期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 27, 期 22, 页码 7765-7770出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.00965-07
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资金
- NCI NIH HHS [R37 CA72614, R37 CA072614, R01 CA104282] Funding Source: Medline
Germ line missense mutations in HRAS and KRAS and in genes encoding molecules that function up- or downstream of Ras in cellular signaling networks cause a group of related developmental disorders that includes Costello syndrome, Noonan syndrome, and cardiofaciocutaneous syndrome. We performed detailed biochemical and functional studies of three mutant K-Ras proteins (P34R, D153V, and F156L) found in individuals with Noonan syndrome and cardiofaciocutaneous syndrome. Mutant K-Ras proteins demonstrate a range of gain-of-function effects in different cell types, and biochemical analysis supports the idea that the intrinsic Ras guanosine nucleotide triphosphatase (GTPase) activity, the responsiveness of these proteins to GTPase-activating proteins, and guanine nucleotide dissociation all regulate developmental programs in vivo.
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