ライフサイエンスコーパス: caspase 7

1 tion of ER function depended additionally on caspase 7.

2 h activation of procaspase 9, caspase 3, and caspase 7.

3 d in vitro by both recombinant caspase-3 and caspase-7.

4 its ability to interact with and neutralize caspase-7.

5 downstream effector caspases, caspase-3 and caspase-7.

6 talytic activity as a domain of fully active caspase-7.

7 inhibitor sensitivity compared to processed caspase-7.

8 is as evidenced by the activation of BAK and caspase-7.

9 le approximately 200-kDa complex with active caspase-7.

10 ated with reduced induction of caspase-3 and caspase-7.

11 ification of the activation of caspase-9 and caspase-7.

12 pases that include caspase-9, caspase-3, and caspase-7.

13 th an increase in cleaved PARP and activated caspase-7.

14 rase (PARP) and activated both caspase-9 and caspase-7.

15 ed domain of ORF57 prevents its digestion by caspase-7.

16 ios inactive caspase-9 became complexed with caspase-7.

17 e not inhibitors of downstream caspase-3 and caspase-7.

18 on indirectly by activating caspase-3 and/or caspase-7.

19 amily of cell death proteases: caspase-3 and caspase-7.

20 amily of cell-death proteases, caspase-3 and caspase-7.

21 onformationally dynamic than closely related caspase-7.

22 detectable by analyzing cleavage of PARP and caspase-7.

23 acilitates cell proliferation is mediated by caspase 7, a protein that typically promotes cell death.

24 Indeed, caspase-7, a member of the caspase-3 subfamily, was foun

25 tage transgenic mSOD1 mice is the downstream caspase-7 activated and the inhibitor of apoptosis, XIAP

26 imentally, and we have now characterized the caspase-7 activating apoptosome complex in MCF-7 cell ly

27 but did not involve detectable caspase 3 or caspase 7 activation.

28 drial cytochrome c release and caspase 3 and caspase 7 activation.

29 , which promotes 5-FU mediated p53-dependent caspase-7 activation and hepatocyte growth inhibition.

30 ere that specific expression of GRP78 blocks caspase-7 activation by etoposide both in vivo and in vi

31 The mechanism of caspase-7 activation by granzyme B and caspase-3 has bee

32 in MCF-7 cells because it directly inhibits caspase-7 activation by the apoptosome and also forms a

33 B cells with lytic KSHV infection and caspase-7 activation exhibited a greatly reduced level o

34 not play a detectable role in 5-FU-mediated caspase-7 activation in the absence of functional p53 in

35 Our data suggest that caspase-7 activation proceeds through a previously uncha

36 not trigger endoplasmic reticulum stress or caspase-7 activation, and did not induce tumor cell deat

37 ndergo mitochondrial-dependent apoptosis via caspase-7 activation.

38 with associated increased caspase-3 but not caspase-7 activation.

39 nhibits 1-LN cell proliferation and promotes caspase-7 activity by a mechanism that requires binding

40 ve ductal carcinoma by negatively regulating caspase-7 activity.

41 Caspase-3 (and/or caspase-7) activity, as measured in cell lysates with th

42 ell death, indexed as DEVDase (caspase-3 and caspase-7) activity.

43 ression of exogenous caspase-7 by adenovirus-caspase-7 (Ad-casp-7) in SKBr3 cells resulted in apoptos

44 e of compensatory activation by caspase-6 or caspase-7 after ischemia.

45 pase-3, which then removes the propeptide of caspase-7 allowing activation by GrB.

46 Caspase-7, an executor caspase that is associated with t

47 ave TcapQ647 with a kcat 7-fold greater than caspase 7 and 16-fold greater than caspase 6.

48 ase 9, cooperated with RA in activating both caspase 7 and 9, and amplified the ability of RA to trig

49 ulated the expression of Apaf1 and triggered caspase 7 and caspase 9 cleavage.

50 ion of several proapoptotic genes, including caspase 7 and caspase 9.

51 , and two apoptotic marker proteins, cleaved caspase 7 and cleaved poly(ADP-ribose) polymerase, were

52 ption of the proapoptotic genes CD95/Fas and caspase 7 and de-repressing the expression of the antiap

53 mitochondria-targeted Bak leads to enhanced caspase 7 and PARP cleavage in comparison with the ER-ta

54 atches the activation sites of caspase 3 and caspase 7 and thus is consistent with the role of granzy

55 ers, GrB in vitro most efficiently processes caspase-7 and -10.

56 These studies have demonstrated that caspase-7 and -3 are critical mediators of apoptosis in

57 Moreover, wild-type caspase-7 and a chimeric caspase-3 (bearing the AKPD mot

58 ted in cleavage and nuclear translocation of caspase-7 and caspase-3 in hypoglossal and facial motone

59 arcinoma cell lines and that, in addition to caspase-7 and caspase-3, there are other factors that co

60 Caspase-7 and caspase-8 were not activated.

61 Curcumin also activated caspase-7 and caspase-9 and induced polyadenosine-5'-dip

62 However, Smac is effective in removing caspase-7 and caspase-9 inhibition by XIAP fragments con

63 ring RNA resulted in decreased expression of caspase-7 and cleaved poly(ADP-ribose) polymerase expres

64 t aspartate-directed proteases caspase-3 and caspase-7 and degradation of the caspase substrates poly

65 oted DNA fragmentation more effectively than caspase-7 and endogenous levels of caspase-7 failed to i

66 se-7 and XIAP closely resemble those between caspase-7 and its tetrapeptide inhibitor DEVD-CHO.

67 addition, Smac forms a ternary complex with caspase-7 and linker_BIR2, suggesting that Smac/linker_B

68 F-7 cells after UV treatment, as measured by caspase-7 and PARP cleavage, and IGF-I co-treatment prot

69 Activation of caspase-7 and PARP proteolysis were delayed in LN-56 und

70 erestingly, we found that PAK2 can bind with caspase-7 and phosphorylate caspase-7 at the Ser-30, Thr

71 o-apoptotic protein Bim/Bod, and cleavage of caspase-7 and poly (ADP-ribose) polymerase.

72 on cDDP-induced activation of caspase-3 and caspase-7 and the cleavage of poly(ADP-ribose) polymeras

73 MAF)] stimulated the activation of caspase-3/caspase-7 and the death of EphA2-expressing cells with I

74 dose- and time-dependent increase in active caspase-7 and up-regulation of p53 and p21 protein.

75 ystal structure of the complex between human caspase-7 and XIAP (BIR2 and the proceeding linker).

76 rientation, a subset of interactions between caspase-7 and XIAP closely resemble those between caspas

77 but it did partially regulate activation of caspase-7 and, more importantly, was necessary for late

78 This cell death was mediated through caspases 7 and 4.

79 drial release of cytochrome c, activation of caspases 7 and 9, and apoptosis did not occur unless TRA

80 eported that ectopically expressed GRP78 and caspases-7 and -12 form a complex, thus coupling ER stre

81 that processing of caspases, in particular, caspases-7 and -3, occurs during Fas-induced apoptosis o

82 ns 2 and 3 of the two cIAPs are able to bind caspases-7 and -9.

83 Caspase 3(-/-)/caspase 7(-/-) and caspase 9(-/-) MEFs also exhibited de

84 Both caspase 3(-/-)/caspase 7(-/-) and caspase 9(-/-) MEFs were resistant to

85 the Fas ligand, Fas-associated death domain, caspase 7, and caspase 6, suggesting that apoptotic mole

86 NEDD8 to ubiquitin substrates, such as p53, Caspase 7, and Hif1alpha, demonstrating that overexpress

87 P21 is detected only after activation of caspase 7, and P53 is neither expressed at baseline nor

88 he proapoptotic molecules pro-caspase-3, pro-caspase-7, and Bax to induce therapeutic apoptosis of pr

89 the apoptotic molecules such as caspase-12, caspase-7, and CAAT/enhancer binding protein homologous

90 F into the cytosol and caspase-9, caspase-3, caspase-7, and caspase-8 activation.

91 n substrates with those found for caspase-3, caspase-7, and caspase-8, involved in apoptosis.

92 a reduction in protein levels of caspase-3, caspase-7, and caspase-9 in human colon cancer specimens

93 -PERK, phospho-eIF2alpha, GRP94, caspase-12, caspase-7, and CHOP/GADD153 was significantly muted.

94 regulation of the abundance of p53, cleaved caspase-7, and cleaved PARP.

95 protein levels of cleaved caspase-3, cleaved caspase-7, and cleaved poly(ADP-ribose) polymerase (PARP

96 f Bcl-2 protein, activation of caspase-9 and caspase-7, and degradation of PARP.

97 ting the executioner caspases, caspase-3 and caspase-7, and have a low potency for inhibiting caspase

98 ith IFNgamma-induced expression of STAT2 and caspase-7, and HDAC inhibitors did not preclude IFNgamma

99 rane permeabilization, via the activation of caspase-7, and identify the salvage pathway as the criti

100 ptosis in MM cells via caspase-8, caspase-3, caspase-7, and poly (ADP-ribose) polymerase cleavage.

101 n, decreased full-length Bid, caspase-9, and caspase-7, and significantly increased DNA fragmentation

102 e (H2AX) and apoptotic markers (p53, cleaved caspase-7, and TUNEL-positive cells).

103 Here we report that ataxin-7 is cleaved by caspase-7, and we map two putative caspase-7 cleavage si

104 A majority of the cells expressing active caspase-7 appeared to have no detectable ORF57 and vice

105 Apoptotic caspases, such as caspase-7, are stored as inactive protease zymogens, and

106 Identification of caspase-7 as a potential mediator of lovastatin-induced

107 s (K(38)KKK) within the N-terminal domain of caspase-7 as critical elements for the efficient proteol

108 embrane protein, as well as co-localize with caspase-7, as confirmed by fluorescence microscopy.

109 Caspase-7 associates with caspase-12 and cleaves the pro

110 -8 and cleavage of ORF57 in the cytoplasm by caspase-7 at the aspartate residue at position 33 from t

111 K2 can bind with caspase-7 and phosphorylate caspase-7 at the Ser-30, Thr-173, and Ser-239 sites.

112 sults suggest that cleavage of PKCepsilon by caspase-7 at the SSPD downward arrow G site results in t

113 CD80), regulators of apoptosis (granzyme B, caspase 7, Bak1, Bax, and BclII), interferon-inducible g

114 The x-ray crystal structures of caspase-7 bound by either compound demonstrates that the

115 An X-ray crystal structure of caspase-7 bound to a fragment hit and a thorough kinetic

116 DFF45 can also be cleaved and inactivated by caspase-7 but not by caspase-6 and caspase-8.

117 teraction assays revealed that caspase-3 and caspase-7 (but not caspase-8) blocked the binding of the

118 Caspase-7, but not caspase-3, underwent proteolytic acti

119 nalysis revealed that Fas-ligation activated caspase-7, but not caspase-3.

120 Expression of exogenous caspase-7 by adenovirus-caspase-7 (Ad-casp-7) in SKBr3 c

121 Further, cleavage at amino acid 45/47 of caspase-7 by calpain results in a reduction in nuclear l

122 ther compound demonstrates that they inhibit caspase-7 by trapping a zymogen-like conformation.

123 hanges include activation of caspase 3 (C3), caspase 7 (C7), and nuclear factor kappaB (NFkappaB).

124 olytic maturation to form caspase-3 (C3) and caspase-7 (C7), respectively, which serve overlapping bu

125 sient intermediate of singly cleaved dimeric caspase-7 can be found in a cell-free model of apoptosis

126 nal activation of the ERSR-induced CASP3 and caspase 7 (CASP7) maintains uterine quiescence through p

127 Polymorphisms in Caspase-7 (CASP7) may modulate the programmed cell death

128 cancer cells rely heavily on the activity of caspase-7 (CASP7) to initiate apoptosis, inhibition of a

129 3 expression and variable down-regulation of caspase-7, caspase-8, and caspase-10.

130 ombination enhanced activation of caspase-3, caspase-7, caspase-8, and caspase-9 and the subsequent c

131 f cytochrome c, and activation of caspase-3, caspase-7, caspase-8, and caspase-9.

132 s as characterized by cleavage of caspase-3, caspase-7, caspase-8, caspase-9, caspase-10, BID, and po

133 Using caspase-3, caspase-7, caspase-8, neutrophil elastase, legumain, and

134 egulation of caspase-2 but not of caspase-3, caspase-7, caspase-8, or caspase-9.

135 d processing of caspase 12 in caspase 3(-/-)/caspase 7(-/-) cells.

136 e of CK2alpha phosphorylation, proximal to a caspase 7 cleavage site.

137 ression of caspase-9 did not enhance PARP or caspase-7 cleavage after UV treatment.

138 Inhibiting caspase-7 cleavage of ORF57 in KSHV(+) BCBL-1 cells by z

139 Caspase-7 cleavage of ORF57 is prevented by pan-caspase

140 neurotoxicity, suggesting that inhibition of caspase-7 cleavage of polyQ-ataxin-7 may be a promising

141 The degradation of the caspase-7 cleavage product is mediated by macroautophagy

142 The caspase-7 cleavage site (30)DETD(33) in ORF57 is not cle

143 ndings indicate that proteolysis at the D266 caspase-7 cleavage site is an important mediator of atax

144 ne 257 (K257), an amino acid adjacent to the caspase-7 cleavage site of ataxin-7 regulates turnover o

145 at S95 and S97 residues in proximity of the caspase-7 cleavage site, 30-DETD-33, inhibits caspase-7

146 Site-directed mutagenesis of these two caspase-7 cleavage sites in the polyQ-expanded form of a

147 leaved by caspase-7, and we map two putative caspase-7 cleavage sites to Asp residues at positions 26

148 c mice similar in size to those generated by caspase-7 cleavage.

149 nd forms a stable approximately 200-kDa XIAP-caspase-7 complex, which apparently does not contain cIA

150 osarcoma cells involves enhanced activity of caspase-7, consistent with the disruption of glucose-reg

151 In ectopic expression experiments, caspase-7 constructs with no N-peptide are far more leth

152 Functionally, the phosphorylation of caspase-7 decreases its activity, thereby inhibiting cel

153 Indeed, caspase-7-deficient mice were resistant to LPS-induced l

154 ic stress via a truncated HDAC3 generated by caspase-7-dependent cleavage at aspartic acid 391.

155 However, caspase-6 and caspase-7 did not cleave Bid, although they initiated cy

156 No apoptosis was observed in the cells where caspase-7 did not undergo autocatalytic activation.

157 aspase-7 cleavage site, 30-DETD-33, inhibits caspase-7 digestion of ORF57.

158 In a human cell model, full maturation of caspase-7 does not occur unless caspase-10 is present.

159 ith staurosporine, caspase-3 and -6 (but not caspase-7) enzymatic activities were induced.

160 also increased HSP expression and decreased caspase-7 expression, with changes in protein levels com

161 iptional upregulation of bak, caspase-8, and caspase-7 expression.

162 combination of high miR-106b and low CASP7 (caspase-7) expressions in primary tumors was an independ

163 vely than caspase-7 and endogenous levels of caspase-7 failed to inactivate DFF45/ICAD in caspase-3 n

164 ial loops in the active site, priming active caspase-7 for inhibitor/substrate binding.

165 tant or kinase-inactive mutants also prevent caspase-7 from being activated completely.

166 Proteolytic processing of ataxin-7 by caspase-7 generates N-terminal toxic polyQ-containing fr

167 -2 and caspase-7, whereas immunodepletion of caspase-7 had no effect on Bcl-2 cleavage.

168 Expression of exogenous caspase-7 had no impact on Bcl-2 expression, but promote

169 This new form of caspase-7 has a 6-fold increase in V(max) when compared

170 Cleavage of ataxin-7 by the protease caspase-7 has been demonstrated in vitro, and the accumu

171 tudies suggest the calpain-activated form of caspase-7 has unique enzymatic activity, localization, a

172 Increases in active caspase-7 immunoreactivity were less frequently encounte

173 similar fashion by recombinant caspase-3 or caspase-7 in a dose-dependent manner.

174 at the Apaf-1-caspase-9 apoptosome processes caspase-7 in an analogous manner to that described for c

175 Here we present the crystal structure of caspase-7 in complex with a potent inhibitory fragment f

176 n and subsequent activation of caspase-3 and caspase-7 in each cell line, decreased Bcl-2 and Bcl-X(L

177 of LPS-injected mice, suggesting a role for caspase-7 in lymphocyte apoptosis.

178 yrin and ASC were required for activation of caspase-7 in macrophages stimulated with zymosan or mann

179 l domain (NTD) and the N-terminal peptide of caspase-7 in promoting key substrate proteolysis.

180 astoma cell lines induces CHOP and activates caspase-7 in temozolomide-treated cells.

181 f GrB-mediated activation of the executioner caspase-7 in vitro and in vivo.

182 l for the first time a nonredundant role for caspase-7 in vivo and identify caspase-7 inhibition as a

183 er, the N-peptide modifies the properties of caspase-7 in vivo.

184 effector caspases (caspase-3, caspase-6, and caspase-7) in becoming active, ultimately leading to dea

185 ly the DEVD cleaving caspases, caspase-3 and caspase-7, inactivated DFF45/ICAD and promoted DNA fragm

186 ion but inhibited CD79a, Requiem, c-Fos, and caspase 7 induction when the cells underwent apoptosis.

187 dant role for caspase-7 in vivo and identify caspase-7 inhibition as a component of the mechanism by

188 ficantly rescued TNF effects on SK1, yet the caspase 7 inhibitor DEVD failed to have any effect, sugg

189 y pan-caspase inhibitor z-VAD, caspase-3 and caspase-7 inhibitor z-DEVD, and caspase-7 small interfer

190 d affinity but also sterically excludes XIAP/caspase-7 interaction, demonstrating the requirement of

191 tion does not sterically exclude linker_BIR2/caspase-7 interaction.

192 These studies identified a full-length caspase-7 intermediate that becomes catalytically activa

193 SCA7 transgenic mouse model, recruitment of caspase-7 into the nucleus by polyQ-expanded ataxin-7 co

194 Whereas caspase 7 is an indirect responder to RA signaling, casp

195 Western blot analysis revealed that caspase-7 is activated by cytochrome c at the same level

196 Because caspase-7 is activated in every model of apoptosis that

197 Caspase-7 is an executioner caspase that plays a key rol

198 Caspase-7 is an obligate dimer of catalytic domains, wit

199 Here, we present that recombinant caspase-7 is directly cleaved by calpain-1 within the la

200 ases such as calpains activate or inactivate caspase-7 is not known.

201 ysates containing Smac and Omi/HtrA2, active caspase-7 is released from the apoptosome and forms a st

202 Strikingly, caspase-7 is unprocessed in caspase-3-deficient MCF-7 ce

203 ), tumor necrosis factor [TNF]-alpha(KO), or caspase 7(KO) mice) using quantitative real-time PCR, en

204 Cellular expression of caspase-7 lacking the critical lysine residues resulted

205 tified the calpain cleavage sites within the caspase-7 large subunit at amino acid 36 and 45/47.

206 e XIAP peptide binds the catalytic groove of caspase-7, making extensive contacts to the residues tha

207 Whereas Bcl2L12-mediated neutralization of caspase-7 maturation involves physical interaction, the

208 aling by neutralizing effector caspase-3 and caspase-7 maturation.

209 t that proteolytic processing of ataxin-7 by caspase-7 may contribute to SCA7 disease pathogenesis.

210 Thus, adenoviral-mediated transfer of caspase-7 may offer a new effective approach for the tre

211 e induced activations of caspase-3/CPP32 and caspase-7/Mch3 followed by PARP cleavage, effects that c

212 phism significantly increases caspase 3- and caspase 7-mediated cleavage of Atg16L1, resulting in low

213 onged ER stress may induce apoptosis through caspase-7-mediated caspase-12 activation.

214 rodomain caspases (caspase-3, caspase-6, and caspase-7), MICE preferentially associates with large pr

215 Moreover, the N-peptide of caspase-7 must be removed before efficient activation of

216 matured caspase-3 with less efficiency than caspase-7 or caspase-10.

217 that Smac is ineffective in relieving either caspase-7 or caspase-9 inhibition by XIAP domain fragmen

218 The addition of purified caspase 3, caspase 7, or caspase 8 to the cytosolic extract from Bc

219 , which subsequently activates caspase-3 and caspase-7, or bigger inactive aggregates, depending on t

220 Upon cleavage with caspase-7, ORF57 was deficient in promoting the expressi

221 in vivo as indicated by the accumulation of caspase-7 p18 and p17 subunits in cortical neurons under

222 uct (p20) or the larger calpain-1 product of caspase-7 (p18).

223 ing with XIAP constitutively inhibits active caspase-7 (p19/p12-CASP7).

224 pared with the caspase-3 cleavage product of caspase-7 (p20).

225 ro-apoptotic target genes such as caspase 3, caspase 7, PARP1, and Apaf-1 and activates their express

226 We show that the N-peptide of caspase-7 plays no role in the fundamental activation or

227 Compared to the inhibitor-bound caspase-7, procaspase-7 zymogen exhibits significant str

228 9 in the apoptosome complex, and as a result caspase-7 processing is abrogated.

229 Zymography revealed that the smaller caspase-7 product (p17) is 18-fold more active than eith

230 n with caspase-3 restores the removal of the caspase-7 propeptide and the capacity of GrB to subseque

231 During GrB-mediated apoptosis, the caspase-7 propeptide is removed and cleavage occurs betw

232 processing the accessible caspase-3, and the caspase-7 propeptide regulates trans-activation of the z

233 tion-defective adenovirus, overexpression of caspase-7 protein in both LNCaP and LNCaP-Bcl-2 cells wa

234 th a second-site mutation (D266N) to prevent caspase-7 proteolysis.

235 values up to 2.6 nM (caspase-3) and 3.3 nM (caspase-7), respectively.

236 -based drug discovery campaign against human caspase-7 resulted in the discovery of a novel series of

237 tal structure of one of these compounds with caspase-7 reveals that it binds to the dimerization inte

238 Caspase-7's N-terminal domain binds PARP and improves it

239 In contrast, caspase-7 showed less efficient hydrolysis of the substr

240 in KSHV(+) BCBL-1 cells by z-VAD, z-DEVD, or caspase-7 small interfering RNA led to increased express

241 aspase-3 and caspase-7 inhibitor z-DEVD, and caspase-7 small interfering RNAs.

242 Our results also showed that active caspase-7 specifically cleaved capsid proteins at D420 i

243 mentation, and cleavage of the caspase 3 and caspase 7 substrate poly(ADP-ribose) polymerase (PARP) i

244 amma-induced expression of STAT1, STAT2, and caspase-7, suggesting that HDAC inhibitors impede the ex

245 loop unique to the executioner caspase-3 and caspase-7 that are targeted by XIAP.

246 e and allosteric transition in the apoptotic caspase-7 that shares only a 23% sequence identity with

247 Moreover, for caspase-7, the precise location of the activating cleava

248 the caspase cascade (including caspase-9 and caspase-7), thereby initiating the apoptotic process.

249 on of caspase-1 and subsequent activation of caspase-7; this results in the resolution of type 2 immu

250 y binding to and inhibition of caspase-3 and caspase-7 through its BIR2 domain and caspase-9 through

251 (LPS) and peptidoglycan induce activation of caspase-7 through the Cryopyrin inflammasome.

252 These cells rely on caspase-7 to execute the apoptotic program, yet binding

253 ved by calpain-1 within the large subunit of caspase-7 to produce two novel products, large subunit p

254 and also leads to translocation of cytosolic caspase-7 to the ER surface.

255 In addition, caspase-3, but not caspase-7, translocated from the cytoplasm into the nucl

256 Expression of the caspase-7 truncation product of ataxin-7-69Q or -92Q, wh

257 fingers of c-Cbl and Apc11 failed to promote caspase-7 ubiquitination, suggesting that the Ring finge

258 Of the caspases tested, only caspase-7 underwent proteolytic activation after stimula

259 directly inhibits effector caspases such as caspase-7 via a linker_BIR2 fragment and initiator caspa

260 e report here that the apoptotic executioner caspase-7 was activated in the splenocytes of LPS-inject

261 Caspase-7 was further cleaved to form the catalytically

262 normally while processing of the downstream caspase-7 was markedly attenuated.

263 Caspase-7 was proteolytically activated in every model o

264 Overexpressed pro-caspase-7 was proteolytically cleaved in LNCaP and LnCaP

265 Caspase-7 was the only detected interleukin 1beta conver

266 ates, and an antibody specific for activated caspase 7, we have determined that apoptosis in MCF-7 ce

267 Both caspase-3 and caspase-7 were able to catalyze the cleavage of Cdc42, w

268 Bax increased, and caspase-9, caspase-6, and caspase-7 were activated but not caspase-3 and caspase-8

269 ease calpains and cleavage of caspase-12 and caspase-7 were found in the channel-deficient retinas, s

270 evels of cleaved ATF6, pEIF2alpha, CHOP, and caspase-7 were much higher than those of wild-type rats.

271 lacking the downstream inflammasome effector caspase-7 were partially protected.

272 ting the executioner caspases, caspase-3 and caspase-7, were identified.

273 and wild type STAT1 also induced cleavage of caspase 7 when expressed in STAT1-negative U3A cells, in

274 erminus of the large subunit of fully mature caspase-7, whereas cIAP1 bound to partially processed ca

275 293 extracts abolished cleavage of Bcl-2 and caspase-7, whereas immunodepletion of caspase-7 had no e

276 st caspase-3 with >120-fold selectivity over caspase-7 which shares 77% active site identity.

277 hrough inactivation of p23 and activation of caspase 7, which cleaves p23 at the C terminus.

278 eficient in the two effectors, caspase 3 and caspase 7, which died immediately after birth with defec

279 The activation of caspase-7, which is independent of cytochrome c release

280 In contrast to caspase-7, which rests constitutively in the strand conf

281 However, caspase-7, which shares the same substrate primary seque

282 s endoplasmic reticulum stress and activates caspase-7 with no effect on mitochondria or caspases-3 a

283 caspase zymogen, procaspase-7, and an active caspase-7 without any bound inhibitors.

284 three protein-protein pairs (caspase-9-XIAP, caspase-7-XIAP, FKBP12-FRB) and their small molecule mod

285 e that it serves to physically sequester the caspase-7 zymogen in a cytosolic location that prevents