Researchers are studying melanoma
cells that initially respond to vemurafenib. Over time, some cells develop
resistance. Sequencing reveals a p61 B-RAF(V600E) splice variant lacking a
portion of the regulatory domain. Western blot analysis shows that MEK
phosphorylation remains high even in the presence of the inhibitor.

Which explanation best accounts for
these findings?

Question

Researchers are studying melanoma
cells that initially respond to vemurafenib. Over time, some cells develop
resistance. Sequencing reveals a p61 B-RAF(V600E) splice variant lacking a
portion of the regulatory domain. Western blot analysis shows that MEK
phosphorylation remains high even in the presence of the inhibitor.

Which explanation best accounts for
these findings?

Accepted Answer

The
truncated p61 BRAF variant forms homodimers, allowing continued MEK
phosphorylation despite inhibitor treatment

Answer

The truncated protein
prevents MEK degradation, maintaining MEK signalling indirectly

Answer

The regulatory domain
deletion causes increased RAS activation, which fully bypasses BRAF to activate
MEK

Answer

The p61 splice
variant recruits alternative kinases that directly phosphorylate MEK
independently of BRAF

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Researchers are studying melanoma cells that initially respond to vemurafenib. ...

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