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.
It doesn’t break food down no
Answer:
Below:
Explanation:
The central dogma of molecular biology is an explanation of the flow of genetic information within a biological system. It is often stated as "DNA makes RNA, and RNA makes protein".
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It's Muska..... :)
We have rough and smooth endoplasmic reticulum as the two types of endoplasmic reticulum. They are different from each other in that the rough endoplasmic reticulum has ribosomes on its surface while the smooth reticulum does not...The two also carry out different functions,having ribosomes on their surface,the rough reticulum is in charge of protein synthesis whereas the smooth endoplasmic reticulum is in charge of the synthesis of lipids
With over half the U.S. population infected, most people are familiar with the pesky cold sore outbreaks caused by the herpes virus. The virus outsmarts the immune system by interfering with the process that normally allows immune cells to recognize and destroy foreign invaders.
I cant find anything about the what the role is for the immunologic system in the prevention and recuperation of herpes
so I dont know how much i helped
