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1 aggerated by cotreatment of the cells with a farnesyltransferase inhibitor.
2 at is reversible by treatment with a protein farnesyltransferase inhibitor.
3 were as pronounced as those resulting from a farnesyltransferase inhibitor.
4 , and fail to accumulate when treated with a farnesyltransferase inhibitor.
5 nsformation, and sensitizes tumor cells to a farnesyltransferase inhibitor.
6 nse to growth factors, genotoxic stress, and farnesyltransferase inhibitors.
7 ed as a target for the antitumor activity of farnesyltransferase inhibitors.
8 r growth and that RhoB-F is not a target for farnesyltransferase inhibitors.
9  were abolished by CYP450, lipoxygenase, and farnesyltransferase inhibitors.
10 ibitor LY294002, the Rheb inhibitor FTI-277 (farnesyltransferase inhibitor-277), and the mTOR inhibit
11 a potential target for novel approaches (eg, farnesyltransferase inhibitors) aimed at regulating pulm
12 nyltransferase I inhibitor, GGTI-298, or the farnesyltransferase inhibitor, alpha-hydroxyfarnesylphos
13 17F, and inhibition of Ras by manumycin A, a farnesyltransferase inhibitor, ameliorated erythroid col
14 m axons; BLBP expression was not affected by farnesyltransferase inhibitor, an inhibitor of H-Ras.
15             We select lonafarnib, a licensed farnesyltransferase inhibitor, and phase III candidate f
16 e proapoptotic and antineoplastic effects of farnesyltransferase inhibitors, and we show here that Rh
17                                              Farnesyltransferase inhibitors are compounds that were d
18 r the transduction of extracellular signals, farnesyltransferase inhibitors are discussed as chemothe
19 a target for pharmaceutical development, and farnesyltransferase inhibitors are in clinical trials as
20 fort has been expended on the development of farnesyltransferase inhibitors as novel anticancer agent
21 of Ras proteins, recent studies suggest that farnesyltransferase inhibitors block the farnesylation o
22                     Inhibition of Ras by the farnesyltransferase inhibitor BZA-5B inhibited prostagla
23 EGF stimulation, and this was blocked by the farnesyltransferase inhibitor BZA-5B.
24             These results demonstrate that a farnesyltransferase inhibitor can induce regression of v
25   These results indicate that treatment with farnesyltransferase inhibitors can alter the oxygenation
26 on a farnesylated protein, as treatment with farnesyltransferase inhibitors caused apoptosis.
27           All previously reported CAAX-based farnesyltransferase inhibitors contain a thiol functiona
28                                              Farnesyltransferase inhibitors could therefore be of use
29 riments with a C-terminal-truncated Ras or a farnesyltransferase inhibitor demonstrate that the CAAX
30 ine the efficacy and safety of tipifarnib, a farnesyltransferase inhibitor, dosed at the respective m
31 nknown, the FTase substrates responsible for farnesyltransferase inhibitor efficacy are not yet under
32  trials have demonstrated that lonafarnib, a farnesyltransferase inhibitor, extends the lifespan in p
33 and growth in nude mice are inhibited by the farnesyltransferase inhibitor FTI-276 in H- and N-Ras tr
34                    Third, treatment with the farnesyltransferase inhibitor FTI-277 blocked Ras, but n
35 his study, we investigated the effect of the farnesyltransferase inhibitor FTI-277 on TGFbeta-regulat
36 ltransferase inhibitor GGTI-298, but not the farnesyltransferase inhibitor FTI-277, induced apoptosis
37                                          Ras farnesyltransferase inhibitor (FTI) exhibit antiprolifer
38                                              Farnesyltransferase inhibitor (FTI) induces apoptosis of
39                         We have investigated farnesyltransferase inhibitor (FTI) L-744,832 in an in v
40 Ras-transformed cells in the presence of the farnesyltransferase inhibitor (FTI) LB42722 leads to up-
41                          It follows that the farnesyltransferase inhibitor (FTI) lonafarnib in additi
42 1478; these responses were also abrogated by farnesyltransferase inhibitor (FTI) or PD98059, inhibito
43            R115777 (tipifarnib) is the first farnesyltransferase inhibitor (FTI) that showed clinical
44          We have used a selective and potent farnesyltransferase inhibitor (FTI) to probe a mechanism
45                                              Farnesyltransferase inhibitor (FTI) treatment with R1157
46                      Previously, the protein farnesyltransferase inhibitor (FTI), L-744, 832, has bee
47                                Exposure to a farnesyltransferase inhibitor (FTI), PD169541, caused a
48 eed, when RD fibroblasts were treated with a farnesyltransferase inhibitor (FTI), prelamin A was part
49 phenotypes can be ameliorated with a protein farnesyltransferase inhibitor (FTI), suggesting that pro
50 ell line, MDA-MB-468, by combining it with a farnesyltransferase inhibitor (FTI), which has been show
51 clei can be reduced by treating cells with a farnesyltransferase inhibitor (FTI).
52  this study, we hypothesized that the use of farnesyltransferase inhibitor (FTI, L-744,832) may direc
53 alpha-synuclein toxicity by treatment with a farnesyltransferase inhibitor (FTI-277) reduces alpha-sy
54                                              Farnesyltransferase inhibitors (FTI) are a class of ther
55                                      Protein farnesyltransferase inhibitors (FTI) mislocalize progeri
56            A phenotypic drug screen identify farnesyltransferase inhibitors (FTI) such as tipifarnib
57                                              Farnesyltransferase inhibitors (FTI), such as R115777, h
58  H-Ras activity by intra-NAc infusion of the farnesyltransferase inhibitor, FTI-276, produced a robus
59                                  The protein farnesyltransferase inhibitor, FTI-277, had no effect on
60  demonstrate that the novel antitumor agents farnesyltransferase inhibitors (FTIs) and geranylgeranyl
61                                              Farnesyltransferase inhibitors (FTIs) are a novel class
62                                              Farnesyltransferase inhibitors (FTIs) are a novel class
63                                              Farnesyltransferase inhibitors (FTIs) are in clinical tr
64                                              Farnesyltransferase inhibitors (FTIs) are in clinical tr
65                                              Farnesyltransferase inhibitors (FTIs) are small-molecule
66                                              Farnesyltransferase inhibitors (FTIs) block Ras farnesyl
67                                              Farnesyltransferase inhibitors (FTIs) exhibit the remark
68               In the clinical development of farnesyltransferase inhibitors (FTIs) for HRAS-mutant tu
69                               Treatment with farnesyltransferase inhibitors (FTIs) has been shown to
70 A series of macrocyclic 3-aminopyrrolidinone farnesyltransferase inhibitors (FTIs) has been synthesiz
71 t to mediate the antitransforming effects of farnesyltransferase inhibitors (FTIs) in H-Ras-transform
72               Despite the success of protein farnesyltransferase inhibitors (FTIs) in the treatment o
73  Pre-clinical studies have demonstrated that farnesyltransferase inhibitors (FTIs) induce growth arre
74                                      Protein farnesyltransferase inhibitors (FTIs) inhibit Ras transf
75                                              Farnesyltransferase inhibitors (FTIs) interfere with thi
76                     The clinical interest in farnesyltransferase inhibitors (FTIs) makes it important
77 investigated in more detail the influence of farnesyltransferase inhibitors (FTIs) on CD20 expression
78                                              Farnesyltransferase inhibitors (FTIs) possess antitumor
79                                              Farnesyltransferase inhibitors (FTIs) represent a new cl
80                                              Farnesyltransferase inhibitors (FTIs) represent a novel
81 fected HeLa, HEK 293, and NIH 3T3 cells with farnesyltransferase inhibitors (FTIs) restored normal nu
82             Previous studies have shown that farnesyltransferase inhibitors (FTIs) reverse this cellu
83 MS-225975 are tetrahydrobenzodiazepine-based farnesyltransferase inhibitors (FTIs) that have nearly i
84 ecent results have shown that the ability of farnesyltransferase inhibitors (FTIs) to inhibit maligna
85                                              Farnesyltransferase inhibitors (FTIs) usually cause grow
86  took only 5 years from 1993, when the first farnesyltransferase inhibitors (FTIs) were reported, to
87                                  Even though farnesyltransferase inhibitors (FTIs), a novel class of
88 icated HDAC6 as a new protein target for the farnesyltransferase inhibitors (FTIs), although HDAC6 la
89 New classes of anticancer drugs, such as the farnesyltransferase inhibitors (FTIs), show therapeutic
90 cer therapy, which led to the development of farnesyltransferase inhibitors (FTIs).
91 s no method available to predict response to farnesyltransferase inhibitors (FTIs).
92  trials of a number of independently derived farnesyltransferase inhibitors (FTIs).
93 he chemopreventive efficacy of two different farnesyltransferase inhibitors (FTIs): one is a peptidom
94 diphenyleneiodonium (DPI, 10 microm), by the farnesyltransferase inhibitor H-Ampamb-Phe-Met-OH (2 mic
95          Most unexpectedly, other classes of farnesyltransferase inhibitors had no inhibitory effect.
96                                              Farnesyltransferase inhibitors have ameliorated disease
97                                              Farnesyltransferase inhibitors have recently shown clini
98 and eIF4E and a direct therapeutic target of farnesyltransferase inhibitors in cancer.
99  inhibitor resistance and clinical trials of farnesyltransferase inhibitors in combination with other
100                                Intriguingly, farnesyltransferase inhibitors increase the binding of W
101        Together, these findings suggest that farnesyltransferase inhibitors interrupt the cytoprotect
102             The mechanism of cytotoxicity of farnesyltransferase inhibitors is incompletely understoo
103 action: see text] The total synthesis of the farnesyltransferase inhibitor kurasoin A has been achiev
104      Since we have previously shown that the farnesyltransferase inhibitor l-744, 832 inhibits cell p
105 ave previously shown that the peptidomimetic farnesyltransferase inhibitor L-744,832 (FTI) inhibits p
106   We tested the antineoplastic effect of the farnesyltransferase inhibitor L-744,832 in mammary and l
107                                          The farnesyltransferase inhibitor L-744,832 selectively bloc
108 grafts in nude mice after treatment with the farnesyltransferase inhibitor L744,832.
109 ns between the Chk1 inhibitor UCN-01 and the farnesyltransferase inhibitor L744832 were examined in h
110 ion phase I and pharmacokinetic study of the farnesyltransferase inhibitor lonafarnib (SCH66336) was
111 clinical trial demonstrated that the protein farnesyltransferase inhibitor lonafarnib ameliorates som
112  Twenty-five patients with HGPS received the farnesyltransferase inhibitor lonafarnib for a minimum o
113 re used to evaluate the effect of the potent farnesyltransferase inhibitor, manumycin, on insulin ant
114 renylation-dependent as determined using the farnesyltransferase inhibitor methyl {N-[2-phenyl-4-N [2
115                 To better understand how the farnesyltransferase inhibitors might be used in the trea
116                                          The farnesyltransferase inhibitor mislocalized progerin away
117 blasts, and we then examined the effect of a farnesyltransferase inhibitor on nuclear blebbing.
118 is migratory phenotype is not inhibited by a farnesyltransferase inhibitor or dominant-negative (dn)
119  Ras or Rac1, as well as by treatment with a farnesyltransferase inhibitor or with diphenylene iodoni
120 e phenotypes are largely rescued with either farnesyltransferase inhibitors or a farnesylation-incomp
121 ptor type II solution, 1 mM gliotoxin (a Ras farnesyltransferase inhibitor), or vehicle alone (the co
122 ase, Y361L, exhibits increased resistance to farnesyltransferase inhibitors, particularly a tricyclic
123           Here we show that FTI-277, another farnesyltransferase inhibitor, prevented the production
124 aluation of analogues of previously reported farnesyltransferase inhibitors, pyridyl benzyl ether 3 a
125 f patients with advanced MM treated with the farnesyltransferase inhibitor R115777 (Zarnestra) in a p
126 on of these events by pharmacologic (eg, the farnesyltransferase inhibitor R115777 or the MEK1/2 inhi
127                                              Farnesyltransferase inhibitors represent a new class of
128                       Preclinical studies of farnesyltransferase inhibitor resistance and clinical tr
129            Activating ykt6 by small-molecule farnesyltransferase inhibitors restores lysosomal activi
130 nesyltransferase gene ERA1 or application of farnesyltransferase inhibitors resulted in ABA hypersens
131                                          The farnesyltransferase inhibitor SCH66336 exhibits antitumo
132 s tumors with K-ras mutations implies that a farnesyltransferase inhibitor-sensitive protein other th
133 sferase, the effects of two types of protein farnesyltransferase inhibitors, several chaetomellic aci
134 ndicate that RAS-inactivating drugs, such as farnesyltransferase inhibitors should be examined in hum
135                             Treatment with a farnesyltransferase inhibitor significantly improved nuc
136 owth; dominant negative RhoB or manumycin, a farnesyltransferase inhibitor that targets the vascular
137 or farnesylation, it may be a target for the farnesyltransferase inhibitors that block Ras processing
138                       Clinical trials of two farnesyltransferase inhibitors--the tricyclic SCH66336 a
139                                              Farnesyltransferase inhibitors thus represent an attract
140                                          The farnesyltransferase inhibitor tipifarnib blocked mutant
141                                          The farnesyltransferase inhibitor tipifarnib exhibits modest
142    In this phase 2 study, we tested the oral farnesyltransferase inhibitor tipifarnib in 158 older ad
143                  A phase 2 study of the oral farnesyltransferase inhibitor tipifarnib was conducted i
144 lyzed the potential therapeutic value of the farnesyltransferase inhibitor, tipifarnib, in 25 TCL cel
145 ceptor signaling pathway with 4 courses of a farnesyltransferase inhibitor, tipifarnib.
146 ere that RhoB alteration is also crucial for farnesyltransferase inhibitors to sensitize neoplastic c
147 sible that Rheb function may be inhibited by farnesyltransferase inhibitors treatment and, consequent
148 nitril es have been synthesized as selective farnesyltransferase inhibitors using structure-based des
149 lly relevant to the long-term use of protein farnesyltransferase inhibitors, which lead to an accumul
150        Manumycin A is a potent and selective farnesyltransferase inhibitor with antitumor activity.
151 ations provided 5h, a non-thiol, non-peptide farnesyltransferase inhibitor with excellent bioavailabi
152                              Combinations of farnesyltransferase inhibitors with cytotoxic chemothera

 
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