Discussion of all aspects of biological molecules, biochemical processes and laboratory procedures in the field.
7 posts • Page 1 of 1
On a recent test, this question appeared and I was really sure I had the right answer... Only I didn't. Now I really don't get the question and I would like to ask you to help me! This is the question:
The growth factor Superchick stimulates proliferation of cultured chicken cells. The receptor that binds Superchick is a receptor tyrosine kinase, and many tumor cell lines have mutations in the gene that encodes this receptor.
Which of the following types of mutations would be expected to induce uncontrolled cell proliferation? (2 points):
a) A mutation that prevents localization of the receptor to the plasma membrane.
b) A mutation that prevents dimerization of the receptor.
c) A mutation that destroys the kinase activity of the receptor.
d) A mutation that prevents recognition of the receptor by phosphatases.
e) A mutation that prevents ligand binding.
I won't post my answer and explanation yet, so you can form your own answer and maybe help me understand!
Thank you! Could you please also explain why?
From my distant memories of regulation of kinase cascades, that looks like the more logical response. Now I could probably elaborate more, but only after you tell me what was your answer and how you came to it.
Oh and by the way, I would take my answer with a grain of salt...
Science has proof without any certainty. Creationists have certainty without
any proof. (Ashley Montague)
I thought D as well, because the phosphatases inactivate an active receptor tyrosine kinase by plucking of the phosphategroups, and if the phosphatases cannot recognize the receptor tyrosine kinase anymore it will remain active and keep on stimulating cell proliferation.. Right?
But that's wrong, because it's supposed to be A... Do you have any possible explanation for that answer? I really don't.
Thanks by the way.
I would guess d as well.
Question is, where should it be localised elsewhere? Maybe the mislocalisation would cause loss of dephosphorylation process. However, the kinase activity shouldn't be activated either.
Cis or trans? That's what matters.
7 posts • Page 1 of 1
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