What is the function of the trifunctional protein (TFP) in mitochondrial beta-oxidation?
Explanation
This question tests the specific role and substrate preference of the trifunctional protein (TFP), a key multienzyme complex in the beta-oxidation of long-chain fatty acids.
Other questions
What are the three primary sources from which cells can obtain fatty acid fuels?
What is the role of bile salts in the digestion of dietary fats?
What hormone, secreted in response to low blood glucose levels, stimulates the mobilization of triacylglycerols stored in adipose tissue?
To what blood protein do free fatty acids released from adipocytes bind for transport to other tissues?
What is the purpose of the carnitine shuttle in fatty acid oxidation?
What is the overall result of one pass through the beta-oxidation sequence for a saturated fatty acyl-CoA?
How many cycles of beta-oxidation are required to completely oxidize one molecule of palmitoyl-CoA (a 16-carbon fatty acid) to acetyl-CoA?
What is the energetic cost, in terms of ATP equivalents, for the activation of a fatty acid to a fatty acyl-CoA?
What is the approximate net yield of ATP molecules from the complete oxidation of one molecule of palmitoyl-CoA to CO2 and H2O?
Which auxiliary enzyme is required for the oxidation of oleate, a monounsaturated fatty acid with a cis double bond?
The final product of oxidizing an odd-number fatty acid is acetyl-CoA and what other molecule?
The conversion of propionyl-CoA to succinyl-CoA requires an enzyme that uses a cofactor derived from which vitamin?
What is a key difference in the first step of beta-oxidation in peroxisomes compared to mitochondria?
In humans and most other mammals, what are the three "ketone bodies" produced in the liver from acetyl-CoA?
Why can the liver produce ketone bodies but not use them as fuel?
Under what two conditions does the overproduction of ketone bodies, leading to acidosis and ketosis, typically occur?
What molecule, an intermediate in fatty acid synthesis, inhibits carnitine acyltransferase I to prevent a futile cycle of simultaneous fat synthesis and breakdown?
The alpha-oxidation pathway is important for the catabolism of what type of fatty acid that cannot undergo beta-oxidation?
Which genetic disease is caused by a defect in the medium-chain acyl-CoA dehydrogenase (MCAD) enzyme?