The correct answer is the last statement.
If the regulatory serine is mutated to alanine, then acetyl-CoA carboxylase will get activated spontaneously and will produce malonyl-CoA. The increased concentrations of malonyl-CoA will obstruct the oxidation of fatty acids by preventing the entry of fatty acids into the mitochondria.
It is because the AMP-activated protein kinase phosphorylates the serine residues of acetyl-CoA carboxylase to inactivate it. If a mutation occurs in such residues, then the AMPL cannot phosphorylate acetyl-CoA carboxylase and this enzyme will get activated spontaneously.
In such a situation, there will be more than sufficient production of malonyl-CoA, which will inhibit the admittance of more fatty acid getting inside the mitochondria; this will indirectly prevent the oxidation of fatty acids.
Answer:
True
Explanation:
when you do so many hypothesis it gets turned into a theory
An answer you are looking is maybe some sort of seizing the computer system. Is that one of the choices? I hope this helps :)
NON-SPECIFIC: Skin, Macrophages, Mucous, Fever
SPECIFIC: B cells, T cells, Antibodies (aka: immunoglobins)
What i found on Rift is <span>a crack, split, or break in something. so i think it would be the first one.
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