it is well known that mutations in some genes can leads to cancer condition. if in that case how those mutated gene products can able to participate in different pathways?
especially in the case of receptors how the mutated proteins can still recognize the specific ligand?
It depends on the mutation type occurring in proteins. For eg. some mutations make receptor proteins constitutively activated (like EGFR) thereby activating downstream signaling pathways. Even though u shut off the receptor with drug, downstream is still activated due to mutation in cytoplasmic tail. So u have to target that particular mutation using specific drugs.
Hi Rajesh,
You can consider a tumor and the surrounding tissue to be an environment suitable for accelerated natural selection to occur on a cellular level. For a cell undergoing cancerous mutations it is certainly possible for proteins to become mutated, lose function, and impair function of the cell- in this case, the surrounding tumor cells or the normal tissue are then able to "out-compete" this disadvantaged cell either through autonomous or non-autonomous means (e.g. apoptosis, immune surveillance). So when you observe the expression of a certain kind of mutated protein that is prevalent in the cancer what you are likely seeing is the surviving population of cells with some sort of advantageous genetics (whether it's delta p53, RasV12, EGFR, etc...). In other words, cancer cells are always accumulating some sort of mutations, and the mutations that ruin the cell do not allow the cell to persist for long collectively in the tumor.
In the receptor case you mentioned it just means that one part of the coding sequence for the gene was mutated and not the part that affects ligand binding.
Hope this helps,
--Ryan
it depends upon the context of cellular physiology . consequences of Oncogenic mutations are of two types gain and loss of function, it dose not mean mutated protein can not function.
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