ライフサイエンスコーパス: z-VAD-FMK

1 inhibitor Z-Val-Ala-Asp-fluoromethyl ketone (Z-VAD-fmk).

2 loxycarbonyl-Val-Ala-Asp fluoromethylketone (Z-VAD-FMK).

3 y cotreatment with the pan-caspase inhibitor Z-VAD-FMK.

4 was suppressed by the pan-caspase inhibitor Z-VAD-FMK.

5 ted by a broad specificity caspase inhibitor Z-VAD-fmk.

6 ich only phosphatidylserine was protected by z-VAD-fmk.

7 he same extent in the absence or presence of z-VAD-fmk.

8 of this effect by the pan-caspase inhibitor Z-VAD-fmk.

9 t was inhibited by the pan-caspase inhibitor Z-VAD-fmk.

10 ibitor Z-YVAD-fmk, and pan-caspase inhibitor Z-VAD-fmk.

11 markedly prevented by the caspase inhibitor z-VAD-FMK.

12 inhibited by pretreatment of HeLa cells with Z-VAD-fmk.

13 re blocked by the general caspase inhibitor, Z-VAD-fmk.

14 prominent N-terminal product was blocked by Z-VAD-FMK.

15 lamed cerebrospinal fluid and was blocked by z-VAD-fmk.

16 hibited apoptosis using pancaspase inhibitor Z-VAD-FMK.

17 AD-CMK, and the tripeptide pan-ICE inhibitor Z-VAD-FMK.

18 ocked by the ICE family inhibitors, CrmA and z-VAD-fmk.

19 ivo treatment with the pan-caspase inhibitor Z-VAD-FMK.

20 and was unaffected by the caspase inhibitor Z-VAD-fmk.

21 beta1 was inhibited only in the presence of z-VAD-FMK.

22 was not blocked by the pan-caspase inhibitor z-VAD-FMK.

23 with either CsA or the pan-caspase inhibitor z-VAD-fmk.

24 ited by the broad spectrum caspase inhibitor z-VAD-fmk.

25 was reversed by a peptide caspase inhibitor, Z-VAD-fmk.

26 that is blocked by the pan-caspase inhibitor Z-VAD-fmk.

27 ssing of caspases-3 and -7 were prevented by Z-VAD.FMK.

28 prevented by the general caspase inhibitor, Z-VAD.FMK.

29 ibited by the pan-caspase peptide inhibitor, Z-VAD.FMK.

30 ctive loss of eIF4G, which is inhibitable by Z-VAD.FMK.

31 presence of a broad-range caspase inhibitor, Z-VAD-fmk (100 microM, 24 h), abrogated DNA fragmentatio

32 ing, and inhibition by the caspase inhibitor z-VAD.fmk (100 microM).

33 optosis, because caspase apoptosis inhibitor Z-VAD-FMK (20 microM), had no effect on this response.

34 Caspase inhibition (Z-VAD-FMK, 50 um) attenuated cell death with immunostain

35 yl-leucyl-norleucinal (a calpain inhibitor), z-VAD-fmk (a pan-caspase inhibitor), and ammonium chlori

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

37 oxycarbonyl-val-ala-asp-fluoromethyl ketone (z-VAD.FMK), a nonselective caspase inhibitor, did not af

38 f apoptosis to organ damage, we administered Z-VAD-FMK, a broad-spectrum caspase inhibitor, to mice w

39 iii) the transfected cells were treated with Z-VAD-fmk, a broad-spectrum caspase inhibitor, which red

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

41 optosis could be inhibited by treatment with Z-VAD-fmk, a caspase inhibitor, and by overexpression of

42 optosis was inhibited by treating cells with Z-VAD-fmk, a cell-permeable fluoromethylketone inhibitor

43 Additionally, Z-VAD-fmk, a general inhibitor of caspases which inhibit

44 or without low-density lipoprotein (LDL) and z-VAD-fmk, a pan-caspase inhibitor.

45 9 cells were exposed to 7kCh with or without z-VAD-fmk, a pan-caspase inhibitor.

46 Z-VAD-FMK, a pancaspase inhibitor, inhibits AGN193198-de

47 We show that z-VAD-fmk, a tripeptide inhibitor of ICE homologues, can

48 block the activation-induced cell death with z-VAD-fmk, a tripeptide inhibitor of IL-1 beta-convertin

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

50 Cotreatment with the caspase-3 inhibitor Z-VAD-FMK abrogated the effect of FTY720 on facilitating

51 Conversely, the pancaspase inhibitor Z-VAD-fmk abrogates the CDDO-Im + bortezomib-induced apo

52 loxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD.FMK), acetyl-Tyr-Val-Ala-Asp-chloromethylketone, o

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

54 Z-VAD-FMK also abrogates the inhibitory effect of PS-341

55 z-VAD-fmk also inhibited activation (anti-CD3)- induced

56 z-VAD-fmk also prevented PKCdelta and betaI proteolytic

57 luoromethylornithine, the caspase inhibitors Z-VAD FMK and Z-DEVD FMK, and c-Myc antisense oligodeoxy

58 o effect on TNF alpha-induced apoptosis, and z-VAD-fmk and Boc-D-fmk inhibited TNF alpha-stimulated r

59 ne, and is blocked by the caspase inhibitors Z-VAD-fmk and Boc-D-fmk.

60 tion was inhibited by the caspase inhibitor, z-VAD-fmk and by cycloheximide, which also prevented pro

61 ily blocked by the general caspase inhibitor Z-VAD-Fmk and by the caspase 1 inhibitor Z-YVAD-Fmk.

62 The general caspase inhibitor Z-VAD-FMK and caspase-3 inhibitor Z-DEVD-FMK decreased a

63 is can be rescued by the caspase inhibitors, z-vad-fmk and CrmA.

64 s are not inhibited by the caspase inhibitor z-VAD-fmk and form independently of apoptotic DNA fragme

65 Moreover, coapplication of Z-VAD-FMK and nifedipine produced virtually complete neu

66 efficiently blocked by the caspase inhibitor Z-VAD-fmk and partially blocked by Ac-DEVD-fmk, suggesti

67 were inhibited by the pan-caspase inhibitor Z-VAD-FMK and partially inhibited by the caspase-3 inhib

68 The caspase inhibitors Z-VAD-FMK and Z-DEVD-FMK blocked apoptosis induced by CD

69 trast, the broad-spectrum caspase inhibitors Z-VAD-fmk and Z-DEVD-fmk failed to protect infected cell

70 Furthermore, caspase-specific inhibitors, z-VAD-fmk and z-DEVD-fmk, significantly attenuate the ac

71 and addition of caspase peptide substrates (Z-VAD-FMK and Z-IETD-FMK) to NS3-transfected cells block

72 Only z-VAD.FMK and acetyl-Tyr-Val-Ala-Asp-chloromethylketone

73 ls to a combination of the caspase inhibitor z-VAD.FMK and the survival factor erythropoietin prevent

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

75 oxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD-FMK) and N-benzyloxycarbonyl-Asp-glu-Val-Asp-fluor

76 The pancaspase inhibitor (Z-VAD-FMK) and the caspase-9 inhibitor (Z-LEHD-FMK) were

77 oxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (z-VAD-fmk), and found that it caused partial inhibition

78 arbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (Z-VAD-FMK), and moderately blocked by the specific caspa

79 ere pretreated with a pan-caspase inhibitor, Z-VAD-FMK, and a specific caspase-9 inhibitor, Z-LEHD-FM

80 a (TNFalpha) and the broad caspase inhibitor Z-VAD-FMK, and by immunoblotting of lysates from endothe

81 ase-mediated anoikis, an effect abrogated by Z-VAD-fmk, and decreased Akt phosphorylation (Ser-473) u

82 ally inhibited by the pan-caspase inhibitor, z-VAD-FMK, and has no cross-reactivity with other known

83 revented by a generalized caspase inhibitor, z-VAD-FMK, and the more specific caspase inhibitor, z-DE

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

85 The caspase inhibitor peptides, DEVD-CHO, Z-VAD.fmk, and Boc-Asp.fmk, blocked Fas-induced PS exter

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

87 y blocked by the cysteine protease inhibitor Z-VAD-fmk (benzyloxycarbonyl-Val-Ala-Asp-fluoromethylket

88 Z-VAD.FMK [benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromet

89 Treatment with the pan-caspase inhibitor Z-VAD-fmk blocked MHV-induced apoptosis, suggesting an i

90 Similarly, in intact cells, although Z-VAD.FMK blocked TGF-beta(1)-induced apoptosis, it did

91 itor Z-Val-Ala-Asp(OMe)-fluoromethyl ketone (Z-VAD-FMK) blocked >50% of ouabain-induced neuronal deat

92 tment with caspase inhibitors (Z-DEVD-FMK or Z-VAD-FMK) blocked MMT-induced proteolytic cleavage of P

93 [benzyloxy Val-Ala-Asp-fluoromethyl ketone (z-VAD-fmk)] blocked apoptosis induced by all three of th

94 The caspase inhibitor, Z-VAD-FMK, blocked the decrease in Mdm2 as well as the i

95 reatment of cells with the caspase inhibitor Z-VAD-fmk blocks both TPA-induced apoptosis and monocyti

96 o, the addition of the pan-caspase inhibitor Z-VAD-FMK blocks formation of the 23-kDa ErbB-2 fragment

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

98 pramipexole (PPX) and the caspase inhibitor Z-VAD-FMK but not by the poly (ADP-ribose) polymerase (P

99 e inhibited by the general caspase inhibitor Z-VAD-FMK, but not by NOK-1 or Fas-Fc.

100 was blocked by a general caspase inhibitor, Z-VAD-FMK, but not by specific inhibitors against caspas

101 z-IETD-fmk, as well as pan-caspase inhibitor z-VAD-fmk, but not the calpain inhibitor E-64d, prevents

102 Bcl-x(L) cooperates with Z-VAD-fmk by blocking the Type II pathway at the level o

103 and 86%, respectively, pan-caspase inhibitor Z-VAD-fmk completely abolished the induced apoptosis.

104 The broad-specificity caspase inhibitor z-VAD-fmk completely blocked Mcl-1 cleavage induced by P

105 is study, crmA antagonized, and YVAD-CMK and Z-VAD-FMK completely inhibited, Fas activation of p38 ki

106 ease was blocked by cycloheximide but not by z-VAD-fmk, consistent with caspase activation downstream

107 insensitive to the general caspase inhibitor z-VAD.FMK, consistent with a caspase-independent mechani

108 and breaks using an alkaline comet assay (+/-z-VAD-fmk cotreatment) and by levels of iododeoxyuridine

109 z-VAD.FMK decreased ICE-like cleavage products and tissu

110 Moreover, the pan-Casp inhibitor Z-VAD-FMK delayed cornification, and corneocytes were st

111 , since the broad-spectrum caspase inhibitor z-VAD-fmk delayed T/HS lymph-induced HUVEC cell death, b

112 Furthermore, the pan-caspase inhibitor z-VAD-fmk did not inhibit VX-944-induced apoptosis and c

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

114 In clonogenic assays, Z-VAD-FMK did not rescue cells treated with VP-16 in con

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

116 asome inhibitor MG-132 and caspase inhibitor Z-VAD-FMK do not block ATRA-induced PML-RARalpha cleavag

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

118 a broad-range inhibitor of caspase activity, z-vad-FMK, efficiently blocked DNA fragmentation, (ii) c

119 owever, the broad-spectrum caspase inhibitor z-VAD-fmk enhances tumor necrosis factor-alpha (TNF alph

120 Further, pancaspase inhibitor Z-VAD-fmk failed to rescue these cells from apoptosis me

121 fusion protein or general caspase inhibitor Z-VAD-FMK followed by silicon phthalocyanine 4 photodyna

122 n Fas, Ac-DEVD-CHO (caspase-3 inhibitor), or Z-VAD-FMK (general caspase inhibitor), apoptosis and pro

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

124 The pan-caspase inhibitor Z-VAD-fmk had no effect on AA-induced ceramide generatio

125 apoptotic cells in the CL group, the use of z-VAD-FMK had no effect on the frequency of these cells.

126 non-apoptotic in nature and GM1, LIGA20 and Z-VAD-FMK had no protective effects.

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

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

129 OVA-sensitized mice treated with z-VAD-fmk immediately before allergen challenge showed m

130 of cell death was reduced by the addition of Z-VAD-FMK in chondroitinase ABC-treated explants and was

131 o determine the specificity of the effect of z-VAD-fmk in neutrophils and define the potential mechan

132 activity is inhibited by Ac-IETD-CHO but not Z-VAD-fmk in vitro.

133 Treatment with z-VAD-fmk in vivo prevented subsequent T cell activation

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

135 ingly, blocking of the apoptotic pathway, by Z-VAD-FMK, in p21(-/-) HCT116 cells following treatment

136 was inhibited by treatment of the cells with Z-VAD.FMK, indicating it is caspase-dependent.

137 Treatment of L929 cells with TNFalpha and Z-VAD-FMK induced caspase-independent cell death with ne

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

139 l three cell lines with a caspases inhibitor z-VAD-FMK inhibited apoptosis.

140 The general caspase inhibitor z-VAD-fmk inhibited both early and late phases of apopto

141 loxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-fmk) inhibited PARP cleavage, DNA fragmentation, c

142 The z-VAD-fmk inhibitor also enhanced survival of T cells in

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

144 Z-VAD-FMK inhibits PARP cleavage, but does not alter the

145 administration of the pan caspase inhibitor, Z-VAD-FMK into normal mice protected against Chlamydia-i

146 Thus, Z-VAD-fmk is likely weakening the death-inducing signali

147 The pan-caspase inhibitor Z-VAD-FMK largely restored the growth of ADdlUL38 in nor

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

149 g diabetic mice with a pancaspase inhibitor, z-VAD-fmk (N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylk

150 Finally, we examined the effect of z-VAD.FMK on excitotoxicity and found that it protected

151 loxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk), on airway inflammation in OVA-sensitized/cha

152 Finally, inhibition of caspase-3 activity by z-VAD-fmk only partially protected neurons from KA toxic

153 reatment with either a pan-caspase inhibitor z-VAD-fmk or a more specific caspase 3 inhibitor Ac-DEVD

154 by broad range synthetic caspase inhibitors z-VAD-fmk or a viral protein CrmA.

155 Using z-VAD-fmk or anti-Fas ligand mAb to inhibit cell death,

156 tor Z-DEVD-FMK and general caspase inhibitor Z-VAD-FMK or Fas-deficient mice abrogated the complete d

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

158 z-VAD-FMK or leupeptin delayed, but did not inhibit, cel

159 either the broad-spectrum caspase inhibitor z-VAD-fmk or vehicle and compared with unmanipulated mic

160 The caspase peptide inhibitors z-VAD-FMK or z-DEVD-FMK blocked both cleavage events.

161 -starved or cycloheximide-treated cells with Z-VAD.FMK or Z-DEVD.FMK, which inhibit caspases required

162 ycarbonyl-Val-Ala-DL-Asp-fluoromethylketone (Z-VAD-FMK), or Z-Asp-2,6-dichlorobenzoyloxymethylketone

163 de occurs in the absence of caspase-8 or any Z-VAD-fmk- or Boc-D-fmk-sensitive caspase activities.

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

165 1), and this was reversed with LDL and LDL + z-VAD-fmk (P < 0.001).

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

167 loxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-FMK pan-caspase inhibitor) blocked T lymphocyte pr

168 -3 was detected after MCPIP transfection and Z-VAD-fmk partially inhibited cell death.

169 arbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (z-VAD-FMK) prevented all of these events except release

170 yloxycarbonyl-Val-Ala-Asp-fluromethylketone (z-VAD-fmk) prevented FHV-induced cytopathology and prolo

171 oxycarbonyl-Val-Ala-Asp-fluoromethyl-ketone (z-VAD-fmk) prevented hippocampal neuronal cell death and

172 Moreover, the general caspase inhibitor Z-VAD-FMK protected cells from bFGF-induced cell death.

173 carbonyl-V-A-D-O-methyl fluoromethyl ketone (Z-VAD-FMK; R & D Systems) given to SCID mice 2 h prior t

174 Both NADH and Z-VAD-fmk reduced significantly the rate of decline of s

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

176 val, since addition of the caspase inhibitor z-VAD-FMK rescues cell death associated with loss of Akt

177 as markedly induced and caspase inhibitor 1 (Z-VAD-FMK)-sensitive oligonucleosome-length DNA fragment

178 ed during apoptosis; p27KIP1 is cleaved by a Z-VAD-fmk-sensitive caspase during apoptosis induced by

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

180 The caspase inhibitor Z-VAD-FMK significantly increased cell survival but did

181 Treatment with the caspase inhibitor z-VAD-fmk significantly inhibited depsipeptide-induced a

182 administration of the pan-caspase inhibitor Z-VAD-FMK significantly reduced cartilage degradation, a

183 Although the caspase inhibitor z-VAD-fmk significantly reduced the number of apoptotic

184 at addition of the general caspase inhibitor Z-VAD-FMK substantially increases the number of both mat

185 was inhibited by the pan-caspase inhibitor, z-VAD-FMK suggesting that ABT-263 potentiated caspase-de

186 sed in the presence of the caspase inhibitor Z-VAD-FMK, suggesting a new role of activated caspases i

187 as not inhibited by the pancaspase inhibitor Z-VAD-FMK, suggesting cell necrosis.

188 t MEHP treatment was profoundly inhibited by Z-VAD-FMK, suggesting that 15d-PGJ(2) activates apoptosi

189 etely abrogated by the pan-caspase inhibitor Z-VAD-FMK, suggesting that downregulation of gp130 is me

190 e readily inhibited by the caspase inhibitor z-VAD-fmk, suggesting that high levels of BCL-2 expressi

191 and etoposide was resistant to YVAD-CMK and Z-VAD-FMK, suggesting the existence of an additional mec

192 not by the broad-spectrum caspase inhibitor z-VAD.fmk, suggesting that mitochondria are a major targ

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

194 The caspase inhibitors (Z-DEVD-FMK and Z-VAD-FMK) suppressed CD437-induced CPP32-like caspase a

195 ficantly reduced by the pancaspase inhibitor Z-VAD-FMK, TCR-zeta degradation was not prevented.

196 Direct addition of z-VAD-FMK to infected cultures abolished cellular caspas

197 Using z-VAD-FMK to inhibit Kgp activity and leupeptin to inhib

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

199 aspase inhibitors (B-D-Fluomethyl Ketone and Z-VAD-FMK) to reduce apoptosis, and by using the postpul

200 s described for using the caspase inhibitor, z-VAD-FMK, to block apoptosis and generate a synchronous

201 Interestingly, Z-VAD-fmk-treated cells died in a caspase- and calpain-i

202 PARP p85 and active caspase 3 was reduced in Z-VAD-FMK-treated knees.

203 We found that Z-VAD-FMK-treated septic mice had decreased levels of hi

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

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

206 through caspase activation was confirmed by Z-VAD-FMK treatment.

207 yl-Val-Ala-Asp(O-methyl)-fluoromethylketone (z-VAD-fmk) under conditions that abrogated apoptosis.

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

209 AICD that could be inhibited by z-VAD-fmk was Fas independent and could be inhibited wit

210 Further, pretreatment of cells with Z-VAD-FMK was found to suppress the cleavage of NF-kappa

211 arbobenzoxy-Val-Ala-Asp fluoromethyl ketone [z-VAD-fmk]), were unable to block destruction of CLL tar

212 ), ROS scavengers, and the caspase inhibitor z-VAD-fmk (where z and fmk are benzyloxycarbonyl and flu

213 r benzyloxycarbonyl-VAD-fluoromethyl ketone (Z-VAD-fmk), which inhibits proteolysis of BCL-xL during

214 loxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-fmk), which suggests that an interleukin-1 beta co

215 ceramide production that was also blocked by Z-VAD-fmk, which suggests that ceramide generation requi

216 Furthermore, z-VAD-fmk, which targets the pro-apoptotic interleukin-1

217 preincubated with the pan-caspase inhibitor z-VAD-fmk [Z-Val-Ala-Asp(OMe)-fluoromethyl ketone] and i

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