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1 sm, may be linked to one another and require protein farnesylation.
2 al evidence indicates that AIPL1 can enhance protein farnesylation.
3 tly acted through a mechanism independent of protein farnesylation.
4 be made to probe the biological function of protein farnesylation.
6 m clinical trials administered inhibitors of protein farnesylation aimed at reducing toxicity of the
9 GGTI-298 or lovastatin, which inhibits both protein farnesylation and geranylgeranylation, arrested
10 FTI-277 and GGTI-298) that selectively block protein farnesylation and geranylgeranylation, respectiv
11 se 2 trial as well as its ability to inhibit protein farnesylation and oncogenic pathways in patients
12 nsferase inhibitors (FTIs) selectively block protein farnesylation and reduce the growth of many Ras-
13 s farnesyltransferase (FTase) expression and protein farnesylation and that FTase inhibitor (FTI) pre
14 requires protein geranylgeranylation but not protein farnesylation and that the tyrosine phosphorylat
16 nhibits both protein geranylgeranylation and protein farnesylation, blocked PDGF receptor tyrosine ph
18 y intermediate in the mevalonate pathway and protein farnesylation, can act as an agonist for several
19 esis and suggest that specific inhibition of protein farnesylation could be a potential strategy for
20 ads to a G0/G1 arrest, whereas inhibition of protein farnesylation does not affect cell cycle distrib
22 st, treatment of cells with the inhibitor of protein farnesylation, FTI-277 (10 microM), blocked IL-1
24 nsferase (FTase), the enzyme responsible for protein farnesylation, has become a key target for the r
27 ngs provide the first evidence of a role for protein farnesylation in glucose-mediated regulation of
29 data support the concept that inhibition of protein farnesylation in progeria could be therapeutical
33 mparisons estimating increased survival with protein farnesylation inhibitors provide the first evide
40 farnesol (FOL) with lovastatin, to stimulate protein farnesylation, prevented lovastatin-induced cell
43 had only a modest influence whereas blocking protein farnesylation with manumycin severely disrupted
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