conversion of beta-hydroxyacyl-CoA to beta-ketoacyl-CoA)? NAD+ water FAD CoA-SH
- Discuss the metabolic rationale for phosphorylation of acetyl-CoA carboxylase by AMP-activated protein kinase (AMPK) and cyclic AMP–dependent protein kinase (PKA).1 2 points Order the following TCA cycle metabolites in the order they are produced in one turn of the citric acid cycle. Not all answers will be used. 2 1 4 3 TI Isocitrate Citrate Lactate Pyruvate Oxaloacetate Isocitrate Succinyl-CoA Aconitate 3-Phosphoglycerate -DOA number of genetic deficiencies in acyl CoA dehydrogenases have been described. This deficiency presents early in life after a period of fasting. Symptoms include vomiting, lethargy, and sometimes coma. Not only are blood levels of glucose low ( hypoglycemia), but starvation-induced ketosis is absent. Provide a biochemical explanation for these last two observations.