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Biochemistry · Insulin signalling: receptor tyrosine kinase
Sample itemA gastrointestinal stromal tumour carries a gain-of-function mutation in the KIT surface receptor, which dimerises and signals without ligand. Imatinib controls the tumour by blocking the intrinsic catalytic domain of which receptor class?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
D. Receptor tyrosine kinase
KIT belongs to the receptor family whose intracellular domain phosphorylates tyrosine residues, as do PDGFR and the insulin receptor. Constitutive activation drives proliferation and is blocked by imatinib at the ATP-binding site. This is a targeted therapy aimed at the mutated driver.
Option by option
A. Receptor guanylyl cyclase
Receptor guanylyl cyclases are not involved in this tumour.
B. G protein-coupled receptor
G protein-coupled receptors are not the target of imatinib in this tumour.
C. Cytokine receptor with JAK
Cytokine receptors depend on separate JAK enzymes and KIT does not belong to this group.
D. Receptor tyrosine kinase (correct)
Correct. KIT is a receptor with intrinsic catalytic activity, and imatinib blocks its ATP-binding site.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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