ライフサイエンスコーパス: Apaf-1

1 Apaf-1 also was found to colocalize with huntingtin-cont

2 Apaf-1 and ATP were required to initiate apoptosis upon

3 Apaf-1 and X-linked inhibitor of apoptosis protein (Xiap

4 Apaf-1 binds to and hydrolyses ATP/dATP and their analog

5 Apaf-1 contains a dATP as a cofactor.

6 Apaf-1 deficiency may constitute a significant mode of r

7 Apaf-1 DNA methylation was demonstrated in acute myeloid

8 Apaf-1 exists in normal cells as an autoinhibited monome

9 Apaf-1 facilitates the proteolytic activation of procasp

10 Apaf-1 is also expressed in all neuroblastoma tumor cell

11 Apaf-1 localizes exclusively in the cytosol and, upon ap

12 Apaf-1 oligomerizes to produce approximately 1.4-MDa and

13 Apaf-1 plays an essential role in apoptosis.

14 Apaf-1 protein content in the soleus of TR animals was l

15 Apaf-1 protein deficiency occurs in human leukaemic blas

16 Apaf-1 protein expression did not correlate with Apaf-1

17 Apaf-1, which interacts with cytochrome c and activates

18 Apaf-1-mediated activation of caspase-9 and caspase-3 wa

19 Apaf-1-negative melanomas are invariably chemoresistant

20 The apoptotic protease-activating factor 1 (Apaf-1) controls caspase activation downstream of mitoch

21 The apoptotic protease-activating factor 1 (Apaf-1) controls the onset of many known forms of intrin

22 the apoptotic protease-activating factor 1 (Apaf-1)-dependent apoptotic pathway in human NSCLC cells

23 rial apoptotic protease-activating factor 1 (Apaf-1)-dependent pathway for apoptosis (as type II cell

24 n of apoptotic protease activating factor-1 (Apaf-1) is a key step in the mitochondrial-signaling pat

25 e to apoptotic protease activating factor-1 (Apaf-1) knockout mice, we have investigated the possibil

26 n of apoptotic protease-activating factor-1 (Apaf-1) protein and reduction of X-chromosome-linked inh

27 e c, apoptosis protease-activating factor-1 (Apaf-1), and caspase-9, or a caspase-independent mechani

28 bind apoptotic protease activating factor-1 (Apaf-1), which in turn binds caspase-9 both activating t

29 and apoptotic protease-activating factor-1 (Apaf-1).

30 inst apoptotic protease-activating factor-1 (Apaf-1).

31 n of apoptotic protease-activating factor-1 (Apaf-1).

32 (apoptosis) and on survival pathways (Bcl-2, Apaf-1, AKT, NF-kappaB) involved in multidrug resistance

33 Despite conservation of Bcl-2, Apaf-1, and caspases in invertebrate phyla, the existenc

34 ced-4 (Apaf-1) is required for all previously known apoptotic c

35 res activation of the apoptotic gene, ced-4 (Apaf-1).

36 CED-4/Apaf-1 is essential for HP in C. elegans and acts throug

37 The CED-3 activator, CED-4/Apaf-1, similarly promotes regeneration, but the upstrea

38 Inhibition of the Drosophila CED-4/Apaf-1-related killer (ARK) homologue resulted in pronou

39 n the release of the caspase activator CED-4/Apaf-1.

40 ses are under positive control via the CED-4/Apaf-1/Dark adaptors and negative control via IAPs (inhi

41 inhibition or genetic deletion of caspase-9, Apaf-1, or caspase-3/7 causes dying cells to secrete IFN

42 so inhibits caspase activation by abrogating Apaf-1 oligomerization and apoptosome assembly.

43 ing of cytochrome c to the caspase activator Apaf-1.

44 function mutation in ced-4, which encodes an Apaf-1 homolog that promotes programmed cell death by ac

45 unction mutations in ced-4, which encodes an Apaf-1 homolog, completely blocked HP.

46 both activating this caspase and forming an Apaf-1/caspase-9 holoenzyme.

47 eal arch mesenchyme leads to apoptosis in an Apaf-1-dependent fashion and that, while loss of aortic

48 down the expression of c-Myc, caspase-2, and Apaf-1, an activating component in the apoptosome, in tw

49 elerated the association of procaspase-9 and Apaf-1 in both intact cells and cell-free extracts.

50 been suggested for caspase-8, caspase-9 and Apaf-1 in controlling tumor development and their sensit

51 gnaling components upstream of caspase-9 and Apaf-1.

52 d cytochrome c release and decreased Bax and Apaf-1 protein levels.

53 ntly lower (P < 0.01), and levels of Bax and Apaf-1 were elevated (P < 0.02) in ER carcinomas versus

54 e-9 without concurrent release of cyto-c and Apaf-1 oligomerization.

55 The status of CASP9 and Apaf-1 expression in numerous neuroblastoma cell lines w

56 of postmitotic neurons in which caspases and Apaf-1 are present and functional because quantitatively

57 revious studies have shown that caspases and Apaf-1 are required for the normal programmed cell death

58 type 1 apoptotic pathway (i.e., caspases and Apaf-1) are perturbed in vivo, developing postmitotic ne

59 gion between Ets homologous factor (EHF) and Apaf-1 interacting protein (APIP).

60 lation between Apaf-1 protein expression and Apaf-1 mRNA levels after the demethylation treatment.

61 of initiator caspases; for example, FADD and Apaf-1 engage caspases 8 and 9, respectively.

62 nerated mouse embryos lacking both HAND2 and Apaf-1, a central downstream mediator of mitochondrial d

63 ), Mcl-1, C-IAP-1, C-IAP-2, XIAP, Livin, and Apaf-1.

64 nes such as caspase 3, caspase 7, PARP1, and Apaf-1 and activates their expression after DNA damage.

65 bcl), a mitochondria-associated protein, and Apaf-1 (dark), which links mitochondrial signaling with

66 During apoptosis, Apaf-1 binds to cytochrome c and in the presence of ATP/

67 thologues of the apoptosome components, Ark (Apaf-1) and Dronc (caspase-9), are also required for the

68 oned a novel rat gene product, designated as Apaf-1-interacting protein (AIP), which functions as a d

69 ide exchange in the monomeric, autoinhibited Apaf-1 protein.

70 Structural comparison with autoinhibited Apaf-1 revealed how dATP binding triggers a set of confo

71 On average, Apaf-1 CARDs recruit 3 to 5 pc-9 molecules to the apopto

72 Bcl-2, Bax, Apaf-1, AIF, cleaved PARP, cleaved caspase-3, cleaved/ac

73 promoting the formation of a complex between Apaf-1 and caspase-9 in a caspase-activating structure k

74 There was no correlation between Apaf-1 protein expression and Apaf-1 mRNA levels after t

75 also able to examine the interaction between Apaf-1 and (15)N-labeled ProT alpha.

76 ormation by blocking the interaction between Apaf-1 and ProT.

77 ons that inactivate the interactions between Apaf-1 CARD and the prodomain of caspase-9 also abolishe

78 protein expression of Bcl-2, Bax, Bim, Bid, Apaf-1, and caspase-9 in activated CD4(+) T cells--compo

79 we show that the NB-ARC (nucleotide-binding, Apaf-1, R-proteins, and CED-4) domain of the Rx1 NLR of

80 mitochondria to the cytosol, where it binds Apaf-1.

81 ere we show that apocytochrome c still binds Apaf-1 and that it can block holo-dependent caspase acti

82 tochrome c interaction with Apaf-1, blocking Apaf-1 oligomerization and caspase activation.

83 mitochondrial apoptotic pathway mediated by Apaf-1 is an integral part of ER stress-induced apoptosi

84 Given the key role played by Apaf-1/cytochrome c in the apoptotic process, and the ro

85 ions support a model in which recruitment by Apaf-1 creates high local concentrations of caspase 9 to

86 ivated in the mitochondria in a cytochrome c/Apaf-1-dependent manner, or activated caspase-9 and -3 m

87 -induced cell death through the cytochrome c/Apaf-1-dependent pathway.

88 e demonstrate that tango7, not the canonical Apaf-1-adaptor dark, regulates dronc activity at the cor

89 irst, in addition to a typical CARD-carrying Apaf-1 homologue, sea urchins have at least two novel Ap

90 erein MAPK signalling promotes Rsk-catalysed Apaf-1 phosphorylation and consequent binding of 14-3-3v

91 AP-ATPases (animal apoptosis regulators CED4/Apaf-1, plant disease resistance proteins, and bacterial

92 By comparison, Apaf-1-deficient cells, as well as cells overexpressing

93 By comparison, Apaf-1-deficient Jurkat cells were sensitive to anti-Fas

94 ptional suppression of apoptosome components Apaf-1 and procaspase-9, and limiting caspase-9 activity

95 ptosome is a multiprotein complex comprising Apaf-1, cytochrome c, and caspase-9 that functions to ac

96 In contrast, Apaf-1 forms a single ring that is comprised of seven su

97 In contrast, Apaf-1-deficient cells were sensitive to Fas-induced apo

98 P may have an additional role in controlling Apaf-1-mediated Csp9 activation.

99 HD brain, suggesting a common role for Dark/Apaf-1 in polyglutamine pathogenesis in invertebrates, m

100 In the presence of cytochrome c and dATP, Apaf-1 assembles into an oligomeric apoptosome, which is

101 Upon binding to cytochrome c and dATP, Apaf-1 oligomerizes into a heptameric complex known as t

102 stal structure of an ADP-bound, WD40-deleted Apaf-1, which reveals the molecular mechanism by which A

103 The Drosophila Apaf-1 related killer (Dark) forms an apoptosome that ac

104 transcriptional induction of the Drosophila Apaf-1/ced-4 homolog.

105 that is comprised of seven subunits and each Apaf-1 binds a molecule of cytochrome c.

106 sembly of a heptameric complex in which each Apaf-1 subunit is bound noncovalently to a procaspase-9

107 transcriptomics databases indicated elevated Apaf-1 expression in several hematologic malignancies, i

108 in the cell death-associated genes encoding Apaf-1, caspase-3, and caspase-9, which suggests that ph

109 is induced by UV light and causes endogenous Apaf-1 to form aggregates.

110 Bcr-Abl prevented interaction of endogenous Apaf-1 with the recombinant prodomain of caspase 9, it d

111 rome c in cells expressing or not expressing Apaf-1.

112 ed conformational changes create an extended Apaf-1 monomer and drive apoptosome assembly.

113 ion of apoptotic protease-activating factor (Apaf-1) expression that in turn induced activation of nu

114 e-9 by apoptotic protease-activating factor (Apaf-1) in an oligomeric complex known as the apoptosome

115 This new role for Apaf-1 is unrelated to its proapoptotic function but is

116 This disk contains four Apaf-1/pc-9 CARD pairs arranged in a shallow spiral with

117 nals, an active apoptosome is assembled from Apaf-1 and procaspase-9 (pc-9).

118 itochondria following heat shock, functional Apaf-1.caspase-9 apoptosome complexes were not formed, a

119 ed apoptosis than cell lines with functional Apaf-1 activity.

120 In contrast to HAND2-/- embryos, HAND2-/-Apaf-1-/- embryos at E10.5-11.0 had well-developed phary

121 nalysis through pharyngeal arches of HAND2-/-Apaf-1-/- embryos revealed decreased apoptosis and the e

122 Unlike in the related heptameric Apaf-1 apoptosome, in which each subunit needs to be con

123 tivity to cytochrome c is attributed to high Apaf-1 levels in the tumor tissue compared with low Apaf

124 However, Apaf-1 protein levels might also be controlled at post-t

125 flies lacking Dark, the fly homolog of human Apaf-1, a key regulator of apoptosis.

126 accharomyces cerevisiae overexpressing human Apaf-1 and procaspase-9, critical components of the apop

127 to label any activated initiator caspase in Apaf-1-deficient cells exposed to hyperthermia.

128 demonstrated by the suppression of death in Apaf-1(fog) mutant pro-B cells.

129 uced Apaf-1 levels and that this decrease in Apaf-1 is directly linked to the tight regulation of cas

130 Importantly, this decrease in Apaf-1 protein was directly linked to the increased abil

131 Because a complete deficiency in Apaf-1 usually results in perinatal lethality and fog/fo

132 These differences in Apaf-1 abundance correlate with differences in the level

133 d via its small subunit to the NOD domain in Apaf-1, resulting in the formation of a heterodimer that

134 also accompanied with a marked reduction in Apaf-1, resulting in a significant decrease in apoptosom

135 tide exchange on Apaf-1 and prevent inactive Apaf-1/cytochrome c aggregation.

136 oreover, the N-terminal CARD in the inactive Apaf-1 monomer is not shielded from other proteins by be

137 uced apoptosis in association with increased Apaf-1 protein levels.

138 y, we find that E2F1 is sufficient to induce Apaf-1 expression in developing but not mature neurons.

139 This differential capacity of E2F1 to induce Apaf-1 transcription is because of the association of th

140 y to Apaf-1, preventing cytochrome c-induced Apaf-1 oligomerization and caspase-9 recruitment.

141 Combination treatment induced Apaf-1 and procaspase-9 expression in which cytochrome c

142 tivation in native lysates and also inhibits Apaf-1 oligomerization into an apoptosome complex in a p

143 Cytochrome c (CC)-initiated Apaf-1 apoptosome formation represents a key initiating

144 Here we report that the isolated Apaf-1 caspase recruitment domain (CARD) forms a large h

145 on of endogenous caspase 9 with the isolated Apaf-1 caspase recruitment domain (CARD) or Apaf-1 lacki

146 JNK inhibition abrogated JNK-Apaf-1 association and accelerated the association of pr

147 Cells lacking Apaf-1 or the pro-apoptotic BH3-only protein Bid exhibit

148 ome using a crystal structure of full length Apaf-1 and a single particle, electron density map at ~9

149 These findings suggest that limiting Apaf-1 activity may alleviate both pathological protein

150 n these four adjoining domains, thus locking Apaf-1 in an inactive conformation.

151 we show that metastatic melanomas often lose Apaf-1, a cell-death effector that acts with cytochrome

152 levels in the tumor tissue compared with low Apaf-1 levels in the adjacent brain tissue.

153 ed neuronal apoptosis was reduced with lower Apaf-1 expression, and little NF-kappaB activation was f

154 vation was found in the neurons with mutated Apaf-1 or a deletion of TNFRI compared with the cells fr

155 Nevertheless, Apaf-1 knockout, overexpression of Bcl-XL, and pharmacol

156 greatly reduced expression levels of normal Apaf-1 mRNA.

157 mologue, sea urchins have at least two novel Apaf-1-like proteins that are each linked to a death dom

158 implications of this complex on the observed Apaf-1 function.

159 Consequently, calcium blocks the ability of Apaf-1 to activate caspase-9.

160 ytochrome c- and dATP-mediated activation of Apaf-1.

161 ATP or dATP is a required activator of Apaf-1 for formation of the Apoptosome and thereby activ

162 f E2F1, a previously identified activator of Apaf-1 transcription.

163 s promote the protein-protein association of Apaf-1 into the functional apoptosome.

164 cytochrome c releases the autoinhibition of Apaf-1 through specific interactions with the WD40 repea

165 prevent the cytochrome c-induced binding of Apaf-1 to procaspase 9.

166 uilibrium and kinetic folding of the CARD of Apaf-1 (apoptotic protease activating factor 1), which c

167 A direct comparison of Apaf-1 in the apoptosome and as a monomer reveals confor

168 to mitochondria and, secondly, deficiency of Apaf-1.

169 Methylation and deletion of Apaf-1 and CASP8 results in the loss of their expression

170 ressing Bcl-2/Bcl-x(L) or stably depleted of Apaf-1 were completely resistant to heat-induced apoptos

171 ressing Bcl-2/Bcl-x(L) or stably depleted of Apaf-1 were equally resistant to apoptosis induced by th

172 by binding to the oligomerization domain of Apaf-1.

173 t between the caspase recruitment domains of Apaf-1 and caspase-9.

174 ction between caspase recruitment domains of Apaf-1 and procaspase-9.

175 ptosome model includes N-terminal domains of Apaf-1, cognate beta-propellers, and cytochrome c.

176 eptibility associated with downregulation of Apaf-1 expression as a function of developmental age was

177 ults suggest that differential expression of Apaf-1 and caspase-3 genes may underlie regulation of ap

178 g that E2F1 contributes to the expression of Apaf-1 in brain tumors.

179 Our results suggest that the expression of Apaf-1 may be predictive of the response to proteasome i

180 All lines retained expression of Apaf-1, and all but one remained sensitive to ectopic ex

181 m is not adequate to describe the folding of Apaf-1 CARD at either pH, suggesting the presence of int

182 raising the possibility that the function of Apaf-1 is not only to oligomerize procaspase-9 but also

183 ds to Apaf-1 and triggers heptamerization of Apaf-1 leading to the activation of Csp9.

184 tion might contribute to the inactivation of Apaf-1 expression.

185 hway described previously, is independent of Apaf-1 and cytochrome c.

186 regulate sulforaphane-mediated induction of Apaf-1 protein.

187 V-light was increased; involved induction of Apaf-1, activation of caspase-3, and was dependent on p5

188 Moreover, juxtapositioning of Apaf-1 monomer and apoptosome formation occur about 5h e

189 mouse embryonic fibroblasts with knockout of Apaf-1, the essential mediator of the pathway.

190 e-dependent increase in the protein level of Apaf-1 in wild-type, Bax-/-, and Bak-/- MEFs but not in

191 The protein level of Apaf-1, an activator of procaspase-9, remained constant

192 that it is crucial to evaluate the levels of Apaf-1 and XIAP proteins in patient samples before using

193 ome leukaemic cells expressed high levels of Apaf-1 mRNA but low levels of Apaf-1 protein.

194 high levels of Apaf-1 mRNA but low levels of Apaf-1 protein.

195 r the caspase inhibitor zVAD-fmk nor loss of Apaf-1 affected the efflux of cytochrome c, Smac/Diablo

196 Loss of Apaf-1 expression is accompanied by allelic loss in meta

197 ent regulation because of a complete loss of Apaf-1 expression.

198 ls, is assembled by rapid oligomerization of Apaf-1 and followed by a slower process of procaspase-9

199 initiates dATP-dependent oligomerization of Apaf-1 and formation of the apoptosome.

200 ndicates cooperativity in oligomerization of Apaf-1 upon binding of cytochrome c.

201 Transient silencing of Apaf-1 expression in RPMI 8402 T-cell leukemic cells als

202 y luciferase were fused to amino-terminal of Apaf-1.

203 ility of such transcripts, including that of Apaf-1, the major protein in the apoptosome.

204 Transfection of Apaf-1 conferred sensitivity to apoptosis in resistant c

205 formed a stable association with oligomeric Apaf-1 in a approximately 1.4-2.0 mDa pre-apoptosome com

206 XIAP associates with oligomerized Apaf-1 and/or processed caspase-9 and influences the act

207 to detect early-stages of apoptosis based on Apaf-1 oligomerization and apoptosome formation using th

208 ogether to accelerate nucleotide exchange on Apaf-1 and prevent inactive Apaf-1/cytochrome c aggregat

209 The dATP hydrolysis and exchange on Apaf-1 are two required steps for apoptosome formation.

210 sembly by stimulating nucleotide exchange on Apaf-1 following binding of cytochrome c.

211 xpression of endogenous c-Myc, caspase-2, or Apaf-1 is reduced 80-90%, cisplatin (or etoposide)-induc

212 by reduced expression levels of caspase-9 or Apaf-1.

213 rphic mutations of the genes encoding AIF or Apaf-1.

214 osis to a larger extent compared with Bax or Apaf-1 transfection alone.

215 Apaf-1 caspase recruitment domain (CARD) or Apaf-1 lacking WD-40 repeats.

216 Thus, the CASP9 or Apaf-1 genes do not appear to function as tumor suppress

217 ated GSE, but not by Bcl2 over-expression or Apaf-1 or cytochrome c knock-down.

218 However, Smac failed to overcome Apaf-1-deficiency-mediated resistance to cytochrome c in

219 tified and a number of these, including p53, Apaf-1, and members of the inhibitor of apoptosis protei

220 tion of E2F1 apoptotic targets, such as p73, Apaf-1, and caspases, during DNA damage.

221 se-3 activation pathway using purified ProT, Apaf-1, procaspase-9, procaspase-3, Hsp70, cytochrome c,

222 y, the Bcl-2 family, and the adaptor protein Apaf-1.

223 comprises 16 molecules of the Dark protein (Apaf-1 ortholog), reveals molecular determinants that su

224 regard to the apoptosis signaling proteins, Apaf-1 and Nod1, which share domain arrangements similar

225 -regulated proapoptotic genes Fas, PUMAbeta, Apaf-1, PIG3.

226 Rather, Apaf-1 up-regulation in mature neurons requires both chr

227 on of this pathway with purified recombinant Apaf-1, procaspase-9, procaspase-3, and cytochrome c fro

228 osome reconstitution system with recombinant Apaf-1 and cytochrome c, K(+) also inhibits caspase acti

229 yocytes, like neurons, have markedly reduced Apaf-1 levels and that this decrease in Apaf-1 is direct

230 c factors related to the apoptosis regulator Apaf-1 and a class of plant disease resistance proteins.

231 ochondrial loss of cytochrome c and required Apaf-1 and caspase-9, -6, and -3.

232 fter DNA damage, mature neurons resynthesize Apaf-1 through the cell cycle-related E2F1 pathway and r

233 e the release of cytochrome c and subsequent Apaf-1-dependent activation of caspases.

234 blasts were transfected with siRNA targeting Apaf-1.

235 rain, but at substantially lower levels than Apaf-1 and caspase-9.

236 itochondria during cytotoxic stress and that Apaf-1 is only required following cytochrome c release t

237 enhanced in this complex, demonstrating that Apaf-1 CARD allosterically up-regulates caspase-9 activi

238 f Molecular Cell, Zermati et al. report that Apaf-1 is essential for the DNA damage-induced intra-S p

239 reverse transcription-PCR analysis show that Apaf-1 mRNA is aberrantly processed, resulting in greatl

240 tial mixing stopped-flow studies showed that Apaf-1 CARD folds and unfolds rapidly and suggest a fold

241 We first showed that Apaf-1 is the direct target protein of BETT.

242 These data suggest that Apaf-1 recruitment of caspase 9 is faulty in the presenc

243 This study suggests that Apaf-1 DNA promoter methylation might contribute to the

244 The Apaf-1-deficient Jurkat T cells were resistant to bortez

245 The Apaf-1/cytochrome c complex then oligomerizes either int

246 alysis shows that a single Dark ring and the Apaf-1 apoptosome share many key features.

247 or unprocessed caspase-9 initially binds the Apaf-1 apoptosome in cytochrome c/dATP-activated lysates

248 ChIP assays reveal that E2F1 binds the Apaf-1 promoter specifically in tumor tissue, suggesting

249 the initiator caspase-9 is activated by the Apaf-1 apoptosome and must remain bound to retain signif

250 utoproteolytic processing is mediated by the Apaf-1 apoptosome at the onset of apoptosis.

251 me activity, retains the ability to form the Apaf-1 oligomer; however, there is a diminished amount o

252 vation in the organelle rather than from the Apaf-1-mediated activation.

253 Hence, the Apaf-1 CARD may be free to interact with a procaspase-9

254 possibility that the fog mutation is in the Apaf-1 gene.

255 al cytochrome c release, which nucleates the Apaf-1/caspase-9 apoptosome.

256 nd apoptosis, and suggest that levels of the Apaf-1 and XIAP proteins, but not mitochondrial depolari

257 at cytochrome c/dATP-induced exposure of the Apaf-1 CARD is likely defective.

258 ription is because of the association of the Apaf-1 promoter with active chromatin in developing neur

259 ions as a dominant-negative inhibitor of the Apaf-1-caspase-9 pathway.

260 ults suggest that molecular targeting of the Apaf-1-caspase-9 signaling pathway may be a feasible neu

261 important role of calcium homeostasis on the Apaf-1-dependent apoptotic pathway.

262 It is assumed that the Apaf-1-caspase-9 apoptosome processes caspase-7 in an an

263 Thus, the Apaf-1 apoptosome functions as a proteolytic-based 'mole

264 rom enhanced recruitment of caspase-9 to the Apaf-1 caspase recruitment domain.

265 y consists of some 25 members related to the Apaf-1/Ced-4 family of apoptosis regulators and certain

266 ase-9 may instead form a holoenzyme with the Apaf-1 apoptosome.

267 wever, after transient transfection with the Apaf-1 gene, K/Bax cells were sensitized to etoposide-in

268 dulate cell survival by interfering with the Apaf-1/cytochrome c interaction.

269 ow that the methylation can occur within the Apaf-1 promoter region in leukaemic blasts.

270 stress activates different caspases through Apaf-1-dependent and -independent mechanisms.

271 mode of apoptotic regulation exerted through Apaf-1 phosphorylation by the 90-kDa ribosomal S6 kinase

272 h requires concurrent positive input through Apaf-1-like proteins together with disruption of IAP-cas

273 Thus, Apaf-1 and XIAP may play important roles in the regulati

274 n healthy and chronic periodontitis tissues (Apaf-1, 19.2-fold; caspase-9, 14.5-fold; caspase-3, 6.8-

275 AIP can directly bind to Apaf-1 in vitro through its N-terminal caspase-recruitin

276 l types promoted 14-3-3varepsilon binding to Apaf-1 and rendered the cells insensitive to cytochrome

277 Cytochrome c binding to Apaf-1 induces hydrolysis of dATP to dADP, which is subs

278 of cytochrome c (CytC), dATP or ATP binds to Apaf-1 and triggers heptamerization of Apaf-1 leading to

279 m mitochondria to cytosol, where it binds to Apaf-1 to form a procaspase-9-activating heptameric prot

280 Binding of cytochrome c and dATP to Apaf-1 in the cytosol leads to the assembly of a heptame

281 heat shock enhanced the binding of HSP70 to Apaf-1, which is likely to interfere in stress-mediated

282 binding of nonphosphorylatable Hsp90beta to Apaf-1.

283 some inhibitor, Hsp90beta, bound strongly to Apaf-1, preventing cytochrome c-induced Apaf-1 oligomeri

284 The mechanisms underlying Apaf-1 function are largely unknown.

285 We also noted variable Apaf-1 expression in a panel of samples from patients wi

286 ich reveals the molecular mechanism by which Apaf-1 exists in an inactive state before ATP binding.

287 itotic neuronal populations in mice in which Apaf-1 has been genetically deleted and find that they e

288 of Bax or by coexpression of caspase 9 with Apaf-1, and preincubation of cytosolic extracts with ILP

289 able of forming a productive Apoptosome with Apaf-1.

290 of cytochrome c that forms apoptosomes with Apaf-1 and caspase-9.

291 e that oxidant-activated JNK associates with Apaf-1 and cytochrome c in a catalytically inactive comp

292 We show that Bcl-xL associates with Apaf-1 in NRP-154 cells; but this association does not i

293 ich is essential for direct association with Apaf-1 and activation.

294 ammalian cells, M1 coimmunoprecipitated with Apaf-1-procaspase-9 complexes.

295 -1 protein expression did not correlate with Apaf-1 mRNA levels in human leukaemic blasts.

296 Parcs interacted with Apaf-1 by binding to the oligomerization domain of Apaf-

297 ys-7, a crucial residue for interaction with Apaf-1 during apoptosis, are discussed.

298 nding prevents cytochrome c interaction with Apaf-1, blocking Apaf-1 oligomerization and caspase acti

299 dues and thus preventing CC interaction with Apaf-1.

300 elease of cytochrome c, which interacts with Apaf-1 to trigger caspase activation and apoptosis.