ライフサイエンスコーパス: lovastatin

1 lyzes lactones such as statin prodrugs (e.g. lovastatin).

2 oma to the effects of the proapoptotic agent lovastatin.

3 olesterol, inhibits CYP4F2 mRNA induction by lovastatin.

4 localization in infected cells treated with lovastatin.

5 oA reductase in complex with the statin drug lovastatin.

6 of the medically significant natural product lovastatin.

7 the morphologic and cytoskeletal effects of lovastatin.

8 vastatin/day and 3) hormone replacement plus lovastatin.

9 w diet supplemented with the HMGCR inhibitor lovastatin.

10 bed statin (73%) followed by simvastatin and lovastatin.

11 ate, as evidenced by increased resistance to lovastatin.

12 se I poison topotecan remained unaffected by lovastatin.

13 ivation in response to therapeutic levels of lovastatin.

14 abrogated Ras and MAPK activation induced by lovastatin.

15 cells (RCECs) and in db/db mice treated with lovastatin.

16 in cell lysates was significantly reduced by lovastatin.

17 eld the cholesterol-lowering natural product lovastatin.

18 holesterol content, which is attenuated with lovastatin.

19 ain and reduced serum cholesterol levels and lovastatin (1.5 mg/kg, twice weekly as in the previous s

20 Indeed, combinations as low as 50 nM lovastatin + 1 microM 5c or 250 nM lovastatin + 50 nM 5c

21 ht with vehicle (0.01% ethanol) or activated lovastatin (10 microM).

22 ed for 24 hours in the presence of activated lovastatin (10 muM) to enhance the endogenous synthesis

23 Lovastatin, 10-30 micromol/L, augmented sulindac-induced

24 5 mg/dl) versus moderate LDL-C lowering with lovastatin 2.5 to 5 mg/day (to achieve LDL-C of 130 to 1

25 Treatment with lovastatin (20 to 40 mg/d) resulted in a 25% reduction i

26 n endothelial cells (HUVECs) were exposed to lovastatin (3 microm-30 microm) for 48 h, and cell death

27 Rats received vehicle (controls), lovastatin (30 mg/kg), or atorvastatin (30 mg/kg) as a s

28 ipoprotein cholesterol (LDL-C) lowering with lovastatin 40 to 80 mg/day (to achieve LDL-C of 60 to 85

29 p prenylation but that therapeutic levels of lovastatin (50 nM to 500 nM) do not.

30 as 50 nM lovastatin + 1 microM 5c or 250 nM lovastatin + 50 nM 5c were highly cytostatic in STS-26T

31 However, lovastatin (a cholesterol lowering and anti-inflammatory

32 reated Chinese hamster ovary cell lines with lovastatin (a hydroxymethylglutaryl-CoA reductase inhibi

33 dient, and (ii) in contrast, applications of lovastatin, a cholesterol synthesis inhibitor, which del

34 make important metabolites in fungi, such as lovastatin, a cholesterol-lowering drug from Aspergillus

35 monstrate that treatment of macrophages with lovastatin, a cholesterol-lowering drug that blocks farn

36 entation assays and in planta application of lovastatin, a competitive inhibitor of HMG1, we show tha

37 vented by culturing cells in the presence of lovastatin, a competitive inhibitor of HMGR.

38 Treatment of infected cells with lovastatin, a drug that disrupts protein prenylation, ch

39 We discovered that lovastatin, a drug that is widely prescribed for the tre

40 Here, we have demonstrated the potential of lovastatin, a HMG-CoA reductase inhibitor, for the resto

41 We report that lovastatin, a member of the statin family, effectively i

42 Lovastatin acted by inhibiting both geranylgeranylation

43 d 43 +/- 2.9 (NS), respectively, with 50 ppm lovastatin alone; to 137 +/- 5.4 (P = 0.053) and 36 +/-

44 Binding of lovastatin also displaces the flap domain of the enzyme,

45 Lovastatin altered the morphology of TM cells by disrupt

46 and cDNA microarray analysis confirmed that lovastatin altered the program of gene expression.

47 induced airspace neutrophils were reduced by lovastatin, an effect that was blocked by mevalonic acid

48 Lovastatin, an HMG-CoA reductase inhibitor (statin), was

49 Treatment of En2(-/-) mice with lovastatin, an indirect inhibitor of ERK phosphorylation

50 replication was disrupted by treatment with lovastatin, an inhibitor of 3-hydroxy-3-methyglutaryl Co

51 ved when transfected cells were treated with lovastatin, an inhibitor of the biosynthesis of the isop

52 nto the genetic and physiological control of lovastatin and (+)-geodin biosynthesis, and identifies n

53 the polyketide-derived secondary metabolites lovastatin and (+)-geodin in broths from fermentations o

54 with different mechanisms of action such as lovastatin and 5-aminoimidazole-4-carboxamide-1-beta-D-r

55 0.004) and 28 +/- 3.4 (P = 0.02) when 50 ppm lovastatin and 80 ppm sulindac were combined.

56 Lovastatin and a geranylgeranyltransferase inhibitor red

57 y; clinical scores >/=3.0) when treated with lovastatin and aforementioned agents validated these in

58 Lovastatin and atorvastatin reduced adhesion formation b

59 in or chronic exposure to different statins (lovastatin and atorvastatin) led to a spatial disorganiz

60 ethylglutaryl-coenzyme A reductase inhibitor lovastatin and by the squalene synthase inhibitor zarago

61 sessed the efficacy of combined therapy with lovastatin and cholesterol.

62 Both lovastatin and compactin decreased MLC phosphorylation i

63 his study demonstrates that the statin drugs lovastatin and compactin induce changes in cell shape an

64 clearance of K. pneumoniae was inhibited by lovastatin and extrapulmonary dissemination was enhanced

65 Here, we show that co-administration of lovastatin and ezetimibe (L/E) significantly reverses he

66 cells and in mice fed chow supplemented with lovastatin and ezetimibe (L/E) to decrease dietary stero

67 The combination of lovastatin and forskolin results in a greater inhibitory

68 The results showed that the content of lovastatin and its acid form in dietary supplements were

69 Lovastatin and minidose warfarin were evaluated in a fac

70 Lovastatin and NSC23766 acted in an additive manner.

71 were not significantly different between the lovastatin and placebo groups at 24 weeks (P = .85) and

72 h a low dosage of two CNS-permeable statins (lovastatin and simvastatin) selectively reduced NMDA-ind

73 en evaluating two other hydrophobic statins, lovastatin and simvastatin.

74 metabolites such as the anticholesterol drug lovastatin and the potent natural carcinogen aflatoxin.

75 Both the lipid-lowering drug lovastatin and the Rac1-specific inhibitor NSC23766 atte

76 ffects were similar among those allocated to lovastatin and those allocated to placebo and were modes

77 Lovastatin and zaragozic acid A produced similar effects

78 a lactone moiety, including statins (such as lovastatin) and the isoprenoid inhibitors (such as FTI-2

79 Specific inhibitors of the MVA pathway (lovastatin) and the MVA-independent pathway (fosmidomyci

80 y, higher doses of atorvasatin, fluvastatin, lovastatin, and simvastatin were associated with higher

81 Some examples include perifosine, lovastatin, and UCN-01.

82 patocytes increase LDL uptake in response to lovastatin; and (4) FH iPSC-derived hepatocytes display

83 at various concentrations, with and without lovastatin; and 2) obese human serum with elevated resis

84 Lovastatin appeared to exert its positive effect on effe

85 Here, we identify lovastatin as a potent inhibitor of p21Ras/Mitogen Activ

86 lase activity and systemic clearance of oral lovastatin (at 5 mg/kg).

87 linical strains of R. oryzae were exposed to lovastatin, atorvastatin, and simvastatin and the minimu

88 Lovastatin attenuated epithelial gingival tissue growth

89 Simvastatin and lovastatin attenuated migration and invasion of MDA-MB-2

90 Lovastatin attenuates pulmonary inflammation induced by

91 rter G5/G8 (G5G8(Tg) mice) were treated with lovastatin because they have a compensatory increase in

92 Lovastatin biases the immune response from Th1 to a prot

93 Three pathways were identified as a result: lovastatin biosynthesis, xylan degradation and biosynthe

94 ght possible polyketide intermediates during lovastatin biosynthesis.

95 e addition of mevalonate, which bypasses the lovastatin block.

96 1 was shifted into the low affinity state by lovastatin, both monomeric and dimeric ICAM-1 dissociate

97 The structure shows lovastatin bound in the active site and its interactions

98 strates that the HMG-CoA reductase inhibitor lovastatin can normalize protein synthesis and also redu

99 The assays showed that lovastatin caused a dose-dependent endothelial cell deat

100 rol-enriched) or 4% cholestyramine and 0.15% lovastatin (cholesterol-depletion) were fed to hamsters

101 Topical treatment with lovastatin/cholesterol (but not cholesterol alone) virtu

102 groups (-14% [P<0.01] and -17% [P<0.01] with lovastatin-colestipol and niacin-colestipol, respectivel

103 LDL buoyancy increased with lovastatin-colestipol therapy (7.7%; P<0.01) and niacin-

104 -fold increase in DiI-LDL internalization by Lovastatin compared to FH-MC.

105 terations induced by Abeta were abrogated by lovastatin, consistent with its anti-inflammatory effect

106 tion between Monascus-fermented products and lovastatin contributes to increased risk of rhabdomyolys

107 s significantly enhanced consistent with the lovastatin data.

108 g/day medroxyprogesterone acetate); 2) 20 mg lovastatin/day and 3) hormone replacement plus lovastati

109 Treatment with hCG and lovastatin decreased expression of BCL-(XL) and XIAP, an

110 We report that lovastatin decreased the enhanced brain p21Ras-MAPK acti

111 Actinomycin D prevented lovastatin-dependent increases in RhoB, but not RhoA, pr

112 methylglutaryl (HMG)-CoA reductase inhibitor lovastatin depletes cellular pools of geranylgeranyl pyr

113 tration of RMD, alone or in combination with lovastatin did not cause significant rhabdomyolysis as a

114 ane cholesterol (methyl-beta-cyclodextrin or lovastatin) disrupted caveolae, attenuated CCE, and inhi

115 RMD alone or in combination with lovastatin, does not increase the risk of rhabdomyolysis

116 aracteristic of Nf1(-/-) osteoprogenitors by lovastatin during embryonic development could attenuate

117 Lovastatin effects are blocked fully by mevalonate and l

118 The lovastatin effects are prevented by mevalonate or gerany

119 Pretreatment with lovastatin eliminated excessive expression of TF in the

120 Lovastatin enhances the accumulation of RhoA and RhoB in

121 Cox regression analysis, all statins except lovastatin exerted protective effects on PD incidence an

122 GTM3 cells cultured in the presence of lovastatin exhibited a loss of actin stress fiber organi

123 PTM cells treated with lovastatin exhibited marked decreases in membrane-bound

124 passage or transformed TM cells treated with lovastatin exhibited marked increases in RhoA and RhoB m

125 orcine eye anterior segments with 100 microM lovastatin for 96 hours caused a significant increase in

126 ticipants in a five-year randomized trial of lovastatin for the primary prevention of acute coronary

127 In contrast, cycloheximide prevented lovastatin from increasing both RhoA and RhoB.

128 ractory to the growth-inhibitory activity of lovastatin, FTI-277, and GGTI-298.

129 ith angiographic progression in the low-dose lovastatin group (p trend <0.001) but not in the high-do

130 In the high-dose lovastatin group, higher BMI appeared to be protective a

131 MA and lovastatin had higher antioxidant activities than either

132 Together, these data demonstrate that lovastatin has the potential to augment remyelination in

133 New pharmaceutical treatments such as lovastatin have improved bone healing in vivo and induce

134 ant increases in small intestinal microsomal lovastatin-hydroxylase activity and systemic clearance o

135 d E (800 mg/d) (n=101), or diet and low-dose lovastatin, if needed, to reduce LDL to <130 mg/dL (n=10

136 In addition, we previously documented that lovastatin impedes demyelination and promotes myelin rep

137 in assembly disorders and phenylbutyrate and lovastatin in adrenoleukodystrophy (ALD).

138 rt, contributes to the protective effects of lovastatin in diabetic retinopathy.

139 echanisms underlying the salutary effects of lovastatin in diabetic retinopathy.

140 es of Rho/Ras family GTPases were reduced by lovastatin in glial cells.

141 with induction of a promyelinating milieu by lovastatin in mixed glial cultures stimulated with proin

142 tudy (AFCAPS/TexCAPS), a randomized trial of lovastatin in the primary prevention of acute coronary e

143 diet supplemented with Zetia (ezetimibe) and lovastatin increased and decreased nuclear SREBP-2 and S

144 Finally, lovastatin increased efferocytosis in the naive murine l

145 In this study, we show that lovastatin increased efferocytosis in vitro in an 3-hydr

146 ellular cholesterol by therapeutic levels of lovastatin increased Ras GTP loading and mitogen-activat

147 I3K abrogated Erk1/2 activity in response to lovastatin, indicating the presence of a signal relay be

148 tion treatments, 1-3 microM 5b plus 1 microM lovastatin induced a significant inhibition of RhoB pren

149 Lovastatin induced drastic changes in cell shape in both

150 Lovastatin induced neural morphology and markers includi

151 We report that lovastatin induced the expression of atrogin-1, a key ge

152 We report here that lovastatin-induced atrogin-1 expression and muscle damag

153 ercent (P<0.001), an effect not explained by lovastatin-induced changes in the lipid profile.

154 These lovastatin-induced changes in tPA and PAI-1 production w

155 Pase function is most likely responsible for lovastatin-induced cytoskeletal changes in lens epitheli

156 analysis, and the effects of C3-exoenzyme on lovastatin-induced cytoskeletal changes were evaluated b

157 d DNA synthesis and partially protected from lovastatin-induced cytotoxicity.

158 Lovastatin-induced effects were reversed by cotreatment

159 Lovastatin-induced Erk1/2 activity contributed to BMP-2

160 When we inhibited ERK, we blocked the lovastatin-induced increase in TNF-alpha production.

161 amily members, may play an important role in lovastatin-induced macrophage apoptosis.

162 anyl pyrophosphate dramatically reversed the lovastatin-induced morphologic and cytoskeletal changes,

163 nt of muscle atrophy, dramatically prevented lovastatin-induced muscle damage and abrogated atrogin-1

164 n-1 knockdown in zebrafish embryos prevented lovastatin-induced muscle injury.

165 end, we revealed the underlying mechanism of lovastatin-induced myelin repair in EAE using in vitro a

166 Lovastatin-induced reporter expression is inhibited by o

167 of PI3K signaling, significantly attenuated lovastatin-induced transcription of BMP-2.

168 Either FPP or GGPP completely prevents lovastatin-induced upregulation of RhoB mRNA.

169 We showed previously that lovastatin induces apoptosis in colon cancer cells.

170 We show that high concentrations (50 muM) of lovastatin inhibit Ras, Rho, and Rap prenylation but tha

171 Similarly, pretreatment of U937 cells with lovastatin inhibited PMA-stimulated, but not mAb 8A2-sti

172 how that treatment of brain EC in vitro with lovastatin inhibits Rho-mediated transendothelial T cell

173 ic pancreatitis, has led to the finding that lovastatin inhibits stellate cell activation and could s

174 Lovastatin is a main component of Monascus purpureus fer

175 Lovastatin is a specific inhibitor of three-hydroxy-3-me

176 Lovastatin is an important statin prescribed for the tre

177 Lovastatin is an inhibitor of hydroxymethyl glutaryl (HM

178 Lovastatin is beneficial in reducing disease progression

179 These data suggest that lovastatin is potentially disease modifying and could be

180 esterol with the HMG CoA reductase inhibitor lovastatin leads to a 2-fold increase in the surface exp

181 es that inhibition of protein prenylation by lovastatin leads to disruption of actin cytoskeletal org

182 chip surface for selective determination of lovastatin (LOV) in red yeast rice.

183 Lovastatin (LOV) is a statin, used to lower cholesterol

184 Previously, we documented that lovastatin (LOV) provides protection in EAE animals via

185 (i.e., fluorouracil (5-FU)) and K(OW) (i.e., lovastatin (LOVS)) compounds, indicating that a pharmace

186 osed by the cytokinin biosynthetic inhibitor lovastatin (LVS).

187 thylglutaryl-coenzyme A reductase inhibitor, lovastatin, markedly reduced (IC(50) approximately 1-2 m

188 Therefore, these results demonstrate that lovastatin may prove useful in the treatment of Neurofib

189 Estrogen/progestin plus lovastatin may provide additional benefits via a greater

190 We previously demonstrated that lovastatin may signal through PPARgamma and directly upr

191 Thus, hCG, in combination with radiation and lovastatin, may represent a novel approach to kill prost

192 Lovastatin-mediated activation is blocked by mevalonate

193 he involvement of the Rho and Rac GTPases in lovastatin-mediated effects, changes in distribution of

194 rvation, reduced TAFC biosynthesis following lovastatin-mediated Hmg1 inhibition, and increased TAFC

195 The lovastatin-mediated inhibition of the proteasome suggest

196 oquine (Aralen), amiodarone (Cordarone), and lovastatin (Mevacor)/simvastatin (Zocor) were evaluated

197 We previously showed that lovastatin mitigates blood-retinal barrier (BRB) breakdo

198 he extent of phosphopantetheinylation of the lovastatin nonaketide synthase (LNKS) heterologously exp

199 We report efficient expression of the lovastatin nonaketide synthase (LovB) from an engineered

200 A], NADH-dependent glutamate synthase [NGS], lovastatin nonaketide synthase [LNS], a cell wall mannop

201 Using the lovastatin nonaketide synthase LovB as a model system an

202 spects of human gingival overgrowth and that lovastatin normalizes the tissue morphology and the expr

203 The effect of lovastatin on efferocytosis was investigated in primary

204 The effects of lovastatin on F-actin reorganization (phalloidin stainin

205 The effects of lovastatin on gene expression are often mediated through

206 Here, we investigated the effect of lovastatin on protein prenylation and cell signaling.

207 This study aimed to determine the effect of lovastatin on Rho G-protein expression and activation in

208 geranyl transferase mimicked, the effects of lovastatin on RhoA and RhoB accumulation.

209 ffects of homocysteine, LDL cholesterol, and lovastatin on risk were assessed over 5.2 years of trial

210 he effect of the HMG-CoA reductase inhibitor lovastatin on the Ewing's sarcoma cell line CHP-100.

211 rther investigated the impact of exposure to lovastatin on the virulence of R. oryzae RESULTS: All st

212 The effects of lovastatin on tPA and PAI-1 production were measured in

213 this study with hyperlipidemic hamsters fed lovastatin only, lovastatin with 1-fold red mold dioscor

214 HMC incubated with either lovastatin or atorvastatin showed concentration-dependen

215 We report that inhibition of Rho, by either lovastatin or C3 exoenzyme, can increase the translation

216 PTM and PCB cells treated with lovastatin or compactin exhibited dramatic changes in ce

217 ing de novo biosynthesis of cholesterol with lovastatin or compactin had no detectable effect on vacu

218 ciliary body (PCB) were treated with either lovastatin or compactin, to determine the effects of sta

219 inhibiting the host mevalonate pathway with lovastatin or fluvastatin and fatty acid synthesis with

220 These data also suggest that lovastatin or MEK inhibitors may be useful for treating

221 changes were abrogated by pretreatment with lovastatin or NADPH oxidase inhibitor diphenyleneiodoniu

222 7Bl/6 mice with three oral doses of 10 mg/kg lovastatin (or vehicle) and three intraperitoneal doses

223 s (MC), pretreated with excess free sterols, Lovastatin, or ethanol (control), and exposed to DiI-LDL

224 groups (97/151 [64%] placebo vs 82/149 [55%] lovastatin; P = .13), and were in keeping with the chara

225 ing various secondary metabolites, including lovastatin, penicillin, and aflatoxin.

226 ies in our laboratory have demonstrated that lovastatin potently induces apoptosis in fibroblasts con

227 erevisiae and that lack of production of the lovastatin precursor polyketide was not due to insuffici

228 first time for simultaneous determination of lovastatin present in lactone and hydroxy acid forms and

229 ed to inhibit synthesis of new proteins, and lovastatin-pretreated cells were subsequently incubated

230 lection systems, that we employed to improve lovastatin production by A. terreus.

231 In zebrafish embryos, lovastatin promoted muscle fiber damage, an effect that

232 on of Rho family functions in glial cells by lovastatin promotes myelin repair in ameliorating EAE.

233 Lovastatin promotes osteoblast differentiation by increa

234 activated mixed glial cells suggesting that lovastatin protects against the degeneration of OPs and

235 nt mice with the HMG-CoA reductase inhibitor lovastatin reduced sterol synthesis in Insig-DKO embryos

236 addition, the sterol biosynthesis inhibitor lovastatin reduced TBSV replication by 4-fold, confirmin

237 Furthermore, brief treatment with lovastatin reduces activation of the GTPase Ras-extracel

238 The hormone replacement and lovastatin regimen blocked the estrogen-associated incre

239 Treatment of seedlings with lovastatin resulted in a transient decrease in sterol le

240 In vivo cholesterol depletion using lovastatin resulted in the lack of sorting of CPE and it

241 ion of protein isoprenylation does not mimic lovastatin's ability to increase Ras and RhoA synthesis,

242 Additionally, R. oryzae exposed to lovastatin showed macroscopic loss of melanin, yielded i

243 ethod, three competitive inhibitors of HMGR (lovastatin, simvastatin, and atorvastatin), as well as a

244 dominantly CYP3A4-metabolized (atorvastatin, lovastatin, simvastatin, and cerivastatin) (CYP3A4-MET)

245 ntrations of UCN-01 and various statins (eg, lovastatin, simvastatin, or fluvastatin) dramatically in

246 or all these drugs except for vigabatrin and lovastatin/simvastatin.

247 of this cross-talk, the first evidence that lovastatin stimulates rapid activation of Ras, which ass

248 We demonstrate that lovastatin stimulates tyrosine phosphorylation of the p8

249 eatment with the HMG CoA reductase inhibitor lovastatin suppressed AKT phosphorylation and enhanced t

250 ntercepted a pre-Diels-Alder intermediate in lovastatin synthesis for the first time, shedding light

251 regulators, the HMG-CoA reductase inhibitor lovastatin, the antimetabolite 5-fluorouracil, and the c

252 in with 1-fold red mold dioscorea (RMD), and lovastatin, the functional components of red mold fermen

253 Lovastatin therapy reduced the C-reactive protein level

254 ow LDL subgroups with different responses to lovastatin therapy.

255 derate lipid lowering with diet and low-dose lovastatin to an LDL level of <120 mg/dL.

256 We found lovastatin to be safe and well tolerated in adults with

257 The ability of lovastatin to induce fibroblast apoptosis in vivo was ex

258 eased survival and differentiation of OPs in lovastatin-treated activated mixed glial cells suggestin

259 ue and tPA activity in peritoneal fluid from lovastatin-treated animals were increased by 57% and 379

260 When added to lovastatin-treated cells, geranylgeraniol, but not farne

261 ation of remyelination in the spinal cord of lovastatin-treated EAE animals.

262 e pathway of cholesterol biosynthesis in the lovastatin-treated G5G8(Tg) mice.

263 Immunoblots indicate that lovastatin-treated human hepatocytes display increased p

264 nged ERK activation after LPS stimulation of lovastatin-treated macrophages.

265 In lovastatin-treated MDA468 cells, the mobility of the ass

266 Ex vivo studies of neutrophils isolated from lovastatin-treated mice confirmed inhibitory effects on

267 se, and squalene synthase in livers of Zetia/lovastatin-treated mice despite the decline in total SRE

268 ho GTPase content of membrane fractions from lovastatin-treated PTM cells were assessed by Western bl

269 After the initial drop, sterol amounts in lovastatin-treated seedlings recovered to levels above c

270 Lovastatin treatment also led to the accumulation of non

271 In addition, lovastatin treatment caused a dramatic relocalization of

272 As expected, lovastatin treatment did not alter plasma and hepatic ch

273 Real time PCR and immunoblots indicate that lovastatin treatment increases expression of the endogen

274 In a relapsing-remitting mouse model of MS, lovastatin treatment inhibited leukocyte migration into

275 ae-enriched lipid rafts and demonstrate that lovastatin treatment led to down-regulation of LOX-1 in

276 o-transfection with the mutant tRNA gene nor lovastatin treatment reduced type I deiodinase mRNA leve

277 Lovastatin treatment significantly increased the level o

278 ouse myotubes, atrogin-1 induction following lovastatin treatment was accompanied by distinct morphol

279 ased in retinas of db/db mice and reduced by lovastatin treatment.

280 In contrast, in the Ewing's sarcoma cells lovastatin triggered differentiation without causing cel

281 ayed significantly reduced susceptibility to lovastatin/UCN-01-mediated lethality.

282 Statin users, except lovastatin users, are dose-dependently associated with a

283 Biosynthesis of lovastatin uses an iterative type I polyketide synthase

284 to the different dietary challenges of Zetia/lovastatin versus fasting/refeeding.

285 factory review of a short pilot phase (40 mg lovastatin vs placebo in 30 cases), we performed a rando

286 placebo-controlled trial of 5 days of 80 mg lovastatin vs placebo in 300 Vietnamese adults with a po

287 The promotion of hCG lethality by lovastatin was abolished by overexpression of BCL-(XL),

288 Lovastatin was also associated with reduced parenchymal

289 However, lovastatin was also effective among those with a ratio o

290 Potentiation of UCN-01 lethality by lovastatin was associated with disruption of Ras prenyla

291 Lovastatin was chosen based on previous analyses of tiss

292 The effect of lovastatin was dose dependent, with newly synthesized pr

293 As expected, lovastatin was effective in preventing coronary events i

294 In contrast, lovastatin was ineffective among participants with a rat

295 pids, a consistent benefit of treatment with lovastatin was observed.

296 The enhancing effect of lovastatin was reproduced by incubation with a geranylge

297 These effects of lovastatin were mimicked by inhibitors of geranylgeranyl

298 presence of the HMG-CoA reductase inhibitor, lovastatin, when PP2A activity was inhibited by okadaic

299 Lovastatin, which binds under the conformationally mobil

300 hyperlipidemic hamsters fed lovastatin only, lovastatin with 1-fold red mold dioscorea (RMD), and lov