ライフサイエンスコーパス: farnesylation

1 CAAX motif (the carboxyl-terminal signal for farnesylation).

2 ion and, unlike normal A-type lamins, stable farnesylation.

3 induce invasion and motility is dependent on farnesylation.

4 be linked to one another and require protein farnesylation.

5 otein transferase (FTase) activity and HDJ-2 farnesylation.

6 ein tyrosine phosphatases (PTPs) modified by farnesylation.

7 get oncogenic Ras proteins by inhibiting Ras farnesylation.

8 nce indicates that AIPL1 can enhance protein farnesylation.

9 unction of its CTD and more specifically its farnesylation.

10 d through a mechanism independent of protein farnesylation.

11 hereby inhibits both geranylgeranylation and farnesylation.

12 tases, which are characterized by C-terminal farnesylation.

13 form of SpRheb (SpRheb-CVIL) that can bypass farnesylation.

14 han those required for the inhibition of Ras farnesylation.

15 e, with its partners was largely mediated by farnesylation.

16 to probe the biological function of protein farnesylation.

17 to a previous report, this does not require farnesylation.

18 f inhibiting geranylgeranylation relative to farnesylation.

19 mpounds have been developed that can inhibit farnesylation.

20 ion of lamin A, Delta50 lamin A, retains its farnesylation.

21 n the post-translational modification termed farnesylation.

22 hored into the LCV membrane by host-mediated farnesylation.

23 rine substitution that was used to eliminate farnesylation.

24 myristylation signal can substitute for the farnesylation.

25 While 3-allylfarnesol inhibits protein farnesylation, 3-vinylfarnesol instead leads to abnormal

26 GTPases are post-translationally modified by farnesylation, a lipid modification catalyzed by farnesy

27 Ras is a major contributor to human cancer, farnesylation, a lipid posttranslational modification re

28 e p21ras family, undergoes posttranslational farnesylation, a modification required for their partiti

29 nal modifications including CaaX processing (farnesylation, aaX cleavage and carboxylmethylation), fo

30 al trials administered inhibitors of protein farnesylation aimed at reducing toxicity of the disease-

31 sidues and are not well described by current farnesylation algorithms.

32 rget of farnesyltransferase and suggest that farnesylation alters the function and perhaps specificit

33 st, hind-limb ischemia failed to induce Rac1 farnesylation and activation as well as angiogenic respo

34 Hind-limb ischemia induced Rac1 farnesylation and activation leading to increased angiog

35 l-specific inhibitor BZA-5B that inhibit the farnesylation and Ag-induced activation of Ras species i

36 hed extracellular bacteria followed by rapid farnesylation and anchoring of AnkB to the cytosolic sid

37 Farnesylation and carboxymethylation of KRAS4b (Kirsten

38 nstrate that this deletion leads to a stable farnesylation and carboxymethylation of the mutant LA (L

39 The FTI SCH66336 blocks HRAS farnesylation and delocalizes it from the plasma membran

40 f the post-translational lipid modifications farnesylation and geranylgeranylation in protein localiz

41 ds currently available which can distinguish farnesylation and geranylgeranylation modification in a

42 tin, a cholesterol-lowering drug that blocks farnesylation and geranylgeranylation of target proteins

43 These results document that farnesylation and geranylgeranylation play differential

44 Prenylation of protein (farnesylation and geranylgeranylation) is involved in se

45 Statins simultaneously inhibit farnesylation and geranylgeranylation, and in consequenc

46 These effects were independent of farnesylation and indicate that modulation of FPP levels

47 his asymmetric distribution depended on Ydj1 farnesylation and intact diffusion barriers.

48 reover, Rheb activity toward mTORC1 requires farnesylation and is readily blocked by a pharmacologica

49 e propose a model where coordination of LKB1 farnesylation and kinase activity serve as a multi-step

50 the truncated PKR to RAS sequences mediating farnesylation and membrane localization and found that t

51 Furthermore, we discovered that farnesylation and membrane localization of Rheb is not e

52 Mevalonate rescued 15(S)-HETE-induced Rac1 farnesylation and membrane translocation in HDMVECs and

53 MG-CoA reductase expression caused increased farnesylation and membrane translocation of Rac1 where i

54 ubunit was observed for both proteins as was farnesylation and methylation of the terminal Gtgamma su

55 al as well as its ability to inhibit protein farnesylation and oncogenic pathways in patients with re

56 nduce disease stabilization, and can inhibit farnesylation and oncogenic/tumor survival pathways.

57 terminus which would allow posttranslational farnesylation and palmitoylation, lipid modifications no

58 inhibitors (FTIs) selectively block protein farnesylation and reduce the growth of many Ras-transfor

59 yltransferase (FTase) expression and protein farnesylation and that FTase inhibitor (FTI) prevents bu

60 vides a link between protein modification by farnesylation and the control of meristem size.

61 nocyte-derived macrophages (hMDMs), the host farnesylation and ubiquitination machineries are recruit

62 d by inhibiting both geranylgeranylation and farnesylation, and not by altering expression of key upt

63 fects of the mutant Ras, an inhibitor of Ras farnesylation, and the MEK inhibitor on ouabain-induced

64 onstrated that Pk1b nuclear localization and farnesylation are required during FBMN migration.

65 xperiments show that both Spindly and CENP-E farnesylation are required for efficient chromosome cong

66 Our study identifies protein farnesylation as a potential hub of the signaling networ

67 Farnesylation as measured by HDJ2 analysis was inhibited

68 The complementation is dependent on farnesylation, as the farnesylation-defective SpRheb-SVI

69 G-CoA reductase inhibitors act through a Ras farnesylation-associated mechanism to induce signaling p

70 main of hSpindly and discovered it undergoes farnesylation at the C-terminal cysteine residue.

71 ogerin, retains the CAAX motif that triggers farnesylation, but the 50-aa deletion prevents the subse

72 se data suggest that FTase catalyzes protein farnesylation by an associative mechanism with an "explo

73 ation by GGTI-298, but not via inhibition of farnesylation by FTI-277, enhanced the proapoptotic effe

74 ivated protein kinase kinase by PD98059, Ras farnesylation by PD152440 and B581, p70(S6K) by rapamyci

75 ediate in the mevalonate pathway and protein farnesylation, can act as an agonist for several nuclear

76 beta 352 removes the magnesium activation of farnesylation catalyzed by FTase but does not significan

77 Magnesium ions enhance farnesylation catalyzed by FTase by several hundred-fold

78 s, by decreasing the catalytic efficiency of farnesylation catalyzed by FTase to a level comparable t

79 The farnesylation consensus is conserved in PpPex19p but dis

80 suggest that specific inhibition of protein farnesylation could be a potential strategy for effectiv

81 A farnesylation-defective mutant of Rheb co-immunoprecipit

82 ortant for its biological activity because a farnesylation-defective mutant of Rheb stimulated S6K1 a

83 In contrast, a farnesylation-defective mutant of SpRheb (SpRheb-SVIA) i

84 In contrast, a farnesylation-defective mutant, V12S186Ras (cysteine 186

85 tation is dependent on farnesylation, as the farnesylation-defective SpRheb-SVIA mutant is incapable

86 related to BicD2 and binds RZZ directly in a farnesylation-dependent but membrane-independent manner.

87 iated with KRAS4B on cellular membranes in a farnesylation-dependent fashion, and retention of GPR31

88 e Ras homolog enriched in brain (Rheb), in a farnesylation-dependent manner.

89 localized to the endoplasmic reticulum in a farnesylation-dependent manner.

90 We conclude that farnesylation-dependent nuclear localization of Pk1b is

91 y protein prenylation, because inhibition of farnesylation did not alter fatty acid synthesis in meva

92 Inhibition of farnesylation did not correlate with disease stabilizati

93 y induced KLF2 levels, whereas inhibition of farnesylation did not.

94 ons compared with clonal cell lines and that farnesylation does not account for the membrane associat

95 d by fusing with a strong membrane-targeting farnesylation domain, apoptosis is blocked.

96 lamin B1 is posttranslationally modified by farnesylation, endoproteolysis, and carboxymethylation a

97 with a C-terminal CaaX motif that undergoes farnesylation, endoproteolytic cleavage, and carboxylmet

98 by four post-translational processing steps: farnesylation, endoproteolytic release of the last three

99 Loading RASFs with FPP to promote farnesylation enhanced MMP-1 secretion.

100 nyl cysteine carboxyl methyltransferase host farnesylation enzymes are recruited to the LCV in a Dot/

101 charomyces pombe mutant, cpp1-, defective in farnesylation, exhibits distinct phenotypes, including m

102 s increased, so too was the extent of HDAg-L farnesylation for all three genotypes.

103 To assess the importance of protein farnesylation for B-type lamins, we created knock-in mic

104 GFP-Cdc42hs was not affected by substituting farnesylation for geranylgeranylation.

105 n considerable detail, but the importance of farnesylation for the B-type lamins, lamin B1 and lamin

106 olvement of regulatory proteins that require farnesylation for their function.

107 determines whether peptides are specific for farnesylation, geranylgeranylation, or dual prenylation.

108 In Arabidopsis thaliana, protein farnesylation has been shown to be necessary for negativ

109 Farnesylation has received significant interest as a tar

110 (FTase), the enzyme responsible for protein farnesylation, has become a key target for the rational

111 Inhibition of protein farnesylation improves the hallmark nuclear shape abnorm

112 requires the posttranslation modification of farnesylation in a reaction catalyzed by farnesyl protei

113 Inhibition of prelamin A farnesylation in buccal mucosa cells of patients treated

114 tors, and these compounds also block protein farnesylation in cultured parasites.

115 approaches were used to determine roles for farnesylation in glucose-mediated activation of ERK1/2,

116 ide the first evidence of a role for protein farnesylation in glucose-mediated regulation of the Raf/

117 The role of protein farnesylation in lamin A biogenesis and the pathogenesis

118 m mutants and highlights a broad utility for farnesylation in plant growth and development.

119 pport the concept that inhibition of protein farnesylation in progeria could be therapeutically usefu

120 significantly enhance the rate constant for farnesylation in the absence of Mg2+.

121 l pyrophosphate, however, suggests a role of farnesylation in the LPS-mediated induction of iNOS.

122 The inhibition of farnesylation in the peripheral blood correlated with th

123 Here, we investigated roles of protein farnesylation in the signaling steps involved in Raf-1/e

124 Inhibition of farnesylation in vivo was consistently documented.

125 d, confirming that SCH66336 inhibits protein farnesylation in vivo.

126 h either farnesyltransferase inhibitors or a farnesylation-incompetent mutant progerin/LADelta50.

127 apparatus, proximal to the centrosomes, in a farnesylation-independent manner.

128 r the drug's anti-tumor effects, such that a farnesylation-independent mutant of Rheb renders these t

129 not merely serine 50 phosphorylation, as the farnesylation-induced anchorage of m-calpain triggers a

130 The inhibitors of Ras farnesylation inhibited glucose-induced nitric oxides an

131 Farnesylation inhibition of HDJ-2 in peripheral blood wa

132 investigate this, we studied the effects of farnesylation inhibition on nuclear phenotypes in cells

133 al activity may correlate with the degree of farnesylation inhibition, rather than dose of tipifarnib

134 ns CENP-E and CENP-F are relevant targets of farnesylation inhibition; however, their relative import

135 Using antisense oligonucleotides and the Ras farnesylation inhibitor FTI-277, we showed that o-HA-ind

136 pathways distinct from its role as a protein farnesylation inhibitor.

137 se defects were reversible by treatment with farnesylation inhibitors and statins.

138 s estimating increased survival with protein farnesylation inhibitors provide the first evidence of t

139 Farnesylation involves covalent linkage of eukaryotic pr

140 Farnesylation involves the post-translational attachment

141 Farnesylation is a critical modification to many switch

142 Our results indicate that farnesylation is a major factor contributing to the spec

143 Farnesylation is a posttranslational lipid modification

144 Farnesylation is a posttranslational lipid modification

145 Farnesylation is an important post-translational modific

146 These results demonstrate that protein farnesylation is critical for maintaining normal cell mo

147 Farnesylation is essential both for normal functioning o

148 ed that hSpindly is farnesylated in vivo and farnesylation is essential for its interaction with the

149 We also found that farnesylation is essential for NRAS leukemogenesis, yet

150 Protein farnesylation is important for a number of physiological

151 Our findings suggest that protein farnesylation is important for cell cycle progression of

152 The loss of protein farnesylation is not as severe but also results in polar

153 ribosomal protein S6 kinase, indicating that farnesylation is not required for B-Raf inhibition by Rh

154 Protein farnesylation is required for expression and secretion o

155 Posttranslational farnesylation is required for Ras activation.

156 crystal structures, the transition state for farnesylation is stabilized by interactions between the

157 Specifically, our findings indicate that Ras farnesylation is sufficient for stable association of Ra

158 Although farnesylation is the obligatory first step in post-trans

159 Farnesylation is the prerequisite for subsequent palmito

160 tudies demonstrated that Rheb is modified by farnesylation, is not a substrate for alternative prenyl

161 te that protein geranylgeranylation, but not farnesylation, is required for integrin-dependent post-r

162 e proposed biologic end point, inhibition of farnesylation, is unknown.

163 oprenylation pathway--geranylgeranylation or farnesylation--is inhibited by simvastatin, we demonstra

164 -actin colocalization is dependent upon LKB1 farnesylation leading to RhoA-ROCK-mediated stress fiber

165 and structurally distinct inhibitors of Ras farnesylation, lovastatin and B581, and a specific inhib

166 hows novel localized recruitment of the host farnesylation machinery and its anchoring of an F-box ef

167 Therefore, targeting RAS farnesylation may be a novel approach to treatment of MM

168 Therefore, inhibition of UCH-L1 farnesylation may be a therapeutic strategy for slowing

169 HDJ-2 farnesylation (mean +/- SD) decreased by 33.4% +/- 19.8%

170 Farnesylation mediates membrane targeting and in vivo ac

171 dramatically affecting the rate constant of farnesylation minus magnesium or the binding affinity of

172 In contrast, defective farnesylation mislocalizes nascent adhesion sites, sugge

173 Finally, a mutation in the C-terminal CAAX farnesylation motif resulted in a loss of ScRheb functio

174 bits high enzymatic activity toward the CAAX farnesylation motif substrates (where C represents cyste

175 We also examined a putative farnesylation motif thought to be involved in CLN3 traff

176 CLN3 with a mutation in the farnesylation motif trafficked normally but was function

177 ino acids in length and contains a conserved farnesylation motif.

178 G1 box, and 4) presence of a conserved CAAX farnesylation motif.

179 1b mutant with a disruption in the consensus farnesylation motif.

180 se inhibitors (FTIs), although HDAC6 lacks a farnesylation motif.

181 ellular nanovesicles, yet expressing a K-Ras farnesylation mutant did not decrease the number of nano

182 Our assay is based upon the farnesylation of a CVIM motif-tagged CTA1 polypeptide (C

183 ch revealed that the Y361L variant catalyzed farnesylation of a normal peptide substrate at a rate si

184 molecule inhibitors that selectively inhibit farnesylation of a number of intracellular substrate pro

185 Furthermore, farnesylation of a tagged Pk1b is required for its nucle

186 rotein farnesyltransferase (FTase) catalyzes farnesylation of a variety of peptide substrates.

187 hat farnesyltransferase inhibitors block the farnesylation of additional cellular polypeptides, there

188 One particular prenylation reaction, farnesylation of an mCherry-CAAX fusion construct, was s

189 We show that farnesylation of AnkB is indispensable for its anchoring

190 Also, blocking farnesylation of authentic progerin in transiently trans

191 cell line, A549, showed that preventing the farnesylation of CENP-E and CENP-F by treatment with the

192 Addition of this analogue also inhibits farnesylation of dansyl-GCKVL by FPP.

193 5777 inhibited FT activity at 300 mg bid and farnesylation of FT substrates lamin A and HDJ-2 at 600

194 Farnesylation of full-length H-Ras at C186 does not resu

195 Whereas FTIs inhibit the farnesylation of Ha-Ras, they do not completely inhibit

196 ood mononuclear cells and also inhibited the farnesylation of HDJ-2 in unfractionated mononuclear cel

197 activity was 30% compared with baseline, and farnesylation of HDJ-2 was inhibited in PBMCs.

198 The HIV-PIs did not affect the farnesylation of HDJ-2, nor did they inhibit protein far

199 n domain toxicity by Ydj1 was dependent upon farnesylation of its C-terminal CAAX box and action of a

200 de of the LCV membrane through host-mediated farnesylation of its C-terminal eukaryotic "CaaX" motif.

201 By contrast, farnesylation of K-Ras was required for its packaging wi

202 Whereas farnesylation of Ki-Ras is blocked by FTIs, Ki-Ras remai

203 PM association is mediated, in part, by farnesylation of KRAS4B, but trafficking of nascent KRAS

204 sferase, R115777 competitively inhibited the farnesylation of lamin B and K-RasB peptide substrates,

205 Thus, farnesylation of lamin B1--but not lamin B2--is crucial

206 Our findings suggest that neither farnesylation of leucine-ending CAAX substrates nor gera

207 zinc enzyme that catalyzes posttranslational farnesylation of many key cellular regulatory proteins,

208 erapeutics because it is responsible for the farnesylation of oncogenic p21 Ras proteins which are fo

209 action of FTIs is dependent on blocking the farnesylation of other proteins.

210 farnesyl protein transferase, suggests that farnesylation of p21(ras) or other proteins regulates th

211 Inhibition of farnesylation of p21ras also blocked the ability of insu

212 We hypothesized that the farnesylation of prelamin A is important for its targeti

213 These results implicate the abnormal farnesylation of progerin in the cellular phenotype in H

214 f FTase provides in vivo selectivity for the farnesylation of protein substrates even in the presence

215 ansferase inhibitor that specifically blocks farnesylation of proteins involved in growth-factor-depe

216 The post-translational farnesylation of proteins serves to anchor a subset of i

217 SCH66336 inhibits farnesylation of RAS and other proteins in tumor cells a

218 Hence farnesylation of Ras is a regulatable process that plays

219 Farnesylation of Ras is catalyzed by an enzyme that is d

220 The farnesylation of Ras oncoproteins, which are associated

221 FTI inhibited farnesylation of Ras protein more significantly in MIA P

222 Farnesylation of Ras proteins is necessary for transform

223 ase, an enzyme involved in posttranslational farnesylation of Ras, and alters Ras-dependent cell sign

224 e inhibitors have been identified that block farnesylation of Ras, reverse Ras-mediated cell transfor

225 ltransferase catalyzes the posttranslational farnesylation of several proteins involved in signal tra

226 s unclear, POH has been shown to inhibit the farnesylation of small G-proteins, including Ras, up-reg

227 geranylation of Rap-1A without affecting the farnesylation of small GTP-binding proteins such as Ras.

228 We show that farnesylation of Spindly is essential for its localizati

229 into amoebas and macrophages, host-mediated farnesylation of the AnkB effector enables its anchoring

230 The first modification is the farnesylation of the C-terminus catalyzed by farnesyl tr

231 ional processing pathway of lamin A includes farnesylation of the C-terminus, likely to increase memb

232 C terminus of the different Ras proteins and farnesylation of the CaaX box cysteine affect Ras membra

233 Farnesylation of the cysteine residue within the HDAg-L

234 ave so far been attributed to defects in the farnesylation of the outer kinetochore proteins CENP-E a

235 Inhibition of farnesylation of the surrogate protein HDJ-2 occurred in

236 The synthesis of heme A begins with farnesylation of the vinyl group at carbon C-2 of heme B

237 ipidated proteins such as isoform-specific S-farnesylation of zinc-finger antiviral protein (ZAP).

238 Posttranslational prenylation (e.g., farnesylation) of small G-proteins is felt to be requisi

239 n was used to determine the effect of Ki-Ras farnesylation on cell survival.

240 Swapping geranylgeranylation for farnesylation on Ras proteins or vice versa on Rho prote

241 of the ankB allele in exploiting either host farnesylation or the ER retention motif to be anchored i

242 Strikingly, inhibition of farnesylation pharmacologically with the farnesyl transf

243 g that ScRheb is farnesylated, suggests that farnesylation plays a key role in ScRheb function.

244 (FOL) with lovastatin, to stimulate protein farnesylation, prevented lovastatin-induced cell roundin

245 ferase inhibitors (FTIs) interfere with this farnesylation process, thereby preventing proper membran

246 C-terminal farnesylation promotes the association of UCH-L1 with ce

247 ermore, for these thiol substrates, both the farnesylation rate constant and the apparent magnesium a

248 increases 28-fold to 110 +/- 30 mM, and the farnesylation rate constant at saturating Mg2+ decreases

249 enzyme affinity for FPP but do decrease the farnesylation rate constant by 30-, 10-, and 500-fold, r

250 In addition, these residues enhance the farnesylation rate constant by almost 80-fold in the pre

251 d Y300beta, but not K164alpha, decreases the farnesylation rate constant using farnesyl monophosphate

252 ct on the pH and magnesium dependence of the farnesylation rate constant, demonstrating that the side

253 osphate (GGPP), implicating perturbations in farnesylation rather than geranylgeranylation in synergi

254 Mg2+ ions accelerate the protein farnesylation reaction by up to 700-fold.

255 The farnesylation reaction requires farnesyldiphosphate as t

256 by four post-translational processing steps-farnesylation, release of the last three amino acids of

257 ted mutant form, Ras1-CVIL, which can bypass farnesylation, rescues these morphological defects.

258 results imply that the inhibition of CENP-E farnesylation results in the alteration of the microtubu

259 After farnesylation, Rheb undergoes two additional CAAX-signal

260 teractive PH domain of Akt was replaced by a farnesylation sequence for constitutive membrane anchora

261 nascent adhesion sites, suggesting that LKB1 farnesylation serves as a targeting mechanism for proper

262 However, alteration of the carboxy-terminal farnesylation signal disrupted the functional and physic

263 sformation is also dependent on a C-terminal farnesylation signal that mediates localization to a cel

264 ylation signal to the amino terminus or of a farnesylation signal to the carboxyl terminus of c-P3k.

265 acidic transcription activation domain and a farnesylation signal.

266 w that an AIP-1 mutant lacking the predicted farnesylation site failed to protect against Abeta toxic

267 Further, expression of a farnesylation site PRL-1 mutant results in mitotic defec

268 This farnesylation site was shown by others to be essential f

269 removes 15 amino acids, including a CAAX box farnesylation site, from the lamin A protein.

270 tingly, AIRAPL and AIP-1 contain a predicted farnesylation site, which is absent from AIRAP.

271 The farnesylation status of prelamin A determines its abilit

272 stern blot analysis was performed to monitor farnesylation status of the chaperone protein HDJ-2.

273 e kinetic mechanism that is at or before the farnesylation step.

274 Thus, inhibition of protein farnesylation stimulates TbetaRII expression, which lead

275 nesyltransferase inhibitors (FTIs) block Ras farnesylation, subcellular localization and activity, an

276 suggesting that H-Ras or N-Ras is a critical farnesylation target upstream of c-Raf in lymphoid cells

277 Farnesylation targets Ras to the endoplasmic reticulum (

278 ciates with the plasma membrane (PM) through farnesylation that functions in conjunction with an adja

279 of the beta subunit surrounding the site of farnesylation that is exposed upon dissociation from the

280 Farnesylation, the attachment of a 15-carbon farnesyl gr

281 se fluorescence quantum yield increases upon farnesylation, the rate of FDPS-catalyzed FPP production

282 P) to stabilize the developing charge in the farnesylation transition state.

283 Inhibition of farnesylation using a farnesyl transferase inhibitor (FT

284 The impact on post-translational farnesylation was assessed in 42 patients with refractor

285 t of protein kinase C and was inhibited when farnesylation was blocked, implicating Ras involvement.

286 In vitro assays indicated that farnesylation was compromised or undetectable for 11 a-f

287 Notably, S-farnesylation was crucial for targeting the long-isoform

288 The inhibition of farnesylation was greater in the three responders than t

289 Inhibition of farnesylation was noted at all dose levels, although the

290 ess efficiently than wild-type HDAg-L; thus, farnesylation was required for efficient assembly.

291 l models and its potential to inhibit Ha-ras farnesylation, we conducted an animal study to evaluate

292 novel assay to quantify the extent of HDAg-L farnesylation, we found that genotype 3 HDAg-L was ineff

293 l and dynamic changes that occur in Ras upon farnesylation, we have used NMR spectroscopy to compare

294 everely inhibited assembly without affecting farnesylation were identified.

295 Inhibition of Ras farnesylation with a concomitant inhibition of Ras funct

296 a modest influence whereas blocking protein farnesylation with manumycin severely disrupted the anti

297 ar envelope in RD and HGPS and that blocking farnesylation would ameliorate the nuclear shape abnorma

298 e hypothesized that interfering with protein farnesylation would block the targeting of progerin to t

299 Also, we hypothesized that blocking farnesylation would decrease progerin toxicity.

300 st, folding of luciferase was independent of farnesylation, yet required the zinc finger-like region