ライフサイエンスコーパス: IAP

1 IAP antagonists, such as Reaper, Hid, and Grim, are thou

2 IAP from indoor coal use increases the risk of lung canc

3 IAP is a major regulator of gut mucosal permeability and

4 IAP provides user-friendly interfaces, and its core func

5 IAPs are therefore, not only gatekeepers of cell death,

6 IAPs contain one to three BIR domains that are crucial f

7 IAPs have been proposed as targets for anticancer therap

8 eeded to be treated (NNT-value) to prevent 1 IAP.

9 analyze the DNA methylation pattern of 4799 IAP LTR retrotransposons in embryonic stem, somatic and

10 sion, the risk of EOGBS in settings with 80% IAP coverage was predicted to be 0.3% (95% CI, 0-.9).

11 cles" (LVs) (1) contain catalytically active IAP that can dephosphorylate lipopolysaccharide (LPS), (

12 Systematic identification of additional IAP substrates is challenged by the heterogeneity and sh

13 pper-bound confidence interval for aggregate IAP harm is implausibly high.

14 AP antagonist structurally distinct from all IAP antagonists previously reported.

15 y, we uncover a unique role for BIRC3, as an IAP that is critical in GBM in response to therapy.

16 Of these, 60 of 95 (63%) had an IAP policy; 35 of 60 (58%) used microbiological screenin

17 We have identified an IAP-binding motif (IBM) at the amino terminus of NIK.

18 acts with the BIR2 domain of XIAP through an IAP-binding motif, the mutation of which impairs the ant

19 We included data on whether an IAP policy was in use, and if so whether it was based on

20 fection by pharmacological targeting with an IAP antagonist/second mitochondria-derived activator of

21 The risk of EOGBS in settings without an IAP policy was 1.1% (95% confidence interval [CI], .6%-1

22 ession of survival proteins in the Bcl-2 and IAP families and removed controls on the activation stat

23 ction of survival molecules in the Bcl-2 and IAP families, induced downstream of an IGF-1R/NFkappaB c

24 was diminished, and expression of Bcl-2 and IAP family members were down-regulated, resulting in hig

25 y, preceded by the upregulation of LINE1 and IAP transposons as well as activation of a DNA damage re

26 H4R3me2s chromatin modification on LINE1 and IAP transposons in PGCs, directly implicating this modif

27 e aimed to review GBS screening policies and IAP implementation worldwide.

28 collected from 20 patients postileostomy and IAP levels were compared between fasted and fed states.

29 Astrogenic RG and IAP cells proliferated in a progressive ventral-to-dorsa

30 ursor proliferation involves distinct RG and IAP cells; is subjected to temporal and spatial control;

31 Downregulation of OTUB1 promotes TWEAK- and IAP antagonist-stimulated caspase activation and cell de

32 WT and IAP-KO mice were used to examine gut barrier function an

33 biting DNA-PK reduced expression of RIP1 and IAPs in cisplatin-treated cells.

34 y consisting of histone H4, DNA-PK, RIP1 and IAPs that attenuates ROS-mediated apoptosis, and targeti

35 umber of proapoptotic proteins to antagonize IAP function.

36 40 of 44 (91%) high-income countries had any IAP policy.

37 Drosophila inhibitor of apoptosis (IAP) 1 (DIAP1) is an E3 ubiquitin ligase that regulates

38 Small-molecule inhibitor of apoptosis (IAP) antagonists, called Smac mimetic compounds (SMCs),

39 in, along with other inhibitor of apoptosis (IAP) family members (cIAP1, cIAP2, and X-linked inhibito

40 vin, a member of the inhibitor of apoptosis (IAP) family.

41 ion, a member of the inhibitor of apoptosis (IAP) family.

42 redominantly in the inhibitors of apoptosis (IAP) family.

43 ting gene coding for inhibitor of apoptosis (IAP) into larvae and adults resulted in a significant kn

44 SM antagonize inhibitor of apoptosis (IAP) proteins and simultaneously induce tumor necrosis f

45 Baculovirus-encoded inhibitor of apoptosis (IAP) proteins likely evolved from their host cell IAP ho

46 unique member of the inhibitor of apoptosis (IAP) proteins that is overexpressed in numerous cancers

47 lecule inhibitors of inhibitor of apoptosis (IAP) proteins.

48 Inhibitors of apoptosis (IAP-like proteins; ORF016, ORF025, and ORF074) were expr

49 In insects, inhibitor-of-apoptosis (IAP) proteins act as regulatory sentinels by responding

50 Inhibitor-of-apoptosis (IAP) proteins are key regulators of the innate antiviral

51 Inhibitor-of-apoptosis (IAP) proteins, particularly cIAP1, are essential mediato

52 on of antiapoptotic inhibitors of apoptosis (IAPs) and Bcl2 family members in macrophages, suggesting

53 Survivin, an inhibitor of apoptosis (IAPs) family member, exhibited a decreased expression le

54 Inhibitor of apoptosis (IAPs) proteins are characterized by the presence of evol

55 As IAP increased, the risk of EOGBS decreased, with a linea

56 d to a fragment-derived lead resulting in AT-IAP, a potent, orally bioavailable, dual antagonist of X

57 nked inhibitor of apoptosis, and baculoviral IAP repeat-containing 7 were all up-regulated in SPRIGHT

58 mature form (20.8 kDa) binds to baculoviral IAP repeat (BIR) domains of inhibitor of apoptosis prote

59 displacing active caspases from baculovirus IAP repeat domains in DIAP1, but can themselves become t

60 NIK interacts with the second baculovirus IAP repeat (BIR2) domain of c-IAP1 via the IBM, and this

61 ncluding the conservation of two baculovirus IAP repeat (BIR) domains and a C-terminal RING, viral IA

62 of interest that best discriminated between IAP-determined left or right dominance for language were

63 ates for epilepsy surgery and underwent both IAP and resting-state functional MR imaging as part of p

64 In contrast, in the absence of both IAPs and caspase-8, RIPK3 kinase activity and MLKL are e

65 vered that lepidopteran (moth and butterfly) IAPs, which are degraded upon baculovirus infection, are

66 oduction and consequent cell death caused by IAP depletion was attenuated by loss or inhibition of TN

67 e Beclin 1-dependent autophagy activation by IAPs described in this study.

68 r the vast majority of DALY losses caused by IAPs considered in this analysis, with impacts on par or

69 describe the identification of OTUB1 as a c-IAP-associated deubiquitinating enzyme that regulates c-

70 Through their E3 ligase activity c-IAP proteins promote ubiquitination of receptor-interact

71 The cellular inhibitor of apoptosis (c-IAP) proteins are E3 ubiquitin ligases that are critical

72 OTUB1 expression in zebrafish destabilizes c-IAP (Birc2) protein levels and disrupts fish vasculature

73 Apoptosis negative (c-IAP-2 and Bcl-xL) and positive (DR5) regulators were pot

74 Consequently, in the absence of c-IAP proteins, TNFR-mediated activation of NF-kappaB and

75 by upregulation of antiapoptotic protein (c-IAP-2) through calmodulin-dependent kinase-II activation

76 Thus, c-IAP-2 may prevent Vpr-mediated mitochondrial depolarizat

77 IAP antagonist that specifically triggers c-IAP degradation.

78 s have been developed that also target the c-IAPs and induce their degradation.

79 However, it is not clear how the c-IAPs specifically recognize and ubiquitylate NIK in the

80 NIK is brought into close proximity to the c-IAPs through a TRAF2-TRAF3 bridge where TRAF2 recruits c

81 sly shown to induce the degradation of the c-IAPs, to SM-164, a synthetic IAP antagonist that specifi

82 iota and that oral supplementation with calf IAP (cIAP) rapidly restores the normal gut flora.

83 proteins likely evolved from their host cell IAP homologs, which function as critical regulators of c

84 inhibitor of apoptosis, as well as cellular IAP-1.

85 ns Op-IAP3's requirement for native cellular IAP as a cofactor and the dispensability of caspase inhi

86 tination when bound to its targeted cellular IAP.

87 inating host IAP in such a way that cellular IAP levels and antiapoptotic activities are maintained.

88 unctioning as a protein degron, the cellular IAP leader dramatically shortened the life span of a lon

89 Thus, the leaders of cellular IAPs from diverse insects carry unique signal-responsive

90 Such signal-induced destruction of cellular IAPs is distinct from degradation caused by well-known I

91 spite their striking relatedness to cellular IAPs, including the conservation of two baculovirus IAP

92 Intrapartum antibiotic chemoprophylaxis (IAP) prevents most early-onset group B streptococcal (GB

93 ions that abrogate binding of well-conserved IAP antagonists did not affect Op-IAP3's capacity to pre

94 servations to a single BIR domain containing IAP family member melanoma-IAP (ML-IAP).

95 nique signal-responsive degrons that control IAP turnover.

96 egulates PDCD4 expression but also decreases IAP expression and enhances chemosensitivity in HA-treat

97 f the K-epsilon-GG epitope recognized during IAP, here we developed a large-scale FASP method (LFASP)

98 bsence of analogous degrons in virus-encoded IAPs explains their relative stability and antiapoptotic

99 the development of unprecedented high-energy IAP sources in the near future.

100 Enteral IAP supplementation may represent a novel approach to ma

101 ll-known IAP antagonists, which act to expel IAP-bound caspases.

102 show that the two most active ERV families, IAP and MusD/ETn, are major targets and are strongly inh

103 etically considered multi-colour drivers for IAP generation can be realized with existing high-power

104 and a structurally novel chemical probe for IAP biology.

105 Furthermore, IAP supplementation improves the lipid profile in mice f

106 Animals given IAP maintained their weight, had reduced clinical severi

107 ating with unstable, autoubiquitinating host IAP in such a way that cellular IAP levels and antiapopt

108 Viral IAP-mediated preservation of the host IAP homolog capitalizes on normal IAP-IAP interactions a

109 In insects, wherein the host IAP provides a primary restriction to apoptosis, diverse

110 nction, WT mice were fasted for 48 hours +/- IAP supplementation in the drinking water.

111 However, there is no description of how IAP is used around the world.

112 my in patients with concurrent elevations in IAP and ICP can reduce ICP.

113 Furthermore, although it was found in IAP virus-like particles, it did not affect their incorp

114 There is considerable heterogeneity in IAP screening policies and coverage worldwide.

115 Increasing IAP coverage was linearly associated with decreased risk

116 dipteran DIAP1 also conferred virus-induced IAP depletion by a caspase-independent mechanism.

117 We used Tet-inducible IAP gene expression to uncouple this process from virus-

118 Indeed, MOV10 inhibited IAP RTP.

119 g with reverse transcription, MOV10 inhibits IAP RTP, and this inhibition is independent of P bodies.

120 All recurrent attacks of AP after an initial IAP episode were registered.

121 ere that the N-terminal leader of two insect IAPs, Spodoptera frugiperda SfIAP and Drosophila melanog

122 Most known IAP inhibitors are selective for the BIR3 domain and bin

123 stinct from degradation caused by well-known IAP antagonists, which act to expel IAP-bound caspases.

124 ted arthritis is exacerbated in mice lacking IAPs, and is reduced by deletion of RIPK3, but not MLKL.

125 ed motifs that are not found in lepidopteran IAPs.

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

127 ibitor of apoptosis proteins (IAPs: X-linked IAP, cellular IAP1 and IAP2) regulate RIPK3 and MLKL ubi

128 complex with SfIAP, the native, short-lived IAP of host insect Spodoptera frugiperda.

129 tor zanamivir was therapeutic by maintaining IAP abundance and function.

130 domain containing IAP family member melanoma-IAP (ML-IAP).

131 About half of the variably methylated IAP LTRs tend to be hypomethylated in ES cells, and near

132 esults unveil a thus far unknown role for ML-IAP in controlling C-RAF stability and cell migration.

133 ontaining IAP family member melanoma-IAP (ML-IAP).

134 Furthermore, small molecule IAP antagonists can modulate spontaneous as well as TNF-

135 Consequently, small-molecule IAP antagonists, such as LCL161, have entered clinical t

136 equent optimization gave a potent nonalanine IAP antagonist structurally distinct from all IAP antago

137 f the host IAP homolog capitalizes on normal IAP-IAP interactions and is likely the result of viral I

138 Up to 50% to 75% of IAP may be due to microlithiasis, which is undetectable

139 The administration of IAP or the antiviral neuraminidase inhibitor zanamivir w

140 e regulated by differential amplification of IAP antagonists, unique caspase adaptor proteins, and mu

141 s a second-generation bivalent antagonist of IAP proteins that is currently undergoing clinical devel

142 s (over 18 years) with their first attack of IAP.

143 y of cancers has prompted the development of IAP antagonists as potential antitumor therapies.

144 The diagnosis of IAP was based on the exclusion of common etiological rea

145 viral escape mechanisms and the dynamics of IAP action has the potential to facilitate the developme

146 The profound negative effect of IAP antagonists on T-cell immunity was partially linked

147 and cancer include studies of the effect of IAP on cancers other than lung cancer; studies of geneti

148 To study the effect of IAP supplementation on starvation-induced gut barrier dy

149 studies to determine whether the effects of IAP are mediated via germline, somatic, and/or epigeneti

150 netic changes; and studies of the effects of IAP exposure via dermal and/or oral routes.

151 research is needed regarding the effects of IAP on other cancers and the effects of different types

152 t to induction of apoptosis by expression of IAP-antagonists, DNA-damaging agents and even knockdown

153 letely shared, indicating novel functions of IAP antagonists and consequences of c-IAP1/2 degradation

154 w this approach can enable the generation of IAP with the available high-energy kHz-repetition-rate Y

155 es, it did not affect their incorporation of IAP RNA, primer tRNAPhe (phenylalanine tRNA), or IAP Gag

156 their size and number, and the inhibition of IAP RTP persisted despite the depletion of their RCK sub

157 The loss of IAP expression is associated with decreased expression o

158 ike receptor 4 (TLR4)-dependent mechanism of IAP desialylation with accumulation of the IAP substrate

159 significant correlation between the onset of IAP expression and halted IFN-beta expression in cells w

160 ow-up of 36 (5-58) months, the recurrence of IAP was significantly higher in the control group than i

161 CC can effectively prevent the recurrence of IAP when all other possible etiologies of pancreatitis a

162 es of solid fuels, oral and dermal routes of IAP exposure, genetic and epigenetic mechanisms, and gen

163 of this method was assessed against that of IAP by using a variety of thresholds.

164 s substantially advance our understanding of IAP inhibitor-mediated regulation of TRAIL-induced cell

165 For validation of IAP, we performed an example experiment that contains 33

166 Ablation or antagonism of IAPs potently suppressed TNF- or RIPK1-induced proinflam

167 The corresponding contributions of IAPs to infectious disease outcomes are relatively unexp

168 umulation of cellular ROS and degradation of IAPs (cIAP1 and XIAP).

169 nity, Vince et al. report that inhibition of IAPs results in the processing and secretion of IL-1beta

170 mplex that may be related to optimization of IAPs binding.

171 Overexpression of IAPs occurs in various cancers and has been associated w

172 , along with increased retrotransposition of IAPs.

173 The prominent role of IAPs in controlling cell death and their overexpression

174 To define the role of IAPs in myelopoiesis, we generated a mouse with cIAP1, c

175 In this study, we analyzed the role of IAPs in T-cell immunity during lymphocytic choriomeningi

176 Normally, SETDB1 maintains silencing of IAPs, but in the absence of DNMT1, prolonged binding of

177 ALYs) lost, due to inhalation of a subset of IAPs in U.S. residences.

178 s report, we studied the effects of MOV10 on IAP RTP and its dependence on P bodies.

179 Opportunities for research on IAP and cancer include studies of the effect of IAP on c

180 nique samples, we identify BIRC3 is the only IAP whose differential expression is associated with lon

181 RNA, primer tRNAPhe (phenylalanine tRNA), or IAP Gag.

182 Oral IAP supplementation protected mice from antibiotic-assoc

183 ides) that occurs with dietary fat, and oral IAP supplementation prevents as well as reverses metabol

184 We postulate that oral IAP supplementation could represent a novel therapy to p

185 We hypothesized that oral IAP supplementation would protect against antibiotic-ass

186 hanistically distinct from that of known pan-IAP inhibitors.

187 nt attacks of idiopathic acute pancreatitis (IAP).

188 of the endogenous intracysternal A particle (IAP) by a similar mechanism.

189 osition (RTP) of intracisternal A particles (IAP).

190 ajor satellites, intracisternal A particles (IAPs), and imprinted genes remain relatively resistant t

191 group, the intracisternal A-type particles (IAPs), and performing simple correlations across all ERV

192 family and intracisternal A-type particles (IAPs).

193 ncer therapy, and a number of peptidomimetic IAP antagonists have entered clinical trials.

194 s given a 24 h of inoculation access period (IAP) to inoculate CCYV on cucumber plants showed a trans

195 der enzyme, intestinal alkaline phosphatase (IAP), in preventing a high-fat-diet-induced metabolic sy

196 ins such as intestinal alkaline phosphatase (IAP), which detoxify bacterial products and prevent inte

197 ecretion of intestinal alkaline phosphatase (IAP), which induces changes in the gut bacteria composit

198 learance of intestinal alkaline phosphatase (IAP).

199 re, we present Integrated Analysis Platform (IAP), an open-source framework for high-throughput plant

200 Indoor air pollutants (IAPs) cause multiple health impacts.

201 Indoor air pollution (IAP) derived largely from the use of solid fuels for coo

202 as well as 3,964 fixed and 1,986 polymorphic IAPs, in mouse.

203 We have identified >50 potential IAP substrates of both cytosolic and mitochondrial origi

204 call an 'intermediate astrocyte precursor' (IAP) located in the mantle region of the spinal cord.

205 Elevated intra-abdominal pressure (IAP) is associated with ICP elevation, and decompressive

206 ts of an intracarotid amobarbital procedure (IAP).

207 erage of intrapartum antibiotic prophylaxis (IAP), used to reduce the incidence of EOGBS.

208 s due to intrapartum antibiotic prophylaxis (IAP).

209 pulse of the inhibitor of apoptosis protein (IAP) antagonist reaper.

210 scription of inhibitor of apoptosis protein (IAP) antagonists reaper, hid and grim.

211 at maintains inhibitor of apoptosis protein (IAP) expression by release of microRNA-146a-mediated cat

212 he Bcl-2 and inhibitor of apoptosis protein (IAP) families.

213 mbers of the inhibitor of apoptosis protein (IAP) family and are key regulators of anti-apoptotic and

214 ember of the inhibitor of apoptosis protein (IAP) family, regulates mitosis and chromosome segregatio

215 n causes downregulation of survival protein (IAP) expression and enhancement of chemosensitivity.

216 Inhibitors of Apoptosis Protein (IAPs) are guardian ubiquitin ligases that keep classic p

217 Inhibitors of apoptosis proteins (IAP) exert critical control on the terminal segment of a

218 ression of inhibitors of apoptosis proteins (IAP) has been implicated in drug resistance in several c

219 appaB), and inhibitor of apoptosis proteins (IAP) were assayed by enzyme-linked immunosorbent assay,

220 rough expression of IFN antagonist proteins (IAPs).

221 Inhibitor of apoptosis proteins (IAPs) are important regulators of apoptosis and pro-surv

222 Inhibitors of apoptosis proteins (IAPs) are important regulators of both cell death and in

223 he roles of inhibitor of apoptosis proteins (IAPs) in the regulation of TNF-induced cell death in the

224 Inhibitor of apoptosis proteins (IAPs) play a major role in determining whether cells und

225 domains of inhibitor of apoptosis proteins (IAPs) releasing their inhibitory effects on caspases, th

226 Inhibitors of apoptosis proteins (IAPs) were originally described as regulating apoptosis

227 ) proteins, inhibitor of apoptosis proteins (IAPs), and murine double-minute 2 (MDM2).

228 Loss of inhibitor of apoptosis proteins (IAPs), particularly cIAP1, can promote production of tum

229 function of inhibitor of apoptosis proteins (IAPs), thereby promoting cancer cell death.

230 ists of the inhibitor of apoptosis proteins (IAPs).

231 in TRIF and inhibitor of apoptosis proteins (IAPs: X-linked IAP, cellular IAP1 and IAP2) regulate RIP

232 ibitors of the apoptosis family of proteins (IAPs) as well as chemoresistance in HSC-3 cells.

233 m, we investigated Op-IAP3, the prototypical IAP from baculovirus OpMNPV.

234 es examined, consistent with other published IAP inhibitors.

235 Isolated attosecond pulses (IAP) generated by high-order harmonic generation are val

236 antibodies for immunoaffinity purification (IAP) and subsequent identification of ubiquitination sit

237 to apoptosis, diverse viruses trigger rapid IAP depletion that initiates caspase-mediated apoptosis,

238 ated coverage (percentage of women receiving IAP where indicated).

239 More recently, IAPs have been identified as important modulators of can

240 iR-21 production leading to PDCD4 reduction, IAP upregulation and chemoresistance in HNSCC cells.

241 in distinct instability motifs that regulate IAP turnover and apoptotic consequences.

242 vity of the SfIAP RING, which also regulated IAP stability.

243 0 GBS colonized pregnant women that reported IAP coverage.

244 ed the movement of an endogenous retrovirus (IAP), our finding shed new light on this intracellular r

245 ional activation of ERVs, including CpG-rich IAP (intracisternal A particle) proviruses.

246 -responsive mechanisms by which the sentinel IAPs are actively degraded to initiate host apoptosis.

247 nisms and antagonistic partners for specific IAPs, and provide a powerful technology for labeling bin

248 In summary, IAP provides a multiple set of functionalities for impor

249 that both endogenous and orally supplemented IAP inhibits absorption of endotoxin (lipopolysaccharide

250 Surprisingly, IAP antagonism also led to spontaneous production of che

251 dation of the c-IAPs, to SM-164, a synthetic IAP antagonist that specifically triggers c-IAP degradat

252 However, the extent of a synthetic IAP antagonist's ability to mirror the transcriptional p

253 vide insight into the mechanism of synthetic IAP antagonists, furthering our understanding of their t

254 ondrial origin that bear hallmark N-terminal IAP binding motifs.

255 For the first time, we demonstrate that IAP expression is also decreased in humans who are depri

256 Finally, our data demonstrate that IAP supplementation reverses the gut barrier dysfunction

257 By demonstrating that IAP inhibitors and lexatumumab synergistically trigger a

258 t such as a virus infection, indicating that IAP antagonists may interfere with immune responses.

259 Here, we report that IAP inhibitors synergized with lexatumumab, but not with

260 Our laboratory recently showed that IAP is enriched on vesicles that are released from the t

261 Previously, we have shown that IAP detoxifies bacterial toxins, prevents endotoxemia, a

262 Previously, we have shown that IAP preserves the normal homeostasis of intestinal micro

263 These data indicate that IAPs not only prevent antiviral signalling prior to IFN-

264 Here, we show that IAPs are required for the production of multiple TNF-ind

265 the pro-apoptotic protease caspase-8 and the IAP ubiquitin ligases, how and when necroptosis is trigg

266 ccurred via the BIR3 domain of cIAP1 and the IAP-binding motif of C9b, but did not require proteolyti

267 NA-damaging agents and even knockdown of the IAP diap1.

268 ncoded by BIRC5), the smallest member of the IAP family, has been correlated with both the control of

269 f IAP desialylation with accumulation of the IAP substrate and TLR4 ligand, lipopolysaccharide-phosph

270 Correlation with the IAP was seen in 13 of 14 (93%) prospective patients, wit

271 phosphorylation-sensitive degron within the IAP N-terminal leader.

272 The IAPs are key regulators of the apoptotic pathways and ar

273 The IAPs were first discovered in baculoviruses because of t

274 The applicability of these IAP would be widened drastically by increasing their ene

275 induction of the E3 ligase activity of this IAP family member.

276 Thus, IAPs play a major role in influencing the production of

277 Thus, IAPs play an important role in T-cell expansion and surv

278 lly reduced in LCMV-infected mice exposed to IAP antagonists.

279 loss of maternal-zygotic PRMT5 also leads to IAP upregulation.

280 pporting a role for FADD in sensitization to IAP inhibitor and death ligands.

281 Rapid response pathways that trigger IAP degradation and initiate apoptosis independent of ca

282 ot viable, and 2 mimicked features of triple IAP knockout cells in vitro.

283 arteriovenous malformation who had undergone IAP and MEG.

284 be the state of the science in understanding IAP and its associations with cancer and suggest researc

285 Viral IAP-mediated preservation of the host IAP homolog capita

286 hortened the life span of a long-lived viral IAP (Op-IAP3) when fused to its N terminus.

287 teractions and is likely the result of viral IAP evolution in which degron-mediated destabilization a

288 We show here that the prototypical viral IAP, Op-IAP3, blocks apoptosis indirectly by associating

289 owever, the antiapoptotic mechanism of viral IAPs in host insects has been elusive.

290 t (BIR) domains and a C-terminal RING, viral IAPs use an unresolved mechanism to suppress apoptosis i

291 e dynamics of interference by selected viral IAPs, NS1 from Influenza A virus and NS3/4A from Hepatit

292 nation of these response motifs within viral IAPs, including those of baculoviruses, explains their u

293 Hence, when IAPs are absent, LPS triggers RIPK3 to activate caspase-

294 e suggests higher incidence in Africa, where IAP is rare.

295 However, while IAPs are derepressed in Dnmt1-ablated embryos and embryo

296 MOV10 also associated with IAP RNA.

297 tional MR imaging was highly concordant with IAP results, with up to 96% (22 of 23) accuracy, 96% (22

298 amined the association in risk of EOGBS with IAP coverage.

299 Also, feeding neonate larvae with IAP (inhibitor of apoptosis) or COP (COPI coatomer, beta

300 potential; and apoptosis upon treatment with IAP inhibitor and lexatumumab.