ライフサイエンスコーパス: fmk

1 fmk, or a specific caspase 9 inhibitor reduced DNA fragm

2 Z-Leu-Gln(NMe(2))-fmk (6a) was found to be a potent inhibitor with low tox

3 the caspase inhibitor z-VAD-fmk (where z and fmk are benzyloxycarbonyl and fluoromethyl ketone).

4 r peptides, DEVD-CHO, Z-VAD.fmk, and Boc-Asp.fmk, blocked Fas-induced PS externalization, disruption

5 the caspase-specific inhibitors crmA and BD-fmk partially inhibit TNF-R1-, TRADD, and TNF-induced NF

6 the caspase-specific inhibitors crmA and BD-fmk, suggesting that FADD- and Casper-induced NF-kappaB

7 ad spectrum caspase inhibitor (Boc-D-fmk (BD-fmk)) completely abolished TGF-beta-induced apoptosis an

8 y by the broad spectrum caspase inhibitor BD-fmk significantly attenuated the Par-4-induced increase

9 longed by the addition of broad spectrum (BD.fmk) or caspase-8 targeted (zIETD.fmk) peptide caspase i

10 The broad spectrum caspase inhibitor (Boc-D-fmk (BD-fmk)) completely abolished TGF-beta-induced apop

11 The caspase inhibitor Boc-D-fmk inhibited BAY 43-9006-induced caspase activation but

12 a-induced apoptosis, and z-VAD-fmk and Boc-D-fmk inhibited TNF alpha-stimulated reactive oxygen speci

13 Boc-D-fmk, a similar broad-spectrum caspase inhibitor, and z-I

14 ence of caspase-8 or any Z-VAD-fmk- or Boc-D-fmk-sensitive caspase activities.

15 y the caspase inhibitors Z-VAD-fmk and Boc-D-fmk.

16 ng a broad-spectrum caspase inhibitor, Bok-D-fmk.

17 r Z-VAD-fmk and partially blocked by Ac-DEVD-fmk, suggesting that SN50-mediated apoptosis is caspase-

18 Ac-YVAD-cho, but not by Ac-DEVD-cho or DEVD-fmk.

19 revented by the addition of DEVD-cho or DEVD-fmk.

20 ide inhibitors of the caspase proteins, DEVD-fmk, DEVD-cho, YVAD-cho, and IETD-fmk, were incubated wi

21 yclosporin A, the caspase-3 inhibitor Z-DEVD-fmk (40 microM) and the PARP-1 inhibitor DPQ (10 microM)

22 e inhibitor z-YVAD-fmk had no effect; z-DEVD-fmk also reduced the number of apoptotic cells after com

23 trum caspase inhibitors Z-VAD-fmk and Z-DEVD-fmk failed to protect infected cell cultures, suggesting

24 on with the pharmacological inhibitor Z-DEVD-fmk or by expressing the BIR1/BIR2 domains of X-linked i

25 eavage of beta-catenin was blocked in Z-DEVD-fmk pretreated cells.

26 oxycarbonyl-DEVD-fluoromethyl ketone (Z-DEVD-fmk) attenuates phosphorylation of H2AX by MST1 but cann

27 of a peptide inhibitor of caspase-3 (Z-DEVD-fmk) on the quantity of apoptotic nuclei was determined.

28 z-DEVD-fmk, an inhibitor of caspase-3-like proteases, prevented

29 unpreventable by caspase-3 inhibitor Z-DEVD-fmk, even though the curcumin-induced cleavage of beta-c

30 se-specific inhibitors, z-VAD-fmk and z-DEVD-fmk, significantly attenuate the accumulation of sub-G(1

31 or the caspase-3 selective inhibitor z-DEVD-fmk, whereas the caspase-1 selective inhibitor z-YVAD-fm

32 retreated with the caspase inhibitors z-DEVD-fmk, z-VAD-fmk, and Z-CH2-Asp-DCB.

33 ministration of the caspase inhibitor z-DEVD-fmk.

34 inhibited by the caspase-3 inhibitor Z-DVED-fmk.

35 Likewise, IETD(OMe)-fluoromethylketone (fmk) inhibited fenretinide-induced apoptosis by >80% in

36 IETD-fmk potently inhibited the initial processing of pro-Sf-

37 n, the caspase inhibitors, DEVD-cho and IETD-fmk, inhibited TNFalpha- and Fas-mediated apoptosis.

38 eins, DEVD-fmk, DEVD-cho, YVAD-cho, and IETD-fmk, were incubated with the ECFC to obtain further evid

39 ptosis, whereas the caspase 8 inhibitor IETD-fmk had no effect.

40 rhgas6 (64%) or the caspase inhibitors IETD-fmk [z-Ile-Glu(OMe)-Thr-Asp(OMe)-fluoromethyl ketone] (6

41 n of caspase-8 with either Z-VAD-fmk or IETD-fmk resulted in necrosis of activated microglia.

42 pase 8, and is inhibited by the peptide IETD-fmk, suggesting that reovirus sensitizes cancer cells to

43 ody NOK-1 and the caspase-8 inhibitor Z-IETD-fmk both blocked C. parvum-induced apoptosis in cholangi

44 with the caspase-8-specific inhibitor z-IETD-fmk but not pretreatment with the caspase-9-specific inh

45 reatment with the caspase-8 inhibitor z-IETD-fmk or DR4:Fc significantly inhibited Apo-2L/TRAIL-induc

46 Z-IETD-fmk, a caspase-8 inhibitor, completely blocked caspase-8

47 broad-spectrum caspase inhibitor, and z-IETD-fmk, a selective caspase-8 inhibitor, caused a concentra

48 The caspase-8-specific inhibitor z-IETD-fmk, as well as pan-caspase inhibitor z-VAD-fmk, but not

49 -fmk, but not the caspase-8 inhibitor z-IETD-fmk, blocked ox-LDL-induced activation of caspase-3 and

50 ction was abrogated by the z-VAD-fmk, z-IETD-fmk, or p35 enzyme inhibitors or by a mutation in the ac

51 lts, inhibition of RSK2 by an RSK inhibitor, fmk, did not effectively induce apoptosis in BCR-ABL-exp

52 ,N-dimethyl glutaminyl fluoromethyl ketones (fmk) as severe acute respiratory syndrome coronovirus (S

53 with the caspase-9-specific inhibitor z-LEHD-fmk inhibited mAb 225-induced apoptosis, indicating that

54 f HCAECs with the caspase-9 inhibitor z-LEHD-fmk, but not the caspase-8 inhibitor z-IETD-fmk, blocked

55 Although caspase-4 inhibitor Z-LEVD-fmk and caspase-1 and -4 inhibitor Z-YVAD-fmk reduced tu

56 Furthermore, z-LEVD-fmk completely prevented poly (ADP-ribose) polymerase (P

57 panel showed that the CASP4 inhibitor z-LEVD-fmk was the most active at blocking E(2)-induced apoptos

58 ng the cells with caspase-4 inhibitor Z-LEVD-fmk, caspase-1 and -4 inhibitor Z-YVAD-fmk, and pan-casp

59 rkedly reduced by caspase-4 inhibitor Z-LEVD-fmk.

60 substrate analogue protease inhibitor z-LSTT-fmk was designed based on the dystrophin sequence that i

61 ted by the broad caspase inhibitor, zVAD(OMe)fmk, but instead reflects serine protease activity assoc

62 uma to Mcl-1 that was inhibited by IETD(OMe)-fmk but not SP600125.

63 In contrast, CrmA transfection or IETD(OMe)-fmk treatment did not inhibit fenretinide-induced apopto

64 methyl ester)-fluoromethyl ketone (IETD(OMe)-fmk) or the c-Jun N-terminal kinase inhibitor SP600125.

65 s relatively resistant to CrmA and IETD(OMe)-fmk, nor with the expression of procaspase-8 and -9, apo

66 biotinylated general caspase inhibitor b-VAD-fmk (biotin-Val-Ala-Asp(OMe)-CH(2)F) both inhibited heat

67 Additionally, b-VAD-fmk failed to label any activated initiator caspase in A

68 Affinity labeling with biotin-VAD-fmk of all active caspase species in TNFalpha-mediated a

69 binding of carboxyfluorescein conjugated VAD-fmk peptide to activated caspase enzymes.

70 FITC-VAD-fmk or antibody specific to cleaved caspase 3 was used t

71 caspase-3 were detected in situ by FITC-VAD-fmk staining and caspase-3 substrate, respectively.

72 While confirming that z-VAD-fmk (> 100 microM) enhances TNF alpha-induced neutrophil

73 ce of a broad-range caspase inhibitor, Z-VAD-fmk (100 microM, 24 h), abrogated DNA fragmentation.

74 cyl-norleucinal (a calpain inhibitor), z-VAD-fmk (a pan-caspase inhibitor), and ammonium chloride and

75 ked by the cysteine protease inhibitor Z-VAD-fmk (benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone),

76 etic mice with a pancaspase inhibitor, z-VAD-fmk (N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone)

77 partially with LDL (P < 0.01) or LDL + z-VAD-fmk (P < 0.001) but not with z-VAD-fmk alone.

78 d this was reversed with LDL and LDL + z-VAD-fmk (P < 0.001).

79 ed caspase-3 activation was blocked by z-VAD-fmk (P < 0.001).

80 scavengers, and the caspase inhibitor z-VAD-fmk (where z and fmk are benzyloxycarbonyl and fluoromet

81 cubated with the pan-caspase inhibitor z-VAD-fmk [Z-Val-Ala-Asp(OMe)-fluoromethyl ketone] and in casp

82 with the caspase inhibitor DEVD-CHO or z-VAD-fmk abolished the cleavage.

83 Conversely, the pancaspase inhibitor Z-VAD-fmk abrogates the CDDO-Im + bortezomib-induced apoptosis

84 L + z-VAD-fmk (P < 0.001) but not with z-VAD-fmk alone.

85 z-VAD-fmk also prevented PKCdelta and betaI proteolytic activa

86 ct on TNF alpha-induced apoptosis, and z-VAD-fmk and Boc-D-fmk inhibited TNF alpha-stimulated reactiv

87 d is blocked by the caspase inhibitors Z-VAD-fmk and Boc-D-fmk.

88 as inhibited by the caspase inhibitor, z-VAD-fmk and by cycloheximide, which also prevented proteolyt

89 be rescued by the caspase inhibitors, z-vad-fmk and CrmA.

90 not inhibited by the caspase inhibitor z-VAD-fmk and form independently of apoptotic DNA fragmentatio

91 ently blocked by the caspase inhibitor Z-VAD-fmk and partially blocked by Ac-DEVD-fmk, suggesting tha

92 the broad-spectrum caspase inhibitors Z-VAD-fmk and Z-DEVD-fmk failed to protect infected cell cultu

93 thermore, caspase-specific inhibitors, z-VAD-fmk and z-DEVD-fmk, significantly attenuate the accumula

94 y and that the proapoptotic effects of z-VAD-fmk are compound specific and ROS independent.

95 eatment with the pan-caspase inhibitor Z-VAD-fmk blocked MHV-induced apoptosis, suggesting an involve

96 nt of cells with the caspase inhibitor Z-VAD-fmk blocks both TPA-induced apoptosis and monocytic diff

97 t was blocked by the caspase inhibitor z-VAD-fmk but not by Fas-blocking antibody.

98 Bcl-x(L) cooperates with Z-VAD-fmk by blocking the Type II pathway at the level of cyto

99 %, respectively, pan-caspase inhibitor Z-VAD-fmk completely abolished the induced apoptosis.

100 he broad-specificity caspase inhibitor z-VAD-fmk completely blocked Mcl-1 cleavage induced by PDT, ST

101 eaks using an alkaline comet assay (+/-z-VAD-fmk cotreatment) and by levels of iododeoxyuridine-DNA i

102 e the broad-spectrum caspase inhibitor z-VAD-fmk delayed T/HS lymph-induced HUVEC cell death, but did

103 Furthermore, the pan-caspase inhibitor z-VAD-fmk did not inhibit VX-944-induced apoptosis and cell de

104 Inhibition of caspases with Z-VAD-fmk did not kill non-activated microglia, or astrocytes

105 ered by HNK, the pan-caspase inhibitor z-VAD-fmk does not abrogate HNK-induced apoptosis.

106 , the broad-spectrum caspase inhibitor z-VAD-fmk enhances tumor necrosis factor-alpha (TNF alpha)-ind

107 Further, pancaspase inhibitor Z-VAD-fmk failed to rescue these cells from apoptosis mediated

108 The pan-caspase inhibitor Z-VAD-fmk had no effect on AA-induced ceramide generation but

109 However, the pan-caspase inhibitor Z-VAD-fmk had only a modest protective effect against the drug

110 OVA-sensitized mice treated with z-VAD-fmk immediately before allergen challenge showed marked

111 rmine the specificity of the effect of z-VAD-fmk in neutrophils and define the potential mechanism of

112 ty is inhibited by Ac-IETD-CHO but not Z-VAD-fmk in vitro.

113 Treatment with z-VAD-fmk in vivo prevented subsequent T cell activation ex vi

114 Furthermore, the pan-caspase inhibitor Z-VAD-fmk inhibited AIFL induced apoptosis.

115 The general caspase inhibitor z-VAD-fmk inhibited both early and late phases of apoptosis in

116 The z-VAD-fmk inhibitor blocked caspase-3 activities in the homoge

117 Thus, Z-VAD-fmk is likely weakening the death-inducing signaling com

118 y, inhibition of caspase-3 activity by z-VAD-fmk only partially protected neurons from KA toxicity, i

119 nt with either a pan-caspase inhibitor z-VAD-fmk or a more specific caspase 3 inhibitor Ac-DEVD-CHO i

120 Using z-VAD-fmk or anti-Fas ligand mAb to inhibit cell death, we dem

121 Inhibition of caspase-8 with either Z-VAD-fmk or IETD-fmk resulted in necrosis of activated microg

122 r the broad-spectrum caspase inhibitor z-VAD-fmk or vehicle and compared with unmanipulated mice.

123 detected after MCPIP transfection and Z-VAD-fmk partially inhibited cell death.

124 Both NADH and Z-VAD-fmk reduced significantly the rate of decline of synapti

125 Treatment with the caspase inhibitor z-VAD-fmk significantly inhibited depsipeptide-induced apoptos

126 Although the caspase inhibitor z-VAD-fmk significantly reduced the number of apoptotic cells,

127 The pan-caspase inhibitor z-VAD-fmk suppressed liver injury induced by polyI:C/posthalot

128 e ability of the pan-caspase inhibitor z-VAD-fmk to prevent T/HS lymph-induced cell death.

129 In R28 cultures, the z-VAD-fmk treatment did not blocked 7kCh-induced caspase-3 act

130 z-VAD-fmk treatment had no effect on apoptosis or liver injury

131 Death induced in the presence of Z-VAD-fmk was associated with a partial inhibition of caspase-

132 bonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD-fmk) and Bcl-x(L) in a cooperative fashion.

133 rbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-fmk) inhibited PARP cleavage, DNA fragmentation, calpain

134 arbonyl-Val-Ala-Asp-fluromethylketone (z-VAD-fmk) prevented FHV-induced cytopathology and prolonged c

135 bonyl-Val-Ala-Asp-fluoromethyl-ketone (z-VAD-fmk) prevented hippocampal neuronal cell death and white

136 An inhibitor of the caspase-3 (Z-VAD-fmk) reduced apoptosis in both thymus and spleen.

137 rbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk), a peptide caspase inhibitor.

138 bonyl-Val-Ala-Asp-fluoromethyl ketone (z-VAD-fmk), and found that it caused partial inhibition of hyd

139 rbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk), on airway inflammation in OVA-sensitized/challenge

140 yloxycarbonyl-VAD-fluoromethyl ketone (Z-VAD-fmk), which inhibits proteolysis of BCL-xL during hypoxi

141 tor Z-Val-Ala-Asp-fluoromethyl ketone (Z-VAD-fmk).

142 yloxy Val-Ala-Asp-fluoromethyl ketone (z-VAD-fmk)] blocked apoptosis induced by all three of the comp

143 itor z-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk)in C3HeB/FeJ mice.

144 he transfected cells were treated with Z-VAD-fmk, a broad-spectrum caspase inhibitor, which reduced c

145 caspases-1-10 and was not inhibited by z-VAD-fmk, a broad-spectrum caspase inhibitor.

146 s could be inhibited by treatment with Z-VAD-fmk, a caspase inhibitor, and by overexpression of Bcl-2

147 Additionally, Z-VAD-fmk, a general inhibitor of caspases which inhibited cyt

148 hout low-density lipoprotein (LDL) and z-VAD-fmk, a pan-caspase inhibitor.

149 s were exposed to 7kCh with or without z-VAD-fmk, a pan-caspase inhibitor.

150 the activation-induced cell death with z-VAD-fmk, a tripeptide inhibitor of IL-1 beta-converting enzy

151 diated anoikis, an effect abrogated by Z-VAD-fmk, and decreased Akt phosphorylation (Ser-473) under a

152 ith the caspase inhibitors z-DEVD-fmk, z-VAD-fmk, and Z-CH2-Asp-DCB.

153 -fmk, as well as pan-caspase inhibitor z-VAD-fmk, but not the calpain inhibitor E-64d, prevents Bid c

154 as blocked by cycloheximide but not by z-VAD-fmk, consistent with caspase activation downstream from

155 The pan-caspase inhibitor, Z-VAD-fmk, did not prevent cell death.

156 The caspase inhibitor, z-VAD-fmk, had no effect on the induction of G2/M arrest but c

157 ily inhibited by the caspase inhibitor z-VAD-fmk, suggesting that high levels of BCL-2 expression ind

158 Death induction was abrogated by the z-VAD-fmk, z-IETD-fmk, or p35 enzyme inhibitors or by a mutati

159 urs in the absence of caspase-8 or any Z-VAD-fmk- or Boc-D-fmk-sensitive caspase activities.

160 DIAP1 was depleted despite z-VAD-fmk-mediated caspase inhibition during infection, sugges

161 ing apoptosis; p27KIP1 is cleaved by a Z-VAD-fmk-sensitive caspase during apoptosis induced by growth

162 (139)S and ESQD(108)V, by a sub-set of Z-VAD-fmk-sensitive caspases.

163 Interestingly, Z-VAD-fmk-treated cells died in a caspase- and calpain-indepen

164 y the broad spectrum caspase inhibitor z-VAD-fmk.

165 versed by a peptide caspase inhibitor, Z-VAD-fmk.

166 a broad specificity caspase inhibitor Z-VAD-fmk.

167 ly phosphatidylserine was protected by z-VAD-fmk.

168 e extent in the absence or presence of z-VAD-fmk.

169 inhibited by the pan-caspase inhibitor Z-VAD-fmk.

170 is effect by the pan-caspase inhibitor Z-VAD-fmk.

171 ted by pretreatment of HeLa cells with Z-VAD-fmk.

172 cked by the general caspase inhibitor, Z-VAD-fmk.

173 Z-YVAD-fmk, and pan-caspase inhibitor Z-VAD-fmk.

174 cerebrospinal fluid and was blocked by z-VAD-fmk.

175 as unaffected by the caspase inhibitor Z-VAD-fmk.

176 s blocked by the pan-caspase inhibitor Z-VAD-fmk.

177 ither CsA or the pan-caspase inhibitor z-VAD-fmk.

178 nzoxy-Val-Ala-Asp fluoromethyl ketone [z-VAD-fmk]), were unable to block destruction of CLL target ce

179 nd inhibition by the caspase inhibitor z-VAD.fmk (100 microM).

180 caspase inhibitor peptides, DEVD-CHO, Z-VAD.fmk, and Boc-Asp.fmk, blocked Fas-induced PS externaliza

181 y the broad-spectrum caspase inhibitor z-VAD.fmk, suggesting that mitochondria are a major target in

182 Furthermore, the caspase-6 inhibitor z-VEID-fmk mimicked the effects of caspase-6 deficiency and pre

183 ry tissue samples from CML patients, whereas fmk treatment induced significant apoptotic cell death n

184 n using a specific caspase-1 inhibitor (YVAD-fmk; 100 microM) significantly decreased high glucose-in

185 eas the caspase-1 selective inhibitor z-YVAD-fmk had no effect; z-DEVD-fmk also reduced the number of

186 VD-fmk and caspase-1 and -4 inhibitor Z-YVAD-fmk reduced tunicamycin-induced hRPE apoptotic cell deat

187 -LEVD-fmk, caspase-1 and -4 inhibitor Z-YVAD-fmk, and pan-caspase inhibitor Z-VAD-fmk.

188 The caspase inhibitors, zIETD-fmk and zDEVD-fmk, inhibited apoptosis in AIDS-KS by sApo-2L, suggesti

189 s known to inhibit caspases (zVAD-fmk, zDEVD-fmk, zIETD-fmk) as well as by overexpression of Bcl-2 pr

190 The caspase inhibitor zDEVD-fmk also partially inhibited cytochrome c translocation.

191 l-Asp-Glu-Val-Asp-fluoromethyl ketone (zDEVD-fmk), indicating activation of caspases in the apoptotic

192 inhibit caspases (zVAD-fmk, zDEVD-fmk, zIETD-fmk) as well as by overexpression of Bcl-2 providing add

193 rmA or exposure to caspase-8 inhibitor zIETD-fmk inhibited the processing of procaspase-8 and Bid but

194 of mice with the caspase 8 inhibitor, zIETD-fmk, inhibited apoptosis, inflammation, and fibrotic les

195 The caspase inhibitors, zIETD-fmk and zDEVD-fmk, inhibited apoptosis in AIDS-KS by sAp

196 Me)-Thr-Asp (OMe) fluoromethyl ketone (zIETD-fmk).

197 ectrum (BD.fmk) or caspase-8 targeted (zIETD.fmk) peptide caspase inhibitors.

198 performed with the caspase-9 inhibitor zLEHD.fmk or neutralizing antibodies against either the FAS-re

199 Injection of zLEHD.fmk into the subretinal space of a detached retina resul

200 l-Val-Ala-Asp(OMe)-fluoromethylketone (ZVAD)-fmk.

201 ZVAD-fmk and Ac-YVAD-cho were able to inhibit apoptosis when

202 zVAD-fmk, a broad spectrum inhibitor of most mammalian caspas

203 Asp(OMe)-fluoromethyl ketone] (65%) and zVAD-fmk (N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone

204 the anti-apoptotic agents, curcumin and zVAD-fmk, were tested in gup(m189) embryos.

205 blocked by caspase inhibitors, such as zVAD-fmk and crmA, and involves activation of caspase 8 and c

206 ptotic cell death, which was blocked by zVAD-fmk, a pancaspase inhibitor.

207 festations of apoptosis were blocked by zVAD-fmk, a peptide caspase inhibitor, indicating that caspas

208 e activity was significantly reduced by ZVAD-fmk, and was associated with improved viability and redu

209 cytochrome c release, was inhibited by zVAD-fmk, placing the latter event upstream of caspase activa

210 2 and 6 h posttreatment with avicins by zVAD-fmk.

211 and their toxicity was not inhibited by ZVAD-fmk.

212 combined toxicity also was inhibited by ZVAD-fmk.

213 ulation was only partially inhibited by ZVAD-fmk.

214 e inhibitors known to inhibit caspases (zVAD-fmk, zDEVD-fmk, zIETD-fmk) as well as by overexpression

215 spase inhibitor Z-Val-Ala-Asp(OMe)-CH2 (ZVAD-fmk).

216 n in the apoptotic index with high-dose ZVAD-fmk (P=0.008) and a 33% reduction with low-dose ZVAD-fmk

217 .008) and a 33% reduction with low-dose ZVAD-fmk (P=0.08).

218 spartyl-(0-methyl)- fluoromethylketone (zVAD-fmk) and the caspase-inhibiting protein X-IAP had no eff

219 arbonyl-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) did not prevent increases in deltaPsi(m).

220 onyl-Val-Ala-DL-Asp-fluoromethylketone (ZVAD-fmk) during cryopreservation of porcine hepatocytes.

221 yl-Val-Ala-Asp(Ome)-fluoromethylketone (ZVAD-fmk) or control.

222 roM CBZ-Val-Ala-Asp-fluoromethylketone (zVAD-fmk).

223 dants (propyl gallate and glutathione), zVAD-fmk, and cyclosporin A, indicating requirements of react

224 However, zVAD-fmk was efficacious in inhibiting cell death triggered b

225 <0.005) reduction in neointimal area in ZVAD-fmk-treated arteries.

226 hepatocytes that were cryopreserved in ZVAD-fmk.

227 s by 76+/-8%, and the caspase inhibitor zVAD-fmk (25 micromol/L) decreased betaAR-stimulated apoptosi

228 as, inhibition by the caspase inhibitor zVAD-fmk (zVal-Ala-Asp-fluoro-methyl ketone), activation of D

229 y the addition of the caspase-inhibitor ZVAD-fmk and involved the cytochrome c pathway.

230 e mimicked by the pan-caspase inhibitor zVAD-fmk and the serine protease inhibitor TPCK, but not the

231 blocked by a general caspase inhibitor ZVAD-fmk at 24 hours but hepatocytes still died by necrosis a

232 reatment with the pan-caspase inhibitor zVAD-fmk but not by supplementation with high folate or SAM.

233 ndependent of the pan-caspase inhibitor zVAD-fmk but were blocked fully by the irreversible calpain i

234 In contrast, the pancaspase inhibitor zVAD-fmk did not protect against FA-AKI.

235 ll death, whereas the caspase inhibitor zVAD-fmk did not provide significant protection.

236 r SP600125 or the pan-caspase inhibitor zVAD-fmk did not restore motility or levels of phosphor-cofil

237 an cooperate with the caspase inhibitor zVAD-fmk in a dose-dependent manner to block TNFalpha-induced

238 trophils with the pan-caspase inhibitor zVAD-fmk just before warming to 37 degrees C inhibited the mo

239 ic drugs, neither the caspase inhibitor zVAD-fmk nor loss of Apaf-1 affected the efflux of cytochrome

240 The caspase inhibitor ZVAD-fmk opposed potentiation of paclitaxel-induced loss of m

241 by the broad-spectrum caspase inhibitor zVAD-fmk or by expression of a dominant negative caspase 9 (9

242 reatment with the pan-caspase inhibitor zVAD-fmk partially rescued cells from UV-induced apoptosis bu

243 e pleurisy model, the caspase inhibitor zVAD-fmk prevents R-roscovitine-enhanced resolution of inflam

244 sion of Bcl-2 and the caspase inhibitor zVAD-fmk protected cells against apoptosis in the presence of

245 of cells with the pan-caspase inhibitor zVAD-fmk reduced pneumolysin-induced apoptosis.

246 y protected by the caspase-1 inhibitor (zVAD-fmk) in a dose-dependent manner.

247 nt with the universal caspase inhibitor zVAD-fmk, failed to block MDL-72,527-induced apoptosis in the

248 s: cycloheximide, pan-caspase inhibitor ZVAD-fmk, neutralizing anti-TNFR1, and anti-TNFR2.

249 inhibited by the pan-caspase inhibitor ZVAD-fmk, whereas the increase in sub-G1 population was only

250 lly, we show that the caspase inhibitor zVAD-fmk, which blocks developmentally regulated cell death,

251 prevented by the pan-caspase inhibitor zVAD-fmk.

252 by the broad-spectrum caspase inhibitor zVAD-fmk.

253 V, and inhibition by caspase inhibitor zVAD-fmk.

254 eine and DTT) and the caspase inhibitor ZVAD-fmk.

255 be blocked by the pan-caspase inhibitor zVAD-fmk.

256 uced mortality by the caspase inhibitor zVAD-fmk.

257 was prevented by the caspase inhibitor, zVAD-fmk (zVal-Ala-Asp-CH2F).

258 The pan-caspase inhibitor, ZVAD-fmk, and the caspase-1 inhibitor, Ac-YVAD-cho, both inhi

259 nt manner, but a pan-caspase inhibitor, zVAD-fmk, blocked cytochrome c release.

260 siRNA or employing a caspase inhibitor, zVAD-fmk, did not block p38 MAPK activation suggesting its ac

261 A caspase inhibitor, zVAD-fmk, prevented epitope-tagged PKCzeta processing and act

262 reatment with the pancaspase inhibitor, zVAD-fmk.

263 ted with the peptide Caspase inhibitors zVAD-fmk or DEVD-cho at HH stages 15-20 (looped heart).

264 rbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk) and benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethyl

265 -Val-Ala-Asp (OMe) fluoromethyl ketone (zVAD-fmk) and carbobenzyloxy-Ile-Glu(OMe)-Thr-Asp (OMe) fluor

266 ic inhibitors zVAD-fluoromethyl ketone (zVAD-fmk) and N-acetyl-Asp-Glu-Val-Asp-aldehyde (DEVD-CHO), i

267 rbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk) directly after transduction almost completely preve

268 rbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk), although capable of altering the kinetics and perh

269 rbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk).

270 zVal-Ala-Asp(OMe)-fluoromethyl ketone (zVAD-fmk).

271 9%) were cryopreserved in 60 micromol/L ZVAD-fmk (+ZVAD group) or without ZVAD-fmk (-ZVAD group) for

272 rbonyl-Val-Ala-Asp-fluoro methylketone (zVAD-fmk).

273 Moreover, zVAD-fmk inhibits caspase-1 activity as well as caspase-1 and

274 The local delivery of ZVAD-fmk during balloon injury inhibits smooth muscle cell ap

275 in a 10-fold decrease in the amount of zVAD-fmk required to inhibit TNFalpha-induced apoptosis.

276 blocking apoptosis by administration of zVAD-fmk to wild-type mice resulted in a significant increase

277 tracerebroventricular administration of zVAD-fmk, a broad caspase inhibitor, delays disease onset and

278 rexpressing cells or in the presence of zVAD-fmk.

279 ich was still active in the presence of zVAD-fmk.

280 AIF knockdown, even in the presence of zVAD-fmk.

281 Caspase inhibitors DEVD or zVAD-fmk had no effect on cytochrome c release, suggesting th

282 e cysteine aspartase inhibitory peptide zVAD-fmk conferred protection from NGF withdrawal and SOD1 de

283 Bax insertion was only sensitive to zVAD-fmk when added at the start of the 15 degrees C culture

284 f the population, while two-thirds were ZVAD-fmk insensitive but TUNEL-positive.

285 ignificantly higher virus yields, while zVAD-fmk completely inhibited virus replication until 10 h p.

286 dp27-infected cells by threefold, while ZVAD-fmk reduced sub-G1 to control levels.

287 In contrast, while zVAD-fmk significantly inhibited BeAn virus replication in BH

288 Inactivating caspases with zVAD-fmk also reduced the death rate of E7 and E6 cells.

289 -expressing Bcl-2-/- cells treated with zVAD-fmk was increased under caspase-8 depletion.

290 d also show the same cooperativity with zVAD-fmk.

291 mol/L ZVAD-fmk (+ZVAD group) or without ZVAD-fmk (-ZVAD group) for 24 to 72 hours.

292 Apoptosis was blocked by zVAD.fmk, and partially by a cathepsin inhibitor.

293 Finally, the caspase inhibitor zVAD.fmk attenuates the increased mineralization induced by k

294 The general caspase inhibitor zVAD.fmk blocked caspase activation, poly(ADP-ribose) polymer

295 nd the broad spectrum caspase inhibitor ZVAD.fmk did not block cell death.

296 of apoptosis with the caspase inhibitor ZVAD.fmk reduced calcification in nodules by approximately 40

297 f the broad spectrum caspase inhibitor, zVAD.fmk.

298 rbonyl-Val-Ala-Asp fluoro-methylketone (ZVAD.fmk) had no effect on the induction of hMyD118, indicati

299 s attenuated by caspase inhibition with zVAD.fmk.

300 the addition of a pancaspase inhibitor, zVD.fmk, demonstrating that experimental manipulation of the