ライフサイエンスコーパス: roscovitine

1 ization of pp65 (UL83) in cells treated with roscovitine.

2 which was blocked by the CDC2/CDK2 inhibitor roscovitine.

3 al replication centers in cells treated with Roscovitine.

4 not inhibited during mitosis or affected by roscovitine.

5 t ESFT cell lines are uniformly sensitive to roscovitine.

6 so significantly slowed by i.p. injection of roscovitine.

7 nd investigate gating alterations induced by roscovitine.

8 ked by treating cells with the Cdk inhibitor roscovitine.

9 d following application of the MPF inhibitor roscovitine.

10 tly reduced by inhibiting CDK2 activity with Roscovitine.

11 inhibited with the protein kinase inhibitor roscovitine.

12 ed cells, and this activity was inhibited by roscovitine.

13 y length, similar to what we observed with R-roscovitine.

14 cessing of ICP4 is also affected by R325 and roscovitine.

15 ere cotreated with the potent cdk2 inhibitor roscovitine.

16 cyclin-dependent kinase 2 (CDK2) inhibitor, roscovitine.

17 ld be reverted by acute Cdk5 inhibition with roscovitine.

18 ABT-737, effects that are not potentiated by roscovitine.

19 a known in vitro model of glucotoxicity, and roscovitine (10 mum) was used as a CDK5 inhibitor.

20 A potent inhibitor of cdks, roscovitine [2-(1-ethyl-2-hydroxyethylamino)-6-benzylami

21 Roscovitine (25 microM) inhibited FCS-induced proliferat

22 pyrazole triol (10 nm) or the CDK5 inhibitor roscovitine (28 mum) on day 30 of withdrawal significant

23 eded for HIV-1 transcription using CYC202 (R-roscovitine), a pharmacological cyclin-dependent kinase

24 K), we explored the efficacy against ESFT of roscovitine, a CDK inhibitor shown to be surprisingly sa

25 ition by MAG is abolished in the presence of roscovitine, a Cdk inhibitor that has greater selectivit

26 93T cells transduced with RUNX1 and HDAC1 to roscovitine, a cdk inhibitor.

27 Long-term treatment with roscovitine, a CDK5 inhibitor, blocked the development o

28 We found that roscovitine, a compound that increases the voltage-depen

29 phenotype can be reversed by treatment with roscovitine, a cyclin-dependent kinase inhibitor and aty

30 Roscovitine, a drug that slows N-channel closing by hold

31 Roscovitine, a potent inhibitor of cyclin-dependent kina

32 We further show that administration of roscovitine, a selective and potent inhibitor of cdk5, m

33 Moreover, we show that roscovitine, a selective Cdk5 inhibitor, blocks both lon

34 This phosphorylation is blocked by roscovitine, a selective inhibitor of cyclin-dependent k

35 Roscovitine, a specific cdk1/2 inhibitor, also sensitize

36 Consistent with this idea, roscovitine, a specific cyclin-dependent kinase inhibito

37 ) in the establishment of this site, we used roscovitine, a specific inhibitor of cdk1, cdk2, cdk7, a

38 ex vivo kidney slices and MDCK-AQP2 cells, R-roscovitine, a specific inhibitor of cdks, increased pS2

39 325 or with wild-type virus and treated with roscovitine, a specific inhibitor of cell cycle-dependen

40 With the drug Roscovitine, a specific inhibitor of cyclin-dependent ki

41 Roscovitine, a tri-substituted purine that enhances L-ch

42 (R)-Roscovitine, a trisubstituted purine, has been shown to

43 Treatment with roscovitine-a clinically applicable Cdk5 inhibitor-alone

44 Here, we show that roscovitine; a an orally available cyclin-dependent kina

45 ncreased in these tumors, and treatment with roscovitine abrogated responses to low levels of androge

46 These results suggest that roscovitine acts on extracellular site(s) of calcium cha

47 the cyclin-dependent kinase (CDK) inhibitor roscovitine after S-phase entry reduced MVM replication,

48 st CDK1/2, and the clinical CDK1/2 inhibitor roscovitine all cooperated with the PI3K inhibitor PIK-9

49 Roscovitine, alone or with NGF, reached peak Erk1/2 acti

50 ng that Cdk1 stabilizes AR protein, although roscovitine also decreased AR message levels.

51 (R)-roscovitine also enhances other macrophage functions inc

52 (R)-roscovitine also increased MDM CFTR function compared to

53 Roscovitine also induces stabilization of the p53 Ala-31

54 We show that roscovitine also slows deactivation (EC(50) approximatel

55 Furthermore, roscovitine, an indirect inhibitor of p300 HAT, and hist

56 (Erk)1/2 in cortical neurons with or without roscovitine, an inhibitor of Cdk5.

57 90) both in vitro and in vivo was blocked by roscovitine, an inhibitor of CDKs.

58 Here we show that roscovitine, an inhibitor of cyclin-dependent kinases (C

59 Alternatively, pre-incubation in roscovitine, an inhibitor of maturation-promoting factor

60 Similarly, application of roscovitine, an inhibitor of the NFH side arm kinase Cdk

61 We have previously shown that roscovitine, an olomoucine-related purine analogue and a

62 ) affinity chromatography on immobilized (R)-roscovitine and (S)-CR8, (4) whole genome transcriptomic

63 o understand the mechanisms of action of (R)-roscovitine and (S)-CR8, two related pharmacological inh

64 ontribute to the antitumoral activity of (R)-roscovitine and (S)-CR8.

65 harmacological and molecular CDK5 inhibitors roscovitine and a dominant-negative form of CDK5.

66 Coadministration of roscovitine and ABT-737 untethers Bak from Mcl-1 and Bcl

67 Thus the CDK1 inhibitor roscovitine and an antibody we designed to block the int

68 xamples for this group include flavopiridol, roscovitine and BMS-387032.

69 entiation of tail calcium currents caused by roscovitine and by the L-channel activator Bay K 8644 wa

70 However, kinase inhibitors roscovitine and C16 partially or entirely reversed the a

71 Roscovitine and dominant-negative STAT5 also reduced the

72 Both roscovitine and heat shock treatment caused increased ac

73 ignaling activated by the small molecule (R)-roscovitine and its derivatives.

74 (R)-roscovitine and M3 significantly increased killing of B.

75 pitated protein was reduced and resistant to roscovitine and may represent a contaminating kinase act

76 As other Cdk inhibitors, such as roscovitine and Myt1, did not act like Wee1 to accelerat

77 We found that treatment with roscovitine and olomoucin, which were originally develop

78 The cyclin-dependent kinase (Cdk) inhibitors roscovitine and olomoucine inhibit initiation of DNA rep

79 ine, was ineffective, two potent inhibitors, roscovitine and olomoucine, attenuated significantly the

80 ve cyclin-dependent kinase (Cdk) inhibitors, roscovitine and olomoucine, dramatically enhance this FT

81 In LNCaP cells, in addition to roscovitine and olomoucine, phophatidylinositol 3-kinase

82 Roscovitine and PIK-90, in combination, were well tolera

83 or cyclin-dependent kinase inhibition (using roscovitine and siRNA directed towards cyclin-dependent

84 Three of these compounds, VX-680, Roscovitine and Sunitinib, each eliminate >85% of infect

85 were not greatly affected by treatment with Roscovitine and thus did not correlate with the reduced

86 We show that roscovitine, R-roscovitine, and CGP74514A (collectively referred to as

87 s not blocked by Cdk5 inhibitors CP68130 and roscovitine, and instead the BACE1 level was increased g

88 in-dependent kinase inhibitors flavopiridol, roscovitine, and olomoucine) reduced up-regulation of ce

89 However, the effects of roscovitine appear to be distinct from those of LY294002

90 Effects of (R)-roscovitine are greatest when combined with CFTR modulat

91 Although these cellular effects of roscovitine are thought to be caused directly by its spe

92 inone, but was ineffective in olomoucine- or roscovitine-arrested oocytes, indicating that it acts up

93 excitotoxicity of synaptic origins and about roscovitine as a selective modulator of this process.

94 nd cyclin-dependent kinase inhibitors (e.g., roscovitine), as well as other leukemia cell types (e.g.

95 stal structure of a complex between cdk2 and roscovitine at 0.24-nm (2.4 A) resolution and refined to

96 Cells treated with roscovitine at doses that affected transcription were fo

97 the cyclin-dependent kinase (cdk) inhibitor Roscovitine at the beginning of infection of cells with

98 Addition of Roscovitine at the beginning of the infection was also a

99 not influenced by inhibition of CDK2 (using Roscovitine), ATM (using Caffeine and KU55933), Chk1 (us

100 ermine whether these effects result from (R)-roscovitine binding to a single site.

101 We conclude that (R)-roscovitine binds to distinct sites on L-type channels t

102 KIs, flavopiridol, purvalanol A, and methoxy-roscovitine, block Moloney murine leukemia virus (MLV) t

103 on sites or treatment with the CDK inhibitor roscovitine blocked the ability of APP to signal through

104 HEp-2 cells lacked the D' form of ICP4, and roscovitine blocked the appearance of the most highly ch

105 A Cdk inhibitor, roscovitine, blocked paclitaxel-induced MCL-1 degradatio

106 n this report, we show that a cdk inhibitor, Roscovitine, blocks VP16-dependent IE gene expression.

107 brafish model, we show that encapsulated (R)-roscovitine can speed up inflammation resolution in vivo

108 s with the cyclin-dependent kinase inhibitor roscovitine caused a concentration- and time-dependent i

109 Both p27(kip1) and roscovitine, cdk2 inhibitors, prevented DNA replication

110 e treated with drugs (etoposide, Adriamycin, roscovitine, cisplatin, 5-fluorouracil, or cycloheximide

111 tivity studies and from analysis of the cdk2/roscovitine complex crystal structure should allow the d

112 osphorylation of NHERF-1 could be blocked by roscovitine, consistent with phosphorylation by cyclin-d

113 Low concentrations of roscovitine cooperate with the DNA-damaging agent campto

114 Our investigations revealed that roscovitine coordinately inhibited the expression of col

115 was increased 3- to 6-fold, suggesting that roscovitine could prolong the channel open state and inc

116 We investigated whether roscovitine could regulate fibrotic protein production d

117 -dependent kinase (CDK) inhibitor, CYC202 (R-roscovitine), could attenuate or reverse existing renal

118 ll-molecule cdk modulators, BMS 387032 and R-Roscovitine (CYC202), have commenced with good tolerabil

119 Treatment of the cells with 10 microg/ml roscovitine daily for a length of time ranging from 24 t

120 nt kinase 2 (CDK2) with the purine analogue, Roscovitine, decreased MC proliferation in vitro and in

121 to be distinct from those of LY294002, since roscovitine did not affect Akt activity while LY294002 s

122 R-Roscovitine did not alter cAMP-dependent PKA activity bu

123 Roscovitine did not enhance [3H]DA release mediated by e

124 The cdk2-cyclin E inhibitor roscovitine did not prevent the effects of Cul3 deletion

125 325901 and GW8510) or stalled (CHIR99021 and roscovitine) differentiation, resulting in myotube and m

126 inhibitor of cdk activity), purvalanol A and roscovitine (direct cdk inhibitors), and the reduction o

127 Roscovitine displays high efficiency and high selectivit

128 cyclin-dependent kinase (CDK) inhibitor (R)-roscovitine does indeed yield effective arrest of cystic

129 The cdc2 inhibitor roscovitine dose dependently inhibited in vivo RUNX2 DNA

130 y, intra-NAc injection of the Cdk5 inhibitor roscovitine, dose-dependently decreased wheel running.

131 Roscovitine dramatically slowed the deactivation kinetic

132 Instead, roscovitine enhanced spontaneous [3H]DA outflow and inhi

133 l, the caspase inhibitor zVAD-fmk prevents R-roscovitine-enhanced resolution of inflammation, indicat

134 Using the S enantiomer, we find that (S)-roscovitine enhances inactivation without affecting acti

135 Furthermore, the cdk inhibitor roscovitine enhances the coupling between tetrodotoxin-s

136 Moreover, intracellular perfusion of roscovitine failed to modulate calcium currents.

137 Intracellularly applied roscovitine failed to slow deactivation, which implies a

138 er agents (including doxorubicin, etoposide, roscovitine, flavopiridol, and nutlin-3).

139 In comparison with the parent molecule, (R)-roscovitine, GV-58 has a approximately 20-fold less pote

140 Roscovitine had little effect on the interaction of VP16

141 Roscovitine has been shown to induce the accumulation of

142 the cyclin-dependent kinase (cdk) inhibitor roscovitine has significant effects on several stages of

143 A novel function of roscovitine, i.e. an effect on Ca(2+) channels and trans

144 In the presence of roscovitine, IE2, cyclin T1, Brd4, HDAC1, and HDAC2 accu

145 of CDK5 or treatment with the CDK5 inhibitor roscovitine improved behavioral performance in the water

146 received daily intraperitoneal injections of Roscovitine in DMSO (2.8 mg/kg) starting at day 1.

147 lude that reducing the activity of CDK2 with Roscovitine in experimental glomerulonephritis decreases

148 RNA synthesis is suppressed significantly by roscovitine in human cells.

149 this benzyl ring explains the specificity of roscovitine in inhibiting cdk2.

150 Inhibition of Cdc2 activity with roscovitine in mitotic cells restored ERK activation by

151 own of CDK2, or inhibiting its activity with roscovitine in podocytes increased apoptosis.

152 k6, can overcome inhibition of initiation by roscovitine in vitro.

153 ied 17 putative protein kinases perturbed by roscovitine, including CMGC kinases, AGC kinases and CAM

154 (R)-roscovitine increases CF macrophage-mediated killing of

155 data generated from this study suggest that roscovitine induced apoptosis in the estrogen receptor-n

156 To explore the involvement of Cdk5 in roscovitine-induced down-regulation of DAT activity, Cdk

157 Roscovitine-induced inhibition of dSTR [3H]DA uptake was

158 Roscovitine-induced potentiation of tail calcium current

159 The roscovitine-induced slow deactivation was accompanied by

160 aining L-channel domains I and IV showed (R)-roscovitine-induced slowed activation like that of wild

161 Roscovitine induces down-regulation of MDM2 expression a

162 Cdk5 inhibition by roscovitine infusion prevented depressive-like behavior

163 e persisted at least 2 weeks after the final roscovitine infusion.

164 Taken together, our results suggest that roscovitine inhibits DAT activity independently of Cdk5;

165 hibiting CDC2A following its activation with roscovitine inhibits MSY2 phosphorylation and prevents m

166 results suggest that the mechanism by which roscovitine inhibits RNA synthesis involves the inhibiti

167 In this study, we investigated whether roscovitine interferes with transcription in human cells

168 er the cyclin-dependent kinase inhibitor (R)-roscovitine into human neutrophils to promote apoptosis

169 Repeated infusions of the Cdk5 inhibitor roscovitine into the NAc before cocaine injections augme

170 We conclude that roscovitine is a potent inhibitor of RNA synthesis and t

171 We found that roscovitine is active against cysts originating from dif

172 The RNAP IIo decrease does not occur if roscovitine is added 8 h postinfection, as was previousl

173 Roscovitine is an inhibitor of cyclin-dependent kinases

174 re also reveals that the (R)-stereoisomer of roscovitine is bound to cdk2.

175 We conclude that roscovitine is effective at preventing prolonged diet-in

176 Enhancement of FTI-induced apoptosis by roscovitine is not unique to HL-60 cells, since similar

177 x-MVIIC, indicating that the major target of roscovitine is the P/Q-type calcium channel.

178 Roscovitine is widely used for inhibition of cdk5, a cyc

179 Seliciclib (CYC202 or R-roscovitine) is a potent CDK inhibitor currently undergo

180 CYC202 (R-roscovitine) is a potent inhibitor of CDK2/cyclin E that

181 ne offered a means of testing the ability of roscovitine, known to potentiate frog neuromuscular tran

182 the cyclin-dependent kinase (cdk) inhibitor roscovitine leads to changes in differential splicing an

183 V12)-C/EBPbeta1 cells with the cdk inhibitor roscovitine leads to stabilization of C/EBPbeta1.

184 dk5 kinase activity using the Cdk5 inhibitor roscovitine led to the formation of larger aggregates of

185 ) confirm that Bax is required for ABT-737+/-roscovitine lethality, whereas Bak is primarily involved

186 Extracellular application of roscovitine markedly enhanced the tail calcium current f

187 These results strongly suggest that roscovitine may be an effective therapeutic agent agains

188 cell death, modulation of this parameter by roscovitine may provide a new chemopreventive and chemot

189 Roscovitine may thus be a viable treatment option for SS

190 ranscriptional basis and did not result from roscovitine-mediated cell cycle inhibition.

191 (R)-roscovitine-mediated effects were partially dependent on

192 From a postsynaptic standpoint, roscovitine-mediated excitotoxicity requires the functio

193 (R)-roscovitine-mediated killing of B. cenocepacia was enhan

194 Roscovitine-mediated suppression of matrix proteins coul

195 es with replication inhibitors (hydroxyurea, roscovitine, mimosine) strongly inhibited transcriptiona

196 r knowledge, we are the first to report that roscovitine modulates matrix protein transcription.

197 Flavopiridol and roscovitine, newly identified inhibitors of cyclin-depen

198 (dSTR) synaptosomes with the Cdk5 inhibitors roscovitine, olomoucine, and 4-{[(7-oxo-6,7-dihydro-8H-[

199 n states was able to reproduce the effect of roscovitine on both activation and deactivation.

200 cdk9 does not compensate for the effects of roscovitine on cdk9 localization or viral gene expressio

201 hovanadate ablated the inhibitory effects of roscovitine on STAT5/PDGF alpha receptor interaction, ST

202 1-43, consistent with the positive effect of roscovitine on the P/Q-type calcium channel, the major m

203 Inhibiting CDK2 activity with Roscovitine or dominant negative mutant reduced apoptosi

204 activity was inhibited by the Cdk5 inhibitor roscovitine or dominant-negative (dn) Cdk5, the migratio

205 MDMs were treated with (R)-roscovitine or its main hepatic metabolite (M3).

206 the cyclin-dependent kinase (CDK) inhibitor roscovitine or Mcl-1-shRNA dramatically increases ABT-73

207 ation or to the inhibition of either cdk5 by roscovitine or of CaMK by 2-[N-(2-hydroxyethyl)]-N-(4-me

208 , justifying further clinical testing of (R)-roscovitine or optimized derivatives.

209 We use the Cdk inhibitor roscovitine or RNAi depletion of Cdc7 to inhibit origin

210 acological inhibition of CDK5 using either R-roscovitine or S-CR8 is accompanied by sustained shorten

211 ing CDK2 activity, either pharmacologically (Roscovitine) or by a dominant-negative mutant, inhibited

212 tly inhibited by pharmacological inhibition (roscovitine) or genetic ablation of CDK5.

213 f Cdk5 activity by a specific Cdk inhibitor, roscovitine, or by overexpression of a dominant negative

214 y toxic concentrations of flavopiridol (FP), roscovitine, or CGP74514A for 3 h in conjunction with th

215 Roscovitine potentiated glutamate release at presynaptic

216 Finally, the CDK inhibitor roscovitine potentiated the cytotoxic activity of ZD9331

217 Additional data showed that roscovitine preferentially binds to the open channel to

218 Roscovitine prevented the tyrosine phosphorylation and c

219 was reduced by > 50% at days 5 and 10 in the Roscovitine prevention group, and at day 5 in the treatm

220 We also provide evidence that R-roscovitine promotes apoptosis by reducing concentration

221 ndent kinases--flavopiridol, olomoucine, and roscovitine--protect CGNs from KCl withdrawal-induced ap

222 We show that roscovitine, R-roscovitine, and CGP74514A (collectively

223 A model where roscovitine reduced a backward rate constant between two

224 Early administration of Roscovitine reduced immunostaining for collagen type IV,

225 anistically, inhibiting DNA replication with Roscovitine reduced tubular injury, blocked the developm

226 We suggest that roscovitine reduces the abundance of tyrosine-phosphoryl

227 p35, a neuronal specific activator of cdk5, roscovitine regulated calcium currents in a manner simil

228 ve CDK5 construct, small interfering RNA, or roscovitine resulted in changes in the microtubule cytos

229 e analysis showed that both flavopiridol and roscovitine reversibly suppressed HIV-1 transcription in

230 or cellular cyclin-dependent kinases (cdks), Roscovitine (Rosco) and Olomoucine (Olo), block the repl

231 in the presence of the cell cycle inhibitors roscovitine (Rosco) and olomoucine (Olo).

232 Roscovitine (Rosco) is a purine derivative that inhibits

233 The cyclin-dependent kinase (cdk) inhibitor Roscovitine (Rosco) reduces transcription of herpes simp

234 Roscovitine (Rosco), an inhibitor of cyclin-dependent ki

235 istant to two cdk inhibitors, Olomoucine and Roscovitine (Rosco), we hypothesized that cdks may be re

236 We sought to determine roscovitine's impact on macrophage function and killing

237 We show that the CDK inhibitor R-roscovitine (Seliciclib or CYC202) markedly enhances res

238 (R)-roscovitine (Seliciclib) is a unique drug that has many

239 d a pharmacologic CDK2/cyclin E inhibitor, R-roscovitine (seliciclib; CYC202), which specifically rev

240 tained with anti U(L)42 antibody contained a roscovitine-sensitive kinase activity, (iv) kinase activ

241 rn neurons are more sensitive to Sema3a in a roscovitine-sensitive manner, whereas nestin knockdown r

242 Inhibition of CDK5 activity with roscovitine-sensitized cells to heat induced apoptosis i

243 s-related cyclin-dependent kinases (Cdks) by roscovitine significantly reduced the hyperphosphorylati

244 In addition, roscovitine similarly inhibited STAT5A phosphorylation a

245 Slow deactivation was specific to roscovitine, since it could not be induced by a closely

246 Compared with flavopiridol and roscovitine, SNS-032 was more potent, both in inhibition

247 A treatment group received daily Roscovitine starting at day 3, when MC proliferation was

248 Moreover, the CDK inhibitor roscovitine stimulated the expression of CYP3A4.

249 n the presence of the specific CDK inhibitor roscovitine strongly supported the prior results by demo

250 roteomics analysis of eWAT demonstrated that roscovitine suppressed expression of peptides and phosph

251 further validated that orally administered R-roscovitine suppresses ACTH and corticosterone levels, a

252 analyses in vitro and in vivo showed that R-roscovitine suppresses ACTH expression, induces corticot

253 Roscovitine synergizes with FTI to release cytochrome c

254 e two agents (trastuzumab targeting HER2 and roscovitine targeting cyclin E).

255 In contrast, treatments with roscovitine, the Cdk5 inhibitor, resulted in an opposite

256 hreefold by treatment of infected cells with Roscovitine, the drop did not correspond to the 1- to 2-

257 In the presence of Roscovitine, the level of virion-induced activation of a

258 de-specific antiserum, and the cdk inhibitor roscovitine to demonstrate that S48 and S424 are also ph

259 e used a lentiviral siRNA system or the drug roscovitine to down-regulate survivin expression.

260 pression of MDM2 can abrogate the ability of roscovitine to induce p53 stabilization.

261 , we detected synergistic effects of FTI and roscovitine to inhibit hyperphosphorylation of retinobla

262 s), which contrasts with a slower effect of roscovitine to inhibit N-current (EC(50) approximately 3

263 dditionally, repeated intra-NAc infusions of roscovitine to saline-injected rats enhanced locomotor r

264 Morphological analysis of roscovitine-treated cells by light and fluorescence micr

265 ted STAT5 from extracts of untreated but not roscovitine-treated cells.

266 application of the MEK1 inhibitor PD98095 to roscovitine-treated cortical neurons prevented apoptosis

267 Roscovitine treatment also resulted in decreased levels

268 ar to previous findings in Pkd1(+/-) mice, R-roscovitine treatment caused a significant decrease in i

269 ting comparatively minor cell cycle effects, roscovitine treatment concomitantly caused the up-regula

270 In an in vivo glomerulonephritis model, roscovitine treatment decreased mesangial cell prolifera

271 e cellular processes and targets affected by roscovitine treatment in the estrogen receptor-negative

272 Roscovitine treatment leads to decreased levels of hyper

273 Ect2, induced expression of 90 cyclin B, and roscovitine treatment), such activity generates multiple

274 A combination of roscovitine treatment, transfection with immediate early

275 creatine biosynthesis are enriched following roscovitine treatment.

276 Therefore, roscovitine-triggered necrosis requires spontaneous Na+-

277 -dependent kinases (Cdks) by kenpaullone and roscovitine (two small molecule inhibitors of Cdks that

278 on late viral events by delaying addition of Roscovitine until 24 h postinfection.

279 Delaying the addition of roscovitine until 8 h postinfection prevented all of the

280 uivalent suppression of HIV-1 transcription, roscovitine was a more effective inhibitor of podocyte p

281 When Roscovitine was added after the first 6 h of infection,

282 A slight enhancement of the cytotoxicity of roscovitine was demonstrated in combination with E2F-1 o

283 uction in viral titer was observed even when Roscovitine was first added at 48 h postinfection, indic

284 on of HIV-1 transcription by flavopiridol or roscovitine was marked by re-expression of the podocyte

285 ein expression mediated by the Cdk inhibitor roscovitine was prevented by proteosome inhibitors, indi

286 However, roscovitine was the only inhibitor that did not also dec

287 to Cdk2 inhibitory drugs (flavopiridol and R-roscovitine) was demonstrable in human tumor cells in vi

288 Finally, by using the cdk inhibitor roscovitine, we reveal that E7 activates the cdc25A prom

289 ates Bak activation and apoptosis by ABT-737+roscovitine, whereas cells overexpressing Bcl-2 or Bcl-x

290 de mediated by p16Ink4a or the CDK inhibitor roscovitine, whereas down-regulation of p27Kip1 was main

291 Roscovitine, which down-regulated Mcl-1, also did not pr

292 26 and the cyclin-dependent kinase inhibitor roscovitine, which inhibit the cell cycle at different p

293 GV-58 was developed as a modification of (R)-roscovitine, which was previously shown to be a Ca(2+) c

294 ntaining L-channel domain I responded to (R)-roscovitine with enhanced inactivation.