BRAF is an effector of the Mapk signaling cascade, and incurs a point mutation on nucleotide 1799, which results in a valine to glutamate substitution at residue 600. This mutated form of the BRAF gene has been found to disrupt the hydrophobic interactions in between the activation loop and the ATP binding site, which results in a constitutive expression of MEK, and ultimately transcription factors that perpetuate cellular differentiation, cellular proliferation, and cellular survival7. Research has determined that these mutations involving either the RET/PTC and BRAF mutation do not generally overlap, and that a functional BRAF gene is needed to see the oncogenic effects of the RET/PTC
BRAF is an effector of the Mapk signaling cascade, and incurs a point mutation on nucleotide 1799, which results in a valine to glutamate substitution at residue 600. This mutated form of the BRAF gene has been found to disrupt the hydrophobic interactions in between the activation loop and the ATP binding site, which results in a constitutive expression of MEK, and ultimately transcription factors that perpetuate cellular differentiation, cellular proliferation, and cellular survival7. Research has determined that these mutations involving either the RET/PTC and BRAF mutation do not generally overlap, and that a functional BRAF gene is needed to see the oncogenic effects of the RET/PTC