ライフサイエンスコーパス: farnesyltransferase

1 he crystal structures that are available for farnesyltransferase.

2 may also result from its higher affinity for farnesyltransferase.

3 mine the structure of the Zn site in protein farnesyltransferase.

4 ially purified Plasmodium falciparum protein farnesyltransferase.

5 strates in the crystal structures of protein farnesyltransferase.

6 specificity compared with mammalian protein farnesyltransferase.

7 ch are good substrates for mammalian protein farnesyltransferase.

8 farnesyl group donor and is catalyzed by the farnesyltransferase.

9 is catalyzed by an enzyme that is designated farnesyltransferase.

10 Tipifarnib is an inhibitor of human protein farnesyltransferase.

11 , which encodes one of the subunits of yeast farnesyltransferase.

12 of the other Rho GTPases are substrates for farnesyltransferase.

13 This hypothesis was confirmed by converting farnesyltransferase (15-C prenyl substrate) into GGTase-

14 tetrapeptide substrate of mammalian protein farnesyltransferase, a series of imidazole-containing pe

15 e detection of protein kinase, protease, and farnesyltransferase activities is demonstrated.

16 We have previously shown that inhibition of farnesyltransferase activity results in an increase in T

17 cipitation assay revealed that inhibition of farnesyltransferase activity was associated with increas

18 Inhibition of farnesyltransferase alone was sufficient to radiosensiti

19 Host farnesyltransferase and class I geranylgeranyltransferas

20 nib analogues that no longer bind to protein farnesyltransferase and display increased potency for ki

21 n promotes phosphorylation and activation of farnesyltransferase and geranylgeranyltransferase (GGTas

22 Two prenyltransferases modify CAAX proteins: farnesyltransferase and geranylgeranyltransferase type I

23 Inhibition of farnesyltransferase and mutation or deletion of the CaaX

24 Protein farnesyltransferase and protein geranylgeranyltransferas

25 As in Arabidopsis, protein farnesyltransferase and protein geranylgeranyltransferas

26 des the alpha-subunit shared between protein farnesyltransferase and protein geranylgeranyltransferas

27 esylation, a lipid modification catalyzed by farnesyltransferase and required for the proteins to att

28 ALA1 (AP1) was identified as a substrate for farnesyltransferase and shown to be farnesylated efficie

29 pistatic to mutations in the beta-subunit of farnesyltransferase and shows a synergistic interaction

30 results demonstrate that AP1 is a target of farnesyltransferase and suggest that farnesylation alter

31 targets, such as matrix metalloproteinases, farnesyltransferase, and HIV-1 integrase, for the treatm

32 Inhibitors of G(i/o)-proteins, Ras farnesyltransferases, and MEK decreased epinephrine-indu

33 ructurally and mechanistically distinct from farnesyltransferase, another family of prenyltransferase

34 ckness (Trypanosoma brucei), and the protein farnesyltransferase appears to be a good target for deve

35 series of imidazole-containing inhibitors of farnesyltransferase are described.

36 e non-thiol-containing inhibitors of protein farnesyltransferase are described.

37 e to abscisic acid), a previously identified farnesyltransferase beta-subunit gene of Arabidopsis.

38 authors review recent laboratory insights on farnesyltransferase biology and on the development of in

39 e the thiol substrate specificity of protein farnesyltransferase by demonstrating that a variety of n

40 nylgeranyltransferase I by GGTi-298, but not farnesyltransferase by FTi-277, induced significant cell

41 led catalytic mechanism of mammalian protein farnesyltransferase by measuring the effect of metal sub

42 Protein farnesyltransferase catalyzes the lipid modification of

43 Protein farnesyltransferase catalyzes the modification of protei

44 Protein farnesyltransferase catalyzes the posttranslational farn

45 Analysis of a mutant of protein farnesyltransferase containing a Tyr-to-Leu substitution

46 revealed low heme aa3 compatible with heme A:farnesyltransferase deficiency due to COX10 dysfunction.

47 e analyzed in guard cells of the Arabidopsis farnesyltransferase deletion mutant era1-2 (enhanced res

48 tibody therapy; inhibitors of FLT3, KIT, and farnesyltransferase; diphtheria toxin conjugated to the

49 a key component of complex IV, protohaem IX farnesyltransferase encoded by the COX10 gene, in granul

50 al, serial measurements provided evidence of farnesyltransferase enzyme inhibition, interference with

51 A and HETEs was reduced by inhibitors of Ras farnesyltransferase (farnesyl protein transferase III an

52 Repression of farnesyltransferase (FNTA) by siRNA and the enzyme inhib

53 P. falciparum: a limited specificity of the farnesyltransferase for peptide substrates compared with

54 tance of the two protein prenyltransferases, farnesyltransferase (FT) and geranylgeranyltransferase-1

55 lar pharmacological profiles associated with farnesyltransferase (FT) inhibition.

56 ro-1-(imidazol-4-ylalkyl)-1,4-benzodiazepine farnesyltransferase (FT) inhibitors.

57 atabase to identify prototypic inhibitors of farnesyltransferase (FT) with zinc present in the active

58 epines were found to be potent inhibitors of farnesyltransferase (FT).

59 xpression (2-fold), accompanied by increased farnesyltransferase (FTase) and Erk activities.

60 trate-1 (IRS-1) and Shc in insulin action on farnesyltransferase (FTase) and geranylgeranyltransferas

61 zyme that shares a common alpha-subunit with farnesyltransferase (FTase) and has a distinct beta-subu

62 Here we show that the protein farnesyltransferase (FTase) and HDAC6 are present in a p

63 AGPP is a substrate for protein farnesyltransferase (FTase) and is transferred to Ras by

64 Protein farnesyltransferase (FTase) and protein geranylgeranyltr

65 Protein farnesyltransferase (FTase) and protein geranylgeranyltr

66 Unlike protein farnesyltransferase (FTase) and protein geranylgeranyltr

67 ed as very potent dual inhibitors of protein farnesyltransferase (FTase) and protein geranylgeranyltr

68 Protein farnesyltransferase (FTase) and protein geranylgeranyltr

69 out by a pair of cytosolic enzymes, protein farnesyltransferase (FTase) and protein geranylgeranyltr

70 n motif for two prenylation enzymes, protein farnesyltransferase (FTase) and protein geranylgeranyltr

71 out by the CaaX prenyltransferases, protein farnesyltransferase (FTase) and protein geranylgeranyltr

72 oven to be both potent inhibitors of protein-farnesyltransferase (FTase) and valuable probes for the

73 ing the unknown Mg2+ binding site in protein farnesyltransferase (FTase) are reported.

74 humans, GGTase-I and the homologous protein farnesyltransferase (FTase) are targets of anticancer th

75 w cancer therapeutics has identified protein farnesyltransferase (FTase) as a promising drug target.

76 Protein farnesyltransferase (FTase) catalyses the attachment of

77 Protein farnesyltransferase (FTase) catalyzes farnesylation of a

78 Protein farnesyltransferase (FTase) catalyzes post-translational

79 Protein farnesyltransferase (FTase) catalyzes the addition of a

80 Protein farnesyltransferase (FTase) catalyzes the attachment of

81 Protein farnesyltransferase (FTase) catalyzes the biologically r

82 Protein farnesyltransferase (FTase) catalyzes the post-translati

83 The zinc metalloenzyme protein farnesyltransferase (FTase) catalyzes the transfer of a

84 Farnesyltransferase (FTase) catalyzes the transfer of fa

85 We have previously shown that burn increases farnesyltransferase (FTase) expression and protein farne

86 al-Ile-Met tetrapeptide substrate of protein farnesyltransferase (FTase) have been designed and synth

87 Studies of the yeast protein farnesyltransferase (FTase) have shown that the enzyme p

88 The farnesyltransferase (FTase) inhibitor FTI-2148 induced a

89 ed on the Sebti-Hamilton type peptidomimetic farnesyltransferase (FTase) inhibitor FTI-276 (1) led to

90 aluated the activity and tolerability of the farnesyltransferase (FTase) inhibitor tipifarnib (Zarnes

91 R115777 is a potent farnesyltransferase (FTase) inhibitor with substantial a

92 Farnesyltransferase (FTase) inhibitors (FTI) have broad

93 volved, two structurally distinct classes of farnesyltransferase (FTase) inhibitors (the monoterpenes

94 Protein farnesyltransferase (FTase) is a key enzyme responsible

95 ene silencing or pharmacologic inhibition of farnesyltransferase (FTase) or ERK caused reduction of I

96 id (a process termed prenylation) by protein farnesyltransferase (FTase) or geranylgeranyltransferase

97 C terminus of a substrate protein by protein farnesyltransferase (FTase) or protein geranylgeranyltra

98 ent of an isoprenoid lipid by either protein farnesyltransferase (FTase) or protein geranylgeranyltra

99 alent attachment of a lipid group by protein farnesyltransferase (FTase) or protein geranylgeranyltra

100 Protein farnesyltransferase (FTase) plays important roles in the

101 Protein farnesyltransferase (FTase) requires both Zn(2+) and Mg(

102 Ras proteins are modified by farnesyltransferase (FTase), but many related small GTPa

103 the potential anticancer drug target protein farnesyltransferase (FTase), but these compounds are not

104 s a selective nonpeptidomimetic inhibitor of farnesyltransferase (FTase), one of several enzymes resp

105 of novel CA(1)A(2)X-based inhibitors of Ras farnesyltransferase (FTase), the conformationally constr

106 Protein farnesyltransferase (FTase), the enzyme responsible for

107 med at elucidating the reaction mechanism of farnesyltransferase (FTase), which catalyzes the prenyla

108 ctures of compounds 49 and 66 complexed with farnesyltransferase (FTase)-farnesyl diphosphate (FPP) w

109 of the outer kinetochore that is modified by farnesyltransferase (FTase).

110 proteins in a reaction catalyzed by protein farnesyltransferase (FTase).

111 te (FPP) to proteins is catalyzed by protein farnesyltransferase (FTase).

112 proteins in a reaction catalyzed by protein farnesyltransferase (FTase).

113 Prenylation presumably occurs by farnesyltransferase (FTase).

114 of the gene for the beta subunit (AtFTB) of farnesyltransferase (FTase).

115 n a reaction catalyzed by the enzyme protein farnesyltransferase (FTase).

116 n requires posttranslational modification by farnesyltransferase (FTase).

117 protein substrates, is catalyzed by protein farnesyltransferase (FTase).

118 14662 is a potent and selective inhibitor of farnesyltransferase (FTI).

119 ly blocked by a pharmacological inhibitor of farnesyltransferase (FTI).

120 sferase enzyme inhibition, interference with farnesyltransferase function ( ie, protein processing),

121 kinesin, insulin receptor, tyrosine kinases, farnesyltransferase, gyrase, prions, triosephosphate iso

122 A potent class of anticancer, human farnesyltransferase (hFTase) inhibitors has been identif

123 cture of one of these analogues bound to rat farnesyltransferase illustrates that they are good subst

124 main alone increases the affinity of Ras for farnesyltransferase, implying independent roles for each

125 ation of HDJ-2, nor did they inhibit protein farnesyltransferase in vitro.

126 to evaluate the therapeutic effectiveness of farnesyltransferase inhibition (FTI).

127 The finding that farnesyltransferase inhibition alone radiosensitizes tum

128 Farnesyltransferase inhibition was noted at all tipifarn

129 lar concentrations and are devoid of protein farnesyltransferase inhibition were discovered.

130 eformations and invaginations preventable by farnesyltransferase inhibition.

131 Ras farnesyltransferase inhibitor (FTI) exhibit antiprolifer

132 Farnesyltransferase inhibitor (FTI) induces apoptosis of

133 We have investigated farnesyltransferase inhibitor (FTI) L-744,832 in an in v

134 Ras-transformed cells in the presence of the farnesyltransferase inhibitor (FTI) LB42722 leads to up-

135 1478; these responses were also abrogated by farnesyltransferase inhibitor (FTI) or PD98059, inhibito

136 R115777 (tipifarnib) is the first farnesyltransferase inhibitor (FTI) that showed clinical

137 We have used a selective and potent farnesyltransferase inhibitor (FTI) to probe a mechanism

138 Farnesyltransferase inhibitor (FTI) treatment with R1157

139 Previously, the protein farnesyltransferase inhibitor (FTI), L-744, 832, has bee

140 Exposure to a farnesyltransferase inhibitor (FTI), PD169541, caused a

141 eed, when RD fibroblasts were treated with a farnesyltransferase inhibitor (FTI), prelamin A was part

142 phenotypes can be ameliorated with a protein farnesyltransferase inhibitor (FTI), suggesting that pro

143 ell line, MDA-MB-468, by combining it with a farnesyltransferase inhibitor (FTI), which has been show

144 clei can be reduced by treating cells with a farnesyltransferase inhibitor (FTI).

145 this study, we hypothesized that the use of farnesyltransferase inhibitor (FTI, L-744,832) may direc

146 alpha-synuclein toxicity by treatment with a farnesyltransferase inhibitor (FTI-277) reduces alpha-sy

147 These results demonstrate that a farnesyltransferase inhibitor can induce regression of v

148 riments with a C-terminal-truncated Ras or a farnesyltransferase inhibitor demonstrate that the CAAX

149 nknown, the FTase substrates responsible for farnesyltransferase inhibitor efficacy are not yet under

150 his study, we investigated the effect of the farnesyltransferase inhibitor FTI-277 on TGFbeta-regulat

151 ltransferase inhibitor GGTI-298, but not the farnesyltransferase inhibitor FTI-277, induced apoptosis

152 diphenyleneiodonium (DPI, 10 microm), by the farnesyltransferase inhibitor H-Ampamb-Phe-Met-OH (2 mic

153 action: see text] The total synthesis of the farnesyltransferase inhibitor kurasoin A has been achiev

154 Since we have previously shown that the farnesyltransferase inhibitor l-744, 832 inhibits cell p

155 ave previously shown that the peptidomimetic farnesyltransferase inhibitor L-744,832 (FTI) inhibits p

156 grafts in nude mice after treatment with the farnesyltransferase inhibitor L744,832.

157 ns between the Chk1 inhibitor UCN-01 and the farnesyltransferase inhibitor L744832 were examined in h

158 ion phase I and pharmacokinetic study of the farnesyltransferase inhibitor lonafarnib (SCH66336) was

159 clinical trial demonstrated that the protein farnesyltransferase inhibitor lonafarnib ameliorates som

160 Twenty-five patients with HGPS received the farnesyltransferase inhibitor lonafarnib for a minimum o

161 renylation-dependent as determined using the farnesyltransferase inhibitor methyl {N-[2-phenyl-4-N [2

162 The farnesyltransferase inhibitor mislocalized progerin away

163 blasts, and we then examined the effect of a farnesyltransferase inhibitor on nuclear blebbing.

164 is migratory phenotype is not inhibited by a farnesyltransferase inhibitor or dominant-negative (dn)

165 f patients with advanced MM treated with the farnesyltransferase inhibitor R115777 (Zarnestra) in a p

166 on of these events by pharmacologic (eg, the farnesyltransferase inhibitor R115777 or the MEK1/2 inhi

167 Preclinical studies of farnesyltransferase inhibitor resistance and clinical tr

168 The farnesyltransferase inhibitor SCH66336 exhibits antitumo

169 Treatment with a farnesyltransferase inhibitor significantly improved nuc

170 owth; dominant negative RhoB or manumycin, a farnesyltransferase inhibitor that targets the vascular

171 The farnesyltransferase inhibitor tipifarnib exhibits modest

172 In this phase 2 study, we tested the oral farnesyltransferase inhibitor tipifarnib in 158 older ad

173 A phase 2 study of the oral farnesyltransferase inhibitor tipifarnib was conducted i

174 Manumycin A is a potent and selective farnesyltransferase inhibitor with antitumor activity.

175 ations provided 5h, a non-thiol, non-peptide farnesyltransferase inhibitor with excellent bioavailabi

176 ptor type II solution, 1 mM gliotoxin (a Ras farnesyltransferase inhibitor), or vehicle alone (the co

177 nyltransferase I inhibitor, GGTI-298, or the farnesyltransferase inhibitor, alpha-hydroxyfarnesylphos

178 17F, and inhibition of Ras by manumycin A, a farnesyltransferase inhibitor, ameliorated erythroid col

179 m axons; BLBP expression was not affected by farnesyltransferase inhibitor, an inhibitor of H-Ras.

180 ine the efficacy and safety of tipifarnib, a farnesyltransferase inhibitor, dosed at the respective m

181 H-Ras activity by intra-NAc infusion of the farnesyltransferase inhibitor, FTI-276, produced a robus

182 The protein farnesyltransferase inhibitor, FTI-277, had no effect on

183 re used to evaluate the effect of the potent farnesyltransferase inhibitor, manumycin, on insulin ant

184 Here we show that FTI-277, another farnesyltransferase inhibitor, prevented the production

185 ceptor signaling pathway with 4 courses of a farnesyltransferase inhibitor, tipifarnib.

186 ibitor LY294002, the Rheb inhibitor FTI-277 (farnesyltransferase inhibitor-277), and the mTOR inhibit

187 s tumors with K-ras mutations implies that a farnesyltransferase inhibitor-sensitive protein other th

188 , and fail to accumulate when treated with a farnesyltransferase inhibitor.

189 nsformation, and sensitizes tumor cells to a farnesyltransferase inhibitor.

190 aggerated by cotreatment of the cells with a farnesyltransferase inhibitor.

191 were as pronounced as those resulting from a farnesyltransferase inhibitor.

192 Farnesyltransferase inhibitors (FTI) are a class of ther

193 Protein farnesyltransferase inhibitors (FTI) mislocalize progeri

194 Farnesyltransferase inhibitors (FTI), such as R115777, h

195 demonstrate that the novel antitumor agents farnesyltransferase inhibitors (FTIs) and geranylgeranyl

196 Farnesyltransferase inhibitors (FTIs) are a novel class

197 Farnesyltransferase inhibitors (FTIs) are in clinical tr

198 Farnesyltransferase inhibitors (FTIs) are in clinical tr

199 Farnesyltransferase inhibitors (FTIs) are small-molecule

200 Farnesyltransferase inhibitors (FTIs) block Ras farnesyl

201 Farnesyltransferase inhibitors (FTIs) exhibit the remark

202 Treatment with farnesyltransferase inhibitors (FTIs) has been shown to

203 A series of macrocyclic 3-aminopyrrolidinone farnesyltransferase inhibitors (FTIs) has been synthesiz

204 t to mediate the antitransforming effects of farnesyltransferase inhibitors (FTIs) in H-Ras-transform

205 Despite the success of protein farnesyltransferase inhibitors (FTIs) in the treatment o

206 Pre-clinical studies have demonstrated that farnesyltransferase inhibitors (FTIs) induce growth arre

207 Farnesyltransferase inhibitors (FTIs) interfere with thi

208 The clinical interest in farnesyltransferase inhibitors (FTIs) makes it important

209 investigated in more detail the influence of farnesyltransferase inhibitors (FTIs) on CD20 expression

210 Farnesyltransferase inhibitors (FTIs) possess antitumor

211 Farnesyltransferase inhibitors (FTIs) represent a novel

212 fected HeLa, HEK 293, and NIH 3T3 cells with farnesyltransferase inhibitors (FTIs) restored normal nu

213 Previous studies have shown that farnesyltransferase inhibitors (FTIs) reverse this cellu

214 MS-225975 are tetrahydrobenzodiazepine-based farnesyltransferase inhibitors (FTIs) that have nearly i

215 ecent results have shown that the ability of farnesyltransferase inhibitors (FTIs) to inhibit maligna

216 Farnesyltransferase inhibitors (FTIs) usually cause grow

217 took only 5 years from 1993, when the first farnesyltransferase inhibitors (FTIs) were reported, to

218 Even though farnesyltransferase inhibitors (FTIs), a novel class of

219 icated HDAC6 as a new protein target for the farnesyltransferase inhibitors (FTIs), although HDAC6 la

220 New classes of anticancer drugs, such as the farnesyltransferase inhibitors (FTIs), show therapeutic

221 trials of a number of independently derived farnesyltransferase inhibitors (FTIs).

222 s no method available to predict response to farnesyltransferase inhibitors (FTIs).

223 he chemopreventive efficacy of two different farnesyltransferase inhibitors (FTIs): one is a peptidom

224 Farnesyltransferase inhibitors are compounds that were d

225 r the transduction of extracellular signals, farnesyltransferase inhibitors are discussed as chemothe

226 a target for pharmaceutical development, and farnesyltransferase inhibitors are in clinical trials as

227 fort has been expended on the development of farnesyltransferase inhibitors as novel anticancer agent

228 of Ras proteins, recent studies suggest that farnesyltransferase inhibitors block the farnesylation o

229 These results indicate that treatment with farnesyltransferase inhibitors can alter the oxygenation

230 on a farnesylated protein, as treatment with farnesyltransferase inhibitors caused apoptosis.

231 Farnesyltransferase inhibitors could therefore be of use

232 Most unexpectedly, other classes of farnesyltransferase inhibitors had no inhibitory effect.

233 Farnesyltransferase inhibitors have ameliorated disease

234 Farnesyltransferase inhibitors have recently shown clini

235 and eIF4E and a direct therapeutic target of farnesyltransferase inhibitors in cancer.

236 inhibitor resistance and clinical trials of farnesyltransferase inhibitors in combination with other

237 Intriguingly, farnesyltransferase inhibitors increase the binding of W

238 Together, these findings suggest that farnesyltransferase inhibitors interrupt the cytoprotect

239 The mechanism of cytotoxicity of farnesyltransferase inhibitors is incompletely understoo

240 e phenotypes are largely rescued with either farnesyltransferase inhibitors or a farnesylation-incomp

241 Farnesyltransferase inhibitors represent a new class of

242 ndicate that RAS-inactivating drugs, such as farnesyltransferase inhibitors should be examined in hum

243 Farnesyltransferase inhibitors thus represent an attract

244 ere that RhoB alteration is also crucial for farnesyltransferase inhibitors to sensitize neoplastic c

245 nitril es have been synthesized as selective farnesyltransferase inhibitors using structure-based des

246 Combinations of farnesyltransferase inhibitors with cytotoxic chemothera

247 a potential target for novel approaches (eg, farnesyltransferase inhibitors) aimed at regulating pulm

248 e proapoptotic and antineoplastic effects of farnesyltransferase inhibitors, and we show here that Rh

249 ase, Y361L, exhibits increased resistance to farnesyltransferase inhibitors, particularly a tricyclic

250 aluation of analogues of previously reported farnesyltransferase inhibitors, pyridyl benzyl ether 3 a

251 sferase, the effects of two types of protein farnesyltransferase inhibitors, several chaetomellic aci

252 lly relevant to the long-term use of protein farnesyltransferase inhibitors, which lead to an accumul

253 Clinical trials of two farnesyltransferase inhibitors--the tricyclic SCH66336 a

254 nse to growth factors, genotoxic stress, and farnesyltransferase inhibitors.

255 ed as a target for the antitumor activity of farnesyltransferase inhibitors.

256 r growth and that RhoB-F is not a target for farnesyltransferase inhibitors.

257 ould be abolished by BZA-5B, a compound with farnesyltransferase inhibitory activity.

258 COX10 is a farnesyltransferase involved in the biosynthesis of heme

259 quence that is a known substrate for protein farnesyltransferase; irradiation of the NDBF-caged pepti

260 Protein farnesyltransferase is a zinc metalloenzyme that catalyz

261 ause post-translational processing of Ras by farnesyltransferase is essential for biologic function,

262 Because posttranslational processing by farnesyltransferase is essential for transformation by o

263 rrogate tissues that allow confirmation that farnesyltransferase is inhibited in vivo at clinically a

264 ylgeranylated K-Ras, which is generated when farnesyltransferase is inhibited.

265 es have been shown to reside in the cytosol (farnesyltransferase), or are ER membrane proteins (Zmpst

266 malarial inhibitors of Plasmodium falciparum farnesyltransferase (PfFTase).

267 Here we show that the enzyme protein farnesyltransferase (PFT) from the malaria parasite Plas

268 The protein farnesyltransferase (PFT) inhibitor tipifarnib, now in p

269 e report a new class of antimalarial protein farnesyltransferase (PFT) inhibitors, designed with spec

270 Inhibition of protein farnesyltransferase (PFT) is lethal to the pathogenic pr

271 e, which encodes the beta-subunit of protein farnesyltransferase (PFT), exhibit pleiotropic effects t

272 nib (R115777), an inhibitor of human protein farnesyltransferase (PFT), is shown to be a highly poten

273 ethylenediamine-based inhibitors of protein farnesyltransferase (PFT).

274 anylgeranyltransferase I (PGGT-I) or protein farnesyltransferase (PFT).

275 dentified as inhibitors of mammalian protein farnesyltransferase (PFT).

276 off-target inhibition of the enzyme protein farnesyltransferase (PFTase) by commercially available d

277 Protein farnesyltransferase (PFTase) is a zinc metalloenzyme tha

278 Protein farnesyltransferase (PFTase) is a zinc-containing metall

279 d the high specificity of the enzyme protein farnesyltransferase (PFTase) to site-specifically modify

280 se-I over the closely related enzyme protein farnesyltransferase (PFTase).

281 ion into a peptide via the action of protein farnesyltransferase (PFTase).

282 Remarkably, the protein farnesyltransferase, RCE-1 (Ras-converting enzyme-1), an

283 are targets for pharmacologic inhibitors of farnesyltransferase, Rce1, and Icmt.

284 nant proteins have a C-terminal CVIX protein farnesyltransferase recognition motif that allows us to

285 ; in the absence of mevinolin, inhibition of farnesyltransferase reduced ERK phosphorylation and bloc

286 A deletion of cox10, the gene for the farnesyltransferase required for heme A synthesis, did n

287 cient product formation catalyzed by protein farnesyltransferase requires an enzyme-bound zinc cation

288 sible that the critical target downstream of farnesyltransferase responsible for these effects is not

289 there was a complex relationship among FTIs, farnesyltransferase, ROS, and RhoB.

290 These data indicate that the ERA1 farnesyltransferase targets a negative regulator of ABA

291 lpha- and beta-subunits of T. brucei protein farnesyltransferase (TB-PFT) using nucleic acid probes d

292 Compared with mammalian protein farnesyltransferases, TB-PFT contains a number of insert

293 activity against Trypanosoma brucei protein farnesyltransferase (TbPFT) was evaluated.

294 ng a C-terminal CAAX motif are prenylated by farnesyltransferase to facilitate localization to cellul

295 s of these snoRNAs also increased binding by farnesyltransferase to K-Ras and increased K-Ras prenyla

296 -ras had markedly improved oxygenation after farnesyltransferase treatment.

297 on of the Y361L variant of mammalian protein farnesyltransferase was performed.

298 the cyoE gene, which encodes a protoheme IX farnesyltransferase, was identified.

299 ening effort against the drug target protein farnesyltransferase, we identified a series of disubstit

300 uppressing expression of the beta-subunit of farnesyltransferase with siRNA did not induce ROS, but s