GSE158235
KRAS K104 modification affects KRASG12D-GEF interaction and mediated cell growth and motility
Mutant RAS genes play an important role in regulating tumors through lysine residue 104 to impair GEF-induced nucleotide exchange, but the regulatory role of KRAS K104 modification on the KRASG12D mutant is not yet clear.  We found that KRASG12D/K104Q decreased the bind to RBD of Raf1 and also decreased cell growth, invasion and migration as well as whole-genome cDNA microarray found that KRASG12D/K104Q decrease the expression of NPIPA2, DUSP1 and IL6 in lung and ovarian cancer cells. This study clear implicates computational and experimental studies involving Lys104 of KRASG12D and GEF and provides a target for the analysis of future treatments. Overall design: Examination of 4 different KRASG12D mutation in  H1299 and MCAS