ライフサイエンスコーパス: XIAP

1 XIAP and cIAP1 are members of the inhibitor of apoptosis

2 XIAP and cIAP1 are two members of the inhibitors of apop

3 XIAP has previously emerged as a molecular discriminator

4 XIAP inhibition by lentivirus mediated RNA interference

5 XIAP is a key regulator of apoptosis, and its overexpres

6 XIAP overexpression has been found in many human cancers

7 XIAP polyubiquitylates p47 in a lysine 63-dependent mann

8 XIAP, its vertebrate homolog, is similarly required for

9 Nedd 4-1, XIAP, and WWP2 have been shown to maintain PTEN turnover

10 observed that P. gingivalis targets APAF-1, XIAP, caspase-3, and caspase-9, to inhibit epithelial ce

11 nal cancer-associated survival genes (Mcl-1, XIAP and cIAP2) in a p53 status-independent manner, whil

12 M, caspase-3, BCL-XL) and resistance (MCL-1, XIAP).

13 hed1/2, and Smoothened), Gli targets (Bcl-2, XIAP and Cyclin D1), and EMT markers and transcription f

14 f anti-apoptotic proteins (survivin, cIAP-2, XIAP), induced apoptosis, and arrested cells in G1.

15 However, a XIAP mutant that does not interact with caspase-9 had no

16 These data included a XIAP threshold concentration at which apoptosis executio

17 sing recombinant adeno-associated virus (AAV-XIAP-GFP).

18 To test this scenario, we pre-activated XIAP at mitochondria via mitochondrial depolarization or

19 Upon Wnt pathway activation, XIAP is recruited to TCF/Lef where it monoubiquitylates

20 In addition, XIAP and CAS mRNA expression levels were correlated in H

21 Anti-apoptotic proteins Bcl-2 and XIAP were up-regulated while pro-apoptotic BAX was down-

22 PARP, together with a decrease in Bcl-2 and XIAP.

23 ogates the production of cIAP-1, cIAP-2, and XIAP and HA-CD44v3-mediated cancer stem cell functions.

24 veral survival proteins (cIAP-1, cIAP-2, and XIAP) leading to self-renewal, clonal formation, and cis

25 e increased levels of phosphorylated AKT and XIAP and reduced levels of cleaved caspase 3.

26 l RTECs in which gene expression of Akt1 and XIAP was silenced lost their protection and demonstrated

27 This study identified APAF-1 apoptosome and XIAP as intracellular targets of P. gingivalis, contribu

28 eatment promoted interaction between Bax and XIAP in the cytosol and on mitochondria, suggesting that

29 this ratio but had little effect on BAX and XIAP.

30 , IKK, NF-kappaB, and antiapoptotic BCL2 and XIAP genes, and up-regulation of BAX and BAK proapoptoti

31 itment of p50 onto the promoters of BCL2 and XIAP is dependent upon BRCA1, but independent of its NF-

32 miR-34a directly inhibits Bcl2 and XIAP, both anti-apoptotic proteins.

33 constitutively on the promoters of BCL2 and XIAP, whereas p50 is recruited to these promoters only i

34 the NF-kappaB antiapoptotic targets BCL2 and XIAP.

35 nt antiproliferative activities in cIAP- and XIAP-dependent cell lines.

36 Smac-mimetics reduced levels of cIAP1 and XIAP in MC38 and YAMC cells, and Smac-mimetics and TNF-r

37 ases with the E3 ubiquitin ligases cIAP1 and XIAP was hindered, leading to decreased degradation of R

38 lular ROS and degradation of IAPs (cIAP1 and XIAP).

39 tly to the BIR3 domains of cIAP1, cIAP2, and XIAP (IC50 = 15, 21, and 15 nM, respectively).

40 imals that lack functional cIAP1, cIAP2, and XIAP are not viable, and 2 mimicked features of triple I

41 we generated a mouse with cIAP1, cIAP2, and XIAP deleted in the myeloid lineage.

42 asone cooperate to deplete cIAP1, cIAP2, and XIAP, thereby promoting assembly of the ripoptosome, a R

43 Loss of cIAPs and XIAP in the myeloid lineage caused overproduction of man

44 from bone marrow in the absence of cIAPs and XIAP led to detectable levels of TNF and resulted in red

45 Our results demonstrate that cIAPs and XIAP together restrain RIPK1- and RIPK3-dependent cytoki

46 ellular radiosensitivity and both DIABLO and XIAP might be potential predictive markers of radiation

47 and (v) down regulation of p-AKT, p-ERK and XIAP.

48 ations in understanding the role of HIF1 and XIAP in human disease.

49 sized as antagonists of cIAP1/2, ML-IAP, and XIAP based on the N-terminus, AVPI, of mature Smac.

50 hibitor treatments caused loss of c-IAP1 and XIAP in multiple cancer cell lines and in tumor xenograf

51 4 expression correlates with IL-17 level and XIAP activation in human colon cancer.

52 MDM2 and XIAP are mutually regulated.

53 ISGs together with elevated FGF2, PDGFB, and XIAP, compared with CL derived from day 18 cyclic cows.

54 e a novel signaling circuit between PERK and XIAP that operates in parallel with PERK to CHOP inducti

55 involving concomitant CHOP up-regulation and XIAP down-regulation both induced by PERK.

56 ymphoproliferative disease genes (SH2D1A and XIAP), and others such as NLRC4, CDC42, and the Epstein-

57 poptosis inducers TNF and staurosporine, and XIAP overexpression reduces the lag time between the adm

58 , increasing its association with BCL-XL and XIAP mRNAs to promote their nuclear export.

59 ed cell survival proteins (MCL1, BCL-xL, and XIAP) and reduced the levels of gamma-H2AX, cleaved casp

60 ies and are highly effective in antagonizing XIAP in cell-free functional assays.

61 e find dramatic suppression of antiapoptosis XIAP proteins in response to chronic ER stress.

62 itin ligase X-linked inhibitor of apoptosis (XIAP) acts as a molecular rheostat for the immune defici

63 down of the X-linked inhibitor of apoptosis (XIAP) and partially reverted by XIAP overexpression.

64 tients with X-linked inhibitor of apoptosis (XIAP) deficiency.

65 -IAP2), and X-linked inhibitor of apoptosis (XIAP) in a ROS-dependent manner, and in RIP1 knockdown c

66 ed role for X-linked inhibitor of apoptosis (XIAP) in regulating this critical Wnt signaling event th

67 X-linked inhibitor of apoptosis (XIAP) is the most potent naturally occurring specific in

68 ole for the X-linked inhibitor of apoptosis (XIAP) protein as a regulator of Lys63-linked polyubiquit

69 The X-linked inhibitor of apoptosis (XIAP) protein has been identified as a key genetic drive

70 ic proteins X-linked inhibitor of apoptosis (XIAP), phospho-Akt (pAkt), and phospho-BAD.

71 ions in the X-linked inhibitor of apoptosis (XIAP).

72 ted AKT and X-linked inhibitor of apoptosis (XIAP); incubation of these cells with leflunomide increa

73 HIF1alpha), X-linked inhibitor of apoptosis (XIAP)], promoting cell cycle arrest [growth arrest and D

74 During apoptosis, XIAP is antagonized by SMAC, which is released from the

75 ith the mRNA that encodes the anti-apoptotic XIAP, simultaneously decreasing expression of both prote

76 inding protein with low pI); anti-apoptotic: XIAP (X-linked inhibitor of apoptosis)] are involved, we

77 omain and bind to cIAP1 and cIAP2 as well as XIAP.

78 eles can be replaced with disease-associated XIAP variants expressed at endogenous levels to simultan

79 pression of a mutant CSR1 that does not bind XIAP.

80 indicated that the C-terminus of CSR1 binds XIAP with high affinity.

81 t that cell death is induced when CSR1 binds XIAP, preventing the interaction of XIAP with caspases.

82 nown pathway members RIPK2, RELA, and BIRC4 (XIAP) as well as FRMPD2 (FERM and PDZ domain-containing

83 over, intramitochondrial Smac degradation by XIAP occurs independently of Drp1-regulated cytochrome c

84 ize NOD2 and cell death phenotypes driven by XIAP.

85 significant level of control of the HIF1 by XIAP, with important implications in understanding the r

86 Lys63-linked ubiquitination of HIF1alpha by XIAP is dependent on the activity of E2 ubiquitin conjug

87 enotype of iNKT cells, which is inhibited by XIAP although it exerts a moderate effect in conventiona

88 occurred at Lys-138, which was inhibited by XIAP domain.

89 on of cancer cell invasion and metastasis by XIAP.

90 ated that the regulation of cell motility by XIAP depends on its interaction with the Rho GDP dissoci

91 f apoptosis (XIAP) and partially reverted by XIAP overexpression.

92 ulated gene expression such as COX-2, cIAP2, XIAP, and IL-8 in a dose- and time-dependent manner, whi

93 or enteropathy, with clinical consequences (XIAP, CYBA, SH2D1A, PCSK1).

94 Consequently, XIAP E3 ligase activity recruits endolysosomes into mito

95 ypothesized that prolonged CS would decrease XIAP, whereas upregulation of XIAP with the novel compou

96 and female Ube3A 2X ASD mice show decreased XIAP levels, increased caspase-3 activation, and elevate

97 n vitro demonstrated significantly decreased XIAP and significantly increased apoptosis, caspase-3 pr

98 y proteins and mitochondrial depolarization, XIAP can permeabilize and enter mitochondria.

99 luminescence assay reveal that the designed XIAP domains can bind strongly with the Smac peptides bu

100 Surprisingly, the UbV selective for dimeric XIAP formed a dimer to stimulate E3 activity by stabiliz

101 UBE4B, phosphorylated active CBL, or dimeric XIAP.

102 d framework to rapidly test newly discovered XIAP variants.

103 Endogenous mRNAs encoding XIAP, c-Myc, CYR61, and Pim-1, which are translated in a

104 n expression was only observed in endogenous XIAP, but not in constitutionally exogenously expressed

105 nderstanding of the regulation of endogenous XIAP by a DR antagonist, pointing out at FAIM-L as a pro

106 s in MDM2 protein stabilization and enhanced XIAP translation.

107 Here, we explore XIAP as an important mediator of an immune response agai

108 ot in constitutionally exogenously expressed XIAP in the same cells, excluding the possibility of ISO

109 rolonged CS/REW by the "prosurvival" factors XIAP and pAkt.

110 i-apoptotic proteins, such as BCL2, c-FLIPS, XIAP, and C-IAP2.

111 eased potency against cIAP2 and affinity for XIAP BIR3 and (ii) decreased ability to inhibit XIAP-dep

112 CS with or without UCF-101, and examined for XIAP, caspase-3, and tubular apoptosis.

113 ratio decreased for DIABLO and increased for XIAP.

114 3 ligase within RING domain was required for XIAP inhibition of phosphatase PP2A activity by up-regul

115 Inhibitors selective for XIAP should exert pro-apoptotic effects through competit

116 d upregulation of antiapoptotic genes (e.g., XIAP and GADD45B) and downregulation of proapoptotic gen

117 onists TNFalpha or TRAIL and inhibited cIAP1>XIAP>IAP2.

118 sis protein (XIAP)-overexpressing HeLa (HeLa XIAP(Adv)) cells, only showed delayed and often no caspa

119 D) pathway of the tick Ixodes scapularis How XIAP activates the IMD pathway in response to microbial

120 Human XIAP was delivered with bicistronic expression of green

121 We also demonstrate that (i) XIAP polyubiquitination is dependent on the really inter

122 alone and in complex with the X-linked IAP (XIAP)-BIR2-BIR3 domains.

123 le reconciling the role of XLP-2 and VEO-IBD XIAP mutations in inflammatory cell death and provide a

124 r, the reported effects of XLP-2 and VEO-IBD XIAP mutations on cell death have been inconsistent.

125 ll death data to show that XLP-2 and VEO-IBD XIAP mutations that exhibit a loss-of-function NOD2 phen

126 ved from DNA-programmed chemistry identified XIAP BIR2 and BIR3 domain inhibitors that displace bound

127 sting new gene (RING) catalytic domain, (ii) XIAP polyubiquitination occurs via lysine (K)-63 but not

128 sine (K)-63 but not K-48 residues, and (iii) XIAP-dependent K-63 polyubiquitination requires zinc for

129 Therefore, development of XLP-2 in XIAP-deficient patients could be partly due to sustained

130 ependent cell growth were also attenuated in XIAP-deficient cancer cells compared with those of the p

131 n of activated caspases and are decreased in XIAP-deficient individuals.

132 is the first reported whole gene deletion in XIAP, the causal gene responsible for XLP2 (X-linked lym

133 to identify a de novo whole gene deletion in XIAP.

134 5 children with IBD (including 5 variants in XIAP, 3 in DOCK8, and 2 each in FOXP3, GUCY2C, and LRBA)

135 to reconcile the aforementioned inconsistent XIAP cell death data to show that XLP-2 and VEO-IBD XIAP

136 UCF-101 significantly increased XIAP in donor kidneys and protected against apoptosis.

137 UCF-101 treatment significantly increased XIAP, significantly decreased capsase-3 protein and acti

138 P BIR3 and (ii) decreased ability to inhibit XIAP-dependent signaling pathways.

139 Finally, we report that FAIM-L inhibits XIAP auto-ubiquitinylation and maintains its stability,

140 ta reveal a transcriptional switch involving XIAP-mediated ubiquitylation of Gro/TLE that facilitates

141 vel leads to the activation of an E3-ligase, XIAP, which potentiates IL-17-induced NFkappaB activatio

142 ting enzyme, Ubc12, to the ubiquitin ligase, XIAP or cIAP1.

143 Importantly, one of the MDM2/XIAP inhibitors, MX69, showed minimal inhibitory effect

144 PEI) inhibited tumor growth via AKT-mediated XIAP degradation in both subcutaneous and quasi-orthotop

145 Here, we explored mitochondrial XIAP action within the intrinsic apoptosis signaling pat

146 Importantly, mitochondrial XIAP actions are activated cell-intrinsically by typical

147 To elucidate the role of mitochondrial XIAP action during apoptosis, we integrated our findings

148 istically, we demonstrate that mitochondrial XIAP entry requires Bax or Bak and is antagonized by pro

149 creases of XIAP, combined with mitochondrial XIAP preconditioning, would reduce MOMP signaling.

150 mechanism by which miR-24 directly modulates XIAP expression level and consequently the apoptosis thr

151 Moreover, XIAP knockdown in SW480 cells enhanced the basal and rad

152 Neither XIAP nor Bcl-2 is affected by alphavbeta6 expression.

153 etails our synthetic explorations of a novel XIAP BIR2-selective benzazepinone screening hit with a f

154 which antagonizes the inflammatory action of XIAP without inducing apoptosis.

155 ed a novel function of E3 ligase activity of XIAP in the up-regulation of cyclin D1 expression, provi

156 ent, orally bioavailable, dual antagonist of XIAP and cIAP1 and a structurally novel chemical probe f

157 We found that deficiency of XIAP expression resulted in a marked reduction in cyclin

158 ted by the ubiquitination and degradation of XIAP (X-linked inhibitors of aptosis protein) by E6AP, w

159 The BIR3 domain of XIAP binds and inhibits caspase 9, while the BIR2 domain

160 E3 ligase activity within the RING domain of XIAP is crucial for its ability to regulate cyclin D1 tr

161 of RhoGDI SUMOylation by the RING domain of XIAP may account for modulation of cancer cell invasion

162 FAIM-L interacts with the BIR2 domain of XIAP through an IAP-binding motif, the mutation of which

163 s critically dependent on the BIR2 domain of XIAP.

164 Targeted knock-down of XIAP enhanced CSR1-induced cell death, while overexpress

165 rates, cleavage of PARP-1, downregulation of XIAP and MCL-1, and activation of caspases, which collec

166 stance in cancer cells via downregulation of XIAP expression, and the resulting cancer cell death ind

167 many human cancers, and forced expression of XIAP blocks apoptosis.

168 Expression of XIAP protein, but not mRNA, was highly increased in neur

169 ; this process was mediated by expression of XIAP, which bound to cleaved caspase-3.

170 The antiapoptotic function of XIAP derives from its BIR domains, which bind to and inh

171 Inactivation of XIAP, a direct target of ARTS, abrogated these phenotype

172 mulations suggest that moderate increases of XIAP, combined with mitochondrial XIAP preconditioning,

173 onstitutive activation of p53, inhibition of XIAP and sensitization of cancer cells to apoptosis.

174 egulation resulted not only in inhibition of XIAP expression, but also in activation of p53, which co

175 rexpressed and pharmacological inhibition of XIAP in these cell lines reduced autophagosome biogenesi

176 In conclusion, inhibition of XIAP rescues cellular radiosensitivity and both DIABLO a

177 sistent with this observation, inhibition of XIAP suppresses cell proliferation, resulting in cell de

178 Notably, we show that combined inhibition of XIAP, SRD5A1 and AR pathways overcomes castration resist

179 R1 binds XIAP, preventing the interaction of XIAP with caspases.

180 IM-L requires sustained endogenous levels of XIAP to protect Type II cells as well as murine cortical

181 intestinal crypts expressed lower levels of XIAP, cIAP1, cIAP2, and cFLIP than liver tissue.

182 It is possible that the loss of XIAP and its antiapoptotic functions contributes to the

183 e kidneys ex vivo is associated with loss of XIAP and subsequent tubular cell apoptosis.

184 UCF-101 protects against the loss of XIAP during prolonged CS both in vitro and ex vivo, and

185 Loss of XIAP leads to increased cell death, whereas XIAP overexp

186 -induced cell death, while overexpression of XIAP antagonized CSR1 activity.

187 showed that CagA induces phosphorylation of XIAP E3 ubiquitin ligase, which enhances ubiquitination

188 The pro-survival properties of XIAP come from binding of the BIR domains to the pro-apo

189 chanisms that determine the diverse range of XIAP expression seen in cancer remains unclear.

190 of G. cleistostachyum by down-regulation of XIAP expression and induction of apoptosis through speci

191 ent with a posttranscriptional regulation of XIAP expression.

192 Of interest, PERK's down-regulation of XIAP occurs independently of CHOP activity.

193 udies have shown that ISO down-regulation of XIAP protein expression was only observed in endogenous

194 dentified miR-24 as a candidate regulator of XIAP expression.

195 The results of this work support the role of XIAP in mediating NOD2 signaling while reconciling the r

196 Molecularly, the role of XIAP mutations in the pathogenesis of these disorders is

197 e peptides, in a manner analogous to that of XIAP-mediated inhibition of caspases-3 and -7.

198 effect is mediated by the ubiquitination of XIAP (X-linked inhibitor of aptosis protein) by E6AP, su

199 would decrease XIAP, whereas upregulation of XIAP with the novel compound UCF-101 would protect again

200 innate-like T-cell homeostasis depending on XIAP and PLZF.

201 significantly abrogated miR-24's effects on XIAP expression.

202 g of MDM2 RING protein to the IRES region on XIAP mRNA results in MDM2 protein stabilization and enha

203 nts revealed multiple Hsp70-binding sites on XIAP, suggesting that it is a direct, physical Hsp70 cli

204 In conclusion, targeting E6 or XIAP in combination with cisplatin can efficiently poten

205 wild-type C57BL/6 mice, cIAP2-null mice, or XIAP-null mice.

206 ), which has high levels of selectivity over XIAP BIR3 and cIAP1 BIR2/3 and shows efficacy in a xenog

207 the biomedical significance of overexpressed XIAP in cancer development, further offering a new molec

208 e identified and studied three novel patient XIAP mutations and used this system to characterize NOD2

209 IAP synthesis through eIF2alpha and promotes XIAP degradation through ATF4.

210 the expression of the anti-apoptotic protein XIAP.

211 t the X-linked inhibitory apoptosis protein (XIAP) associates with the C terminus of Ptch1 (Ptch1-C)

212 hat X-linked inhibitor of apoptosis protein (XIAP) interacted with RhoGDI via its RING domain and neg

213 X-linked inhibitor of apoptosis protein (XIAP) is a potent caspase inhibitor and an important bar

214 The X-linked inhibitor of apoptosis protein (XIAP) is a potent caspase inhibitor, best known for its

215 by X-linked inhibitor of apoptosis protein (XIAP) is a potential mechanism by which apoptosis is pre

216 The X-linked inhibitor of apoptosis protein (XIAP) is a well known potent inhibitor of apoptosis; how

217 ced X-linked inhibitor-of-apoptosis protein (XIAP) levels in these cells.

218 med x-linked inhibitor of apoptosis protein (XIAP) restricts bacterial colonization of this arthropod

219 aB- X-linked inhibitor of apoptosis protein (XIAP) signaling pathway.

220 bit X-linked inhibitor of apoptosis protein (XIAP) suppression of executioner caspases, respectively.

221 the X-linked inhibitor of apoptosis protein (XIAP) using a benzamide-sulfonyl fluoride warhead.

222 of X-linked inhibitor of apoptosis protein (XIAP), activation of NF-kappaB, and proteasome activity

223 een x-linked inhibitor of apoptosis protein (XIAP), an E3 ubiquitin ligase, and the E2 conjugating en

224 P), X-linked inhibitor of apoptosis protein (XIAP), and perforin expression, respectively.

225 and X-linked inhibitor of apoptosis protein (XIAP), are obligate Hsp70 clients that are rapidly (with

226 or, X-linked inhibitor of apoptosis protein (XIAP), has been associated with chemotherapy resistance

227 ith X-linked Inhibitor of Apoptosis Protein (XIAP), using yeast two-hybrid screening analyses.

228 the X-linked inhibitor of apoptosis protein (XIAP), whose primary function is to suppress the cell de

229 in X-linked inhibitor of apoptosis protein (XIAP), with poorly understood molecular mechanisms.

230 to X-linked inhibitor of apoptosis protein (XIAP)-overexpressing HeLa (HeLa XIAP(Adv)) cells, only s

231 the X-linked inhibitor of apoptosis protein (XIAP).

232 osome-linked inhibitor of apoptosis protein (XIAP).

233 and X-linked inhibitor of apoptosis protein (XIAP).

234 of X-linked inhibitor of apoptosis protein (XIAP).

235 ght inhibitors that blocked the MDM2 protein-XIAP RNA interaction, leading to MDM2 degradation.

236 egulates short-lived antiapoptotic proteins, XIAP and c-FLIPL by inhibiting global protein synthesis.

237 accelerate Hsp70 drug discovery by providing XIAP as a pharmacodynamic biomarker.

238 in E6-supressed cells was related to reduced XIAP levels and not due to reduced p21 levels.

239 We also identified that ISO down-regulated XIAP gene transcription via inhibition of Sp1 transactiv

240 ing protein human antigen R (HuR), regulated XIAP mRNA stability and expression.

241 We find that PERK down-regulates XIAP synthesis through eIF2alpha and promotes XIAP degra

242 excluding the possibility of ISO regulating XIAP expression at the level of protein degradation.

243 Mechanistically, [pIC](PEI) repressed XIAP and survivin expression and activated an immune res

244 will focus on the optimization of selective XIAP BIR2 inhibitors leading to the discovery of highly

245 ffer a further theoretical basis for setting XIAP as a potential prognostic marker and specific targe

246 Recent work has consistently shown XIAP to be critical for signaling downstream of the Croh

247 n summary, this study reveals a IL-17-STEAP4-XIAP axis through which the inflammatory response induce

248 occurring V30E mutant also did not suppress XIAP and HuR.

249 f cells transfected with exogenous HA-tagged XIAP.

250 depolarization or by artificially targeting XIAP to the intermembrane space.

251 In the current study, we discovered that XIAP and its E3 ligase played a crucial role in regulati

252 Here, we report preclinical evidence that XIAP offers an effective therapeutic target in neuroblas

253 We find that XIAP and Ubc13 dependent Lys63-linked polyubiquitination

254 Taken together, we propose that XIAP enters mitochondria through a novel mode of mitocho

255 Here we report that XIAP and cIAP1 induce autophagy by upregulating the tran

256 Together, our findings show that XIAP targeting sensitizes neuroblastoma to chemotherapy-

257 Here we showed that XIAP deficiency selectively impaired B-cell chronic lymp

258 Recent studies suggest that XIAP is involved in immune signaling.

259 cytosol and on mitochondria, suggesting that XIAP plays a critical role in the activation and translo

260 The XIAP expression was maintained in ground squirrel RTECs

261 ro recombinant protein-binding analyses, the XIAP-binding motif in CSR1 was determined to include ami

262 ewly synthesized drug is able to disrupt the XIAP:p19/p12-CASP7 complex and induce apoptosis in caspa

263 for the first time that Shigella evades the XIAP-mediated immune response by inducing the BID-depend

264 Here, we identified the XIAP enzymatic substrate p47 as a positive regulator of

265 in different human conditions including the XIAP immunodeficiency.

266 Using a luciferase construct of the XIAP 3'UTR, we showed that miR-24 specifically coordinat

267 hat miR-24 directly targets the 3'UTR of the XIAP messenger RNA (mRNA) to exert translational repress

268 n-protein interaction (PPI) inhibitor of the XIAP:p19/p12-CASP7 complex.

269 treat CASP3/DR malignancies by targeting the XIAP:p19/p12-CASP7 complex, but also elucidate the molec

270 profile of these compounds; it binds to the XIAP BIR3 domain, the BIR domain of ML-IAP, and the BIR3

271 that miR-24 specifically coordinates to the XIAP mRNA.

272 GDP dissociation inhibitor (RhoGDI) via the XIAP RING domain.

273 s critical for stimulating apoptosis through XIAP and survivin degradation.

274 with a diazabicyclic core structure bind to XIAP, cIAP1, and cIAP2 with low to subnanomolar affiniti

275 ion of compound 12 (SM-1200), which binds to XIAP, cIAP1, and cIAP2 with Ki values of 0.5, 3.7, and 5

276 CAS/imp-alpha1 transport cycle is linked to XIAP and is required to maintain tumor cell survival in

277 vity; however, the function of the wild-type XIAP can be eliminated by the binding of Smac peptides.

278 ctivity in vitro compared with the wild-type XIAP protein.

279 the brain and face is dependent in part upon XIAP mediation of Hh/Ptch1-regulated cell survival and a

280 SATB2 overexpression also upregulated XIAP and cyclin D1, suggesting its role in cell survival

281 Using XIAP as a model system, we further investigated a variet

282 offering a new molecular basis for utilizing XIAP E3 ligase as a cancer therapeutic target.

283 rsed the actions of THBS1 on cell viability, XIAP, and cleaved caspase-3.

284 ent B-cell lymphoma-derived cell lines where XIAP is overexpressed and pharmacological inhibition of

285 m apoptosis in pathological situations where XIAP levels are decreased.

286 XIAP leads to increased cell death, whereas XIAP overexpression significantly enhances resistance to

287 ights into the molecular mechanisms by which XIAP regulates cancer invasion and offer a further theor

288 em for cells of the myeloid lineage in which XIAP alleles can be replaced with disease-associated XIA

289 While XIAP BIR3 inhibitors have previously been reported, they

290 rence enhanced EF24-induced apoptosis, while XIAP overexpression reduced it in CCA cells.

291 vely and rapidly form a covalent adduct with XIAP-BIR3 in vitro and in cell, approaching the rate of

292 the chemotherapy resistance associated with XIAP and cIAP1 overexpression observed in several human

293 cute the apoptotic program, yet binding with XIAP constitutively inhibits active caspase-7 (p19/p12-C

294 y cocrystal structures of key compounds with XIAP BIR2 suggested potency-enhancing structural modific

295 The binding of CSR1 with XIAP enhanced caspase-9 and caspase-3 protease activitie

296 egimens should not be used for patients with XIAP deficiency.

297 on the treatment of the cancer patients with XIAP overexpression.

298 identifies the expression patterns of XAF1, XIAP and SRD5A1 as a predictive and actionable signature

299 d in a recent publication that reveals XAF1, XIAP, and SRD5A1 as novel predictive biomarkers and ther

300 cells, which overexpress CDK6, BCL2, Bcl-xL, XIAP, and AKT, but lack ibrutinib resistance-conferring

301 aB targets of antiapoptotic proteins Bcl-xL, XIAP, and cIAP2.