This question pertains to the KRAS wikipedia page, and I just want to double check and clarify my own understanding of how this mutation works in cancer.
K-Ras protein acts like a switch that is turned on and off by the GTP and GDP molecules.
So if K-Ras is a switch, does that mean that when there is K-Ras mutation, it functions defectively so that it does not shut off? So for example when it binds to GTP and converts it to GDP, KRAS does not shut off regardless of GTP is converted to GDP and this would lead to / cause cancer.
So I guess I have several questions to my reasoning above..
Why does excess conversion of GTP to GDP lead to cancer? Is it because this is specifically pertaining to the the RAS pathway?
When I referenced above "it" is the K-Ras binding event the K-Ras protein binding to GTP then converting to GDP caused by the K-RAS gene not being able to function correctly? I'm just confused if its the K-Ras gene causing the problem or the K-Ras protein being the problem, or is it both?
If K-Ras acts as a molecular switch, how to GEFs/GAPs effect K-Ras mutations? Because I know GEFS activate the conversion of of GTP to GDP, but what is its relationship to KRAS/K-Ras?
In the next line it states:
When the protein is bound to GDP, it does not relay signals to the cell's nucleus.
- Is this saying when K-Ras is bound to GDP, that the conversion of GTP to GDP won't ever stop? I kind of just don't understand why this was written or what its relevance is. Or is it simply stating K-Ras can only turn on GTP to convert it in to GDP but not the other way around?