ライフサイエンスコーパス: RIP

1 RIP and esophageal manometry can objectively identify su

2 RIP is conserved from bacteria to humans and governs man

3 RIP is not recruited to this complex in Sam68 knockout c

4 RIP limits radiation dosage, interrupts treatment, and l

5 RIP-B7.1 mice homozygous for targeted disruption of TLR9

6 RIP-B7.1 transgenic mice express B7.1 costimulatory mole

7 RIP-Chip studies (and parallel assessments of total inpu

8 RIP-LCMV islets express CXCL10 after isolation and maint

9 The gene of a type 1 RIP related with the actual Euphorbiaceae type 1 RIPs fu

10 underwent deletions rendering either type 1 RIPs (like those from Cucurbitaceae, Rosaceae and Iridac

11 related with the actual Euphorbiaceae type 1 RIPs fused with a double beta trefoil lectin gene simila

12 nces revealed that the most primitive type 1 RIPs were similar to that of the actual monocots (Poacea

13 They have been classified as type 1 RIPs, consisting of single-chain proteins, and type 2 RI

14 is a type of receptor-interacting protein-1 (RIP-1)-dependent programmed necrosis called necroptosis,

15 Here, we demonstrate that RFS-1/RIP-1 acts by shutting down RAD-51 dissociation from ssD

16 hich nucleates RAD-51-ssDNA filaments, RFS-1/RIP-1 binds and remodels pre-synaptic filaments to a sta

17 stopped-flow experiments, we show that RFS-1/RIP-1 confers this dramatic stabilization by capping the

18 ating that remodeling is essential for RFS-1/RIP-1 function.

19 a heterodimeric Rad51 paralog complex, RFS-1/RIP-1, and uncovered the molecular basis by which Rad51

20 RAD51 paralog complex from C. elegans, RFS-1/RIP-1, functions predominantly downstream of filament as

21 leotide binding, but not hydrolysis by RFS-1/RIP-1.

22 Cucurbitaceae lectins to generate the type 2 RIPs and finally this gene underwent deletions rendering

23 Type 2 RIPs contain two polypeptide chains (usually named A, fo

24 The best known example of type 2 RIPs is ricin.

25 in the cell intoxication operated by type 2 RIPs ricin and abrin.

26 sisting of single-chain proteins, and type 2 RIPs, consisting of an A chain with RIP properties coval

27 is highly abundant among reads in our TDP-43 RIP-seq library.

28 ngle antigen-mismatched mouse model (C57BL/6 RIP-GP in C57BL/6) was used to evaluate the antigen-spec

29 Here we develop a RIP-seq method to capture the PRC2 transcriptome and ide

30 ctly activates programmed necrosis through a RIP homotypic interaction motif-dependent association of

31 upon RIP-specific Cre recombination using a RIP-Cre line first described by Herrera (RIP(HER)-Cre).

32 Additionally, pharmacologic treatment with a RIP kinase inhibitor attenuated histological and functio

33 Using this approach to ablate RIP(HER) neurons in the brain, but not in the pancreas,

34 SRF activated RIP II, and SRF binding to RIP II and the exon 5-encoded

35 obox-1 (Pdx-1) and synergistically activated RIP II.

36 ported for their protection of cells against RIPs.

37 racemate and showed cell protection against RIPs.

38 AGO2 RIP-Seq analysis revealed the differential recruitment o

39 We used a combined AGO2 RIP-seq and AGO2 PAR-CLIP-seq (photoactivatable-ribonucl

40 Using AGO2 RIP-seq and PAR-CLIP-seq, we show that the DNA damage-in

41 A-Seq) and AGO2-immunoprecipitated RNA (AGO2-RIP-Seq).

42 ecipitation followed by microarray analysis (RIP-chip) to recover and identify the endogenous RNA tar

43 ecipitation followed by microarray analysis (RIP-chip) was used to identify mRNA species preferential

44 antibodies, followed by microarray analysis (RIP-Chip).

45 d prevented by inhibiting both caspase-8 and RIP-1 activities.

46 can be applied on all variations of CLIP and RIP-seq technologies, (ii) it accurately models the unde

47 inking with immunoprecipitation- (CLIP-) and RIP-seq] for probing their activities have advanced rapi

48 ecroptosis execution downstream of IFN-I and RIP signaling remain elusive.

49 erage and vessel perfusion both in mPDAC and RIP-Tag2 tumors, in parallel to an inhibition of tumor h

50 approach involving expression profiling and RIP-Chip analysis, we have identified a cohort of transl

51 pitation)-seq datasets for 60 human RBPs and RIP-ChIP (RNP immunoprecipitation-microarray) data for 6

52 and RNA modification sites from CLIP-seq and RIP-seq data, and reveals the significant contribution o

53 hed fractions were digested with trypsin and RIP-II peptides were identified based on accurate mass L

54 of A. suum: these include the paired URX and RIP neurons, two pairs of lateral ganglion neurons in th

55 onstrate that, using a single protocol, APEX-RIP can isolate RNAs from a variety of subcellular compa

56 Since APEX-RIP is simple, versatile, and does not require special i

57 Here, we develop such a method, termed APEX-RIP, which combines peroxidase-catalyzed, spatially rest

58 ray analyses and downstream bioinformatics, 'RIP-Chip' experiments enable direct analyses of miRNA ta

59 st responsive mRNA target candidates in both RIP competition assays and expression profiling experime

60 by inspiratory flow limitation (measured by RIP and esophageal manometry) and classified as subglott

61 as Howardula rRNA in vitro at the canonical RIP target site within the alpha-sarcin/ricin loop (SRL)

62 eral high-throughput technologies (PAR-CLIP, RIP-chip, 4sU-tagging, and SILAC) provides strong eviden

63 rgeting technologies, specifically PAR-CLIP, RIP-chip, and whole-transcript expression profiling.

64 A bisulfite sequencing, m(1)A-Seq, Par-CLIP, RIP-Seq, etc.

65 This suggested the presence of an SC-cMRF-RIP pathway.

66 her oligodendroglial markers such as CNPase, RIP, and APC.

67 ree partners-RIP1, DAI, or TRIF-via a common RIP homotypic interaction motif.

68 ing the formation of 2 cell death complexes, RIP 1 (receptor-interacting protein 1)-FADD (Fas-associa

69 e substrates through a spatially coordinated RIP mechanism.

70 own-regulation was associated with decreased RIP II activity and increased SRF phosphorylation on ser

71 slets from either normal or CXCL10-deficient RIP-LCMV mice and transferred them under the kidney caps

72 We further show that DIM-2-dependent RIP requires DIM-5, HP1, and other known heterochromatin

73 Unlike any previously described RIP family member, the encoded protein carries an RNA re

74 Nonobese diabetic RIP-IL35 transgenic mice exhibited decreased islet infil

75 Combination therapy of diabetic RIP-LCMV and NOD mice with anti-CD3 and anti-CXCL10 anti

76 ed them under the kidney capsule of diabetic RIP-LCMV mice.

77 at contains a pair of truncated RIP domains (RIP-RIP).

78 e employed a rat insulin II promoter-driven (RIP-driven) Cre recombinase to disrupt the GH receptor i

79 comprehensive information than using either RIP-Chip or total mRNA profiling alone after miRNA trans

80 Five minutes after extubation, RIP and esophageal manometry better identified patients

81 Xbp1(f/f);RIP-cre mice displayed modest hyperglycemia and glucose

82 tein/multiple organellar RNA editing factor (RIP/MORF) boxes, which are required for ORRM1 to interac

83 l, which protects against both TNF-alpha/Fas-RIP-1-dependent necroptosis and TNF-alpha/Fas-independen

84 erties render a given substrate amenable for RIP, and how the lipid environment affects the substrate

85 nto lead identification and optimization for RIP antidote development to minimize the global health t

86 that the mechanism of repeat recognition for RIP involves direct interactions between homologous doub

87 in Rip1 or Rip3 revealed a critical role for RIP proteins in heme-induced cell death.

88 H-2d) mice transplanted with 400 islets from RIP.B7-H4 (H-2b) mice under the kidney capsule.

89 icantly up-regulated in isolated islets from RIP.B7-H4 compared with wild-type B6 mice (56%+/-23% vs.

90 lly, mice lacking synaptic GABA release from RIP-Cre neurons have reduced energy expenditure, become

91 response is dependent upon GABA release from RIP-Cre neurons.

92 e, selective activation of arcuate GABAergic RIP-Cre neurons, which monosynaptically innervate PVH ne

93 Thus, GABAergic RIP-Cre neurons in the arcuate selectively drive energy

94 erance in rat insulin promoter-glycoprotein (RIP-GP) mice.

95 g a RIP-Cre line first described by Herrera (RIP(HER)-Cre).

96 To define the function of hypothalamic RIP-expressing neurons, we set out to acutely and select

97 Using the OT-I RIP-mOVA model, we found that Nur77 deficiency did not s

98 he analyses support four major findings: (i) RIP-Chip studies correlated with total input mRNA profil

99 SRF bound to the rat insulin promoter II (RIP II) serum response element, an element conserved in

100 tification have used co-immunoprecipitation (RIP-Chip and others) and transfection-based experimental

101 using ribonucleoprotein immunoprecipitation (RIP) analysis, we discovered a novel function for MYF5 a

102 RNA immunoprecipitation (RIP) assay identified several putative target RNAs of At

103 In vivo RNA immunoprecipitation (RIP) assays revealed that SFPS associates with EARLY FLO

104 Here, we utilized RNA immunoprecipitation (RIP) combined with competitive binding assays to identif

105 ution than standard RNA immunoprecipitation (RIP) profiling or purely computational approaches.

106 tion into myotubes, RNP immunoprecipitation (RIP) analysis indicated that AUF1 binds prominently to M

107 quencing data from RNA immunoprecipitations (RIPs) and report that mRNAs associated with the cell cyc

108 cyclophosphamide and reduced tumor burden in RIP-Tag2 mice, without evidence of tumor cell sensitizat

109 ted cross priming of diabetogenic T cells in RIP-mOVA mice, a situation phenocopied in wild-type RIP-

110 legans, flp-8 expression was not detected in RIP, PQR, and PDA or -B or in the pharynx.

111 These actions were examined in RIP-Tag2 transgenic mice with pancreatic neuroendocrine

112 n tumor cell proliferation also was found in RIP-Tag2 tumors.

113 fferentiation by inducing 2-fold increase in RIP(+) cells (p<0.01) while the presence of miRs further

114 pancreatic neuroendocrine tumors (PNETs) in RIP-Tag2 mice and cervical carcinomas in HPV16/E2 mice.

115 ndicate that inhibition of VEGF signaling in RIP-Tag2 mice upregulates c-Met expression in lymphatic

116 f other macaques labeled axonal terminals in RIP, confirming this cMRF projection.

117 r proliferation in AI4alphabeta mice than in RIP-B7xAI4alphabeta mice.

118 or near pancreatic neuroendocrine tumors in RIP-Tag2 transgenic mice and whether lymph node metastas

119 findings outline a mechanism of IFN-induced RIP kinase-dependent necrotic cell death and identify FA

120 However, an intact RIP homotypic interaction motif (RHIM) is essential.

121 We use metaseq to integrate RIP- and ChIP-seq data for Shep and the core gypsy insul

122 OPNs) within the nucleus raphe interpositus (RIP) help gate the transition between fixation and sacca

123 ns labeled retrogradely from injections into RIP had numerous anterogradely labeled terminals closely

124 Thus, necrotic mechanisms involving RIP kinase are crucial in cone cell death in inherited r

125 ipitation (IP)-based methods such as RNA IP (RIP) and crosslinking and IP (CLIP) are key starting poi

126 nt to suppress TNF-induced necrosis, and its RIP homotypic interaction motif (RHIM) domain was requir

127 with pentatricopeptide transfactors via its RIP-RIP domain.

128 nd receptor-interacting protein (RIP) kinase RIP 3 (RIPK3) driving extrinsic apoptosis and necroptosi

129 interacting serine/threonine-protein kinase (RIP) 1/3 were observed in the cells transfected with the

130 Receptor-interacting protein kinase (RIP) 3 (also called RIPK3) mediates RIP homotypic intera

131 Because receptor-interacting protein kinase (RIP) 3-mediated necroptosis, a nonapoptotic cell death p

132 interacting serine/threonine-protein kinase (RIP)-3-mediated intestinal necroptosis was linked to inc

133 tion of receptor-interacting protein kinase (RIP)1 by necrostatin 1 partially inhibited TNF-alpha/ZVA

134 ated by receptor interacting protein kinase (RIP)3 (also called RIPK3) has emerged as an alternate de

135 ted by receptor-interacting protein kinases (RIPs).

136 Crossing with insulin-Cre lines (RIP-Cre and IPF1-Cre) to obtain pancreas-selective delet

137 kinase (RIP) 3 (also called RIPK3) mediates RIP homotypic interaction motif (RHIM)-dependent program

138 B7-H4 transgenic C57BL/6 (B6) mice (RIP.B7-H4) were developed by inserting the entire B7-H4

139 immunoprecipitation followed by microarray (RIP-chip) analysis showed that DHTS treatment of HeLa ce

140 rosynteny analyses, indicating that mosquito RIP genes derived from a single Horizontal Gene Transfer

141 induced receptor activation, but unlike most RIP target proteins, it requires endocytosis and does no

142 affinity-purified Puf3-TAP associated mRNAs (RIP-seq) identified mRNAs encoding mitochondrially-targe

143 ospora crassa repeat-induced point mutation (RIP) as a model system, we show that a pair of DNA segme

144 also mediate repeat-induced point mutation (RIP) of repetitive DNA in N. crassa.

145 profile of a repeat-induced point mutation (RIP) process distinctly different from what has been obs

146 nisms, namely repeat-induced point mutation (RIP), DNA methylation and small RNA-mediated gene silenc

147 Collectively, our study identifies a novel RIP in an insect defensive symbiont and suggests an unde

148 In addition, ablation of RIP(HER) neurons caused increased c-Fos immunoreactivity

149 A systematic phylogenetic analysis of RIP sequences revealed that the most primitive type 1 RI

150 f the alpha-helical substrate in the case of RIP may be associated with a hinge motion triggered by t

151 In this study, we employ a combination of RIP-seq and short- and long-wave individual-nucleotide r

152 event apoptosis together with competitors of RIP homotypic interaction motif (RHIM)-dependent signal

153 Necroptosis is mediated by engagement of RIP kinases and a downstream pseudokinase, MLKL.

154 een suggested to be two downstream events of RIP kinases.

155 ted for the first time in silico evidence of RIP encoding genes in metazoans, in two closely related

156 ines are likely not the dominant inducers of RIP kinase-driven embryonic lethality in FADD-deficient

157 to apoptosis, and simultaneous inhibition of RIP kinases and caspases is essential for effective neur

158 essed by the MCMV-encoded viral inhibitor of RIP activation (vIRA).

159 -encoded RHIM competitor, viral inhibitor of RIP activation, sustains viability of human cells like i

160 The performance of RIP scheme under heavy traffic load scenario is also qua

161 enzyme activity and required the presence of RIP.

162 pected cell death-independent requirement of RIP kinase activity in coordinating neuroinflammation, r

163 s work we have carried out a broad search of RIP sequence data banks from angiosperms in order to stu

164 Moreover, transsynaptic tracing of RIP(HER) neurons revealed labeling of neurons located in

165 ative method for more effective treatment of RIP and promises to improve quality of life of cancer pa

166 Treatment of RIP-Tag2 mice with XL999 resulted in 43% reduction in va

167 ions concerning mechanistic underpinnings of RIP and therapeutic interventions remain.

168 s of intracellular retrograde trafficking of RIPs.

169 cyclophosphamide in Lewis lung carcinomas or RIP-Tag2 tumors.

170 d pro-NGF do not induce homerdimerization or RIP, homodimers of p75(NTR) are gamma-secretase substrat

171 pitation followed by sequencing (CLIP-seq or RIP-seq) allows transcriptome-wide discovery of RNA regu

172 ein should be applicable to studies of other RIP events and amenable to developing in vitro assays fo

173 u interaction assay confirmed genes from our RIP-Seq data as the ZNF804A targets.

174 the RPM-1.FSN-1 complex inhibitory peptide (RIP), yields similar phenotypes and enhancer effects to

175 ated respiratory inductance plethysmography (RIP) and esophageal manometry to identify clinically sig

176 man retrotransposon insertion polymorphisms (RIPs), yielding an unprecedented catalog of common and r

177 nd that the nature of reactant ion positive (RIP) is dependent on the discharge/carrier gas compositi

178 The primitive RIPs evolved to the dicot type 1 related RIPs (like thos

179 Radiation-induced proctitis (RIP) is the most common clinical adverse effect for pati

180 3-dihydroquinazolin-4(1H)-one as a promising RIP inhibitor and for chemical characterization of drug

181 to beta-cells via the rat insulin promoter (RIP) II.

182 enic mouse model using rat insulin promoter (RIP)-driven Cre-loxP recombination system to specificall

183 cence imaging (BLI) of rat insulin promoter (RIP)-driven luciferase was used to monitor the fate of t

184 Rat insulin promoter (RIP)-expressing neurons in the hypothalamus control body

185 (OVA(323-339)) in the rat insulin promoter (RIP)-mOVA self-antigen model for their ability to trigge

186 n is controlled by the rat insulin promoter (RIP).

187 eading frame under the rat insulin promoter (RIP).

188 ell-specific promoter (rat insulin promoter [RIP]) stimulates proliferation of both alpha and beta ce

189 mericana is a ribosome-inactivating protein (RIP) and an RNA N-glycosidase that removes specific puri

190 sma encodes a ribosome-inactivating protein (RIP) related to Shiga-like toxins from enterohemorrhagic

191 , a notorious ribosome inactivating protein (RIP).

192 ave re-named ORF145 RNAP Inhibitory Protein (RIP).

193 LR9 results in receptor interacting protein (RIP) 3 kinase-dependent programmed necrosis that occurs

194 pe C57BL/6 and receptor interacting protein (RIP) 3(-/-) mice were randomized to chow or HFD.

195 the RNA-editing factor interacting protein (RIP) family and Organelle RNA Recognition Motif-containi

196 psis RNA-editing factor interacting protein (RIP) family and ORRM1 (Organelle RNA Recognition Motif-c

197 the RNA-editing factor interacting protein (RIP) family in Arabidopsis have recently been shown to b

198 ) that contain receptor-interacting protein (RIP) homotypic interaction motifs (RHIM) play a key role

199 this involves receptor-interacting protein (RIP) kinase 1/3, this study aimed to establish the role

200 , we show that receptor-interacting protein (RIP) kinase mediates necrotic cone cell death in rd10 mi

201 caspase-8 and receptor-interacting protein (RIP) kinase RIP 3 (RIPK3) driving extrinsic apoptosis an

202 evidence for a receptor-interacting protein (RIP) kinase-caspase-8-dependent macrophage apoptotic dea

203 e execution of receptor-interacting protein (RIP) kinase-dependent necroptosis, is upregulated and ac

204 onse to induce receptor-interacting protein (RIP) kinase-mediated necroptosis in macrophages.

205 es (IRAK), and receptor-interacting protein (RIP) kinases contribute to inflammasome functions.

206 is known that receptor interacting protein (RIP) kinases, RIP1 and RIP3, are key effectors of TNF-in

207 assembles with receptor-interacting protein (RIP)-2 kinase in response to the presence of bacterial m

208 2 (TRAF2), and receptor-interacting protein (RIP).

209 the necrosome, receptor-interacting protein (RIP)1 and RIP3, are highly expressed in PDA and are furt

210 ce precipitous receptor-interacting protein (RIP)1/RIP3 kinase-mediated necrosis when the adaptor pro

211 Receptor interacting protein (RIP)3 kinase (also called RIPK3) becomes active when eit

212 ctive SREBP transmembrane precursor protein, RIP of the anchor intermediate by site-2 protease genera

213 Ribosome inactivating proteins (RIPs) are RNA N-glycosidases that depurinate a specific

214 Ribosome inactivating proteins (RIPs) depurinate a universally conserved adenine in the

215 f the type 2 ribosome-inactivating proteins (RIPs) family (e.g. ricin, abrin) are potent cytotoxins s

216 Ribosome-inactivating proteins (RIPs) from angiosperms are rRNA N-glycosidases that have

217 nd ricin are ribosome-inactivating proteins (RIPs) that are lethal to mammals and pose a global healt

218 king to regulated intramembrane proteolysis (RIP) and expression of megalin.

219 cess of regulated intramembrane proteolysis (RIP) and has a significant impact on receptor function.

220 lled by regulated intramembrane proteolysis (RIP) and requires the site 2 protease RasP.

221 dergoes regulated intramembrane proteolysis (RIP) during late stationary phase in response to nutrien

222 cently, regulated intramembrane proteolysis (RIP) has been recognized as a mechanism whereby proteoly

223 Regulated intramembrane proteolysis (RIP) involves cleavage of a transmembrane segment of a p

224 Regulated intramembrane proteolysis (RIP) is a conserved mechanism crucial for numerous cellu

225 Regulated intramembrane proteolysis (RIP) is a mechanism of transmembrane signal transduction

226 induces regulated intramembrane proteolysis (RIP) of FGFR3.

227 ning in regulated intramembrane proteolysis (RIP) of OASIS, ATF6 and SREBP transcription factors, con

228 nducing regulated intramembrane proteolysis (RIP) to produce a transcriptional effector.

229 nown as regulated intramembrane proteolysis (RIP), thereby inactivating the cascade.

230 called regulated intramembrane proteolysis (RIP).

231 In this study, we used the prototypical RIP-Tag model of multistage pancreatic islet tumorigenes

232 A resources integrated provisioning (RIP) scheme using an auxiliary graph is introduced based

233 tor, and its deficiency dramatically reduces RIP recruitment and ubiquitylation.

234 ive RIPs evolved to the dicot type 1 related RIPs (like those from Caryophyllales, Lamiales and Eupho

235 RNA immunoprecipitation-RNAseq (RIP-Seq) identified transcripts bound to ZFP804A.

236 P-La(WT) and are less enriched in GFP-La(SD) RIPs.

237 pplied it to a wide range of public CLIP-seq/RIP-seq datasets involving numerous splicing factors, mi

238 As CLIP-seq/RIP-seq reads are short, existing computational tools fo

239 oprotein immunoprecipitation and sequencing (RIP-seq) analyses of HuR in oral cancer cells treated wi

240 immunoprecipitation followed by sequencing (RIP-seq), RNA sequencing (RNA-seq), and gene expression

241 tion followed by next-generation sequencing (RIP-seq), and the diversity of RNA species identified su

242 itation coupled with genome-wide sequencing (RIP-Seq) analysis revealed significant LIN28 binding wit

243 an be prevented by necrostatin-1, a specific RIP-1 inhibitor.

244 ratio is lower in islets from islet-specific RIP-iPLA2beta transgenic mice, whereas islets from globa

245 Specifically, RIP-Seq analyses showed that the majority of enriched RN

246 First, we show that recombinant Spiroplasma RIP catalyzes depurination of 28S rRNAs in a cell-free a

247 is cell death pathway requires an N-terminal RIP homotypic interaction motif (RHIM) within R1, acting

248 These mutations provide evidence that RIP plays a fundamental role in normal bone development.

249 e neurons have been limited by the fact that RIP expression is predominantly found in pancreatic beta

250 Thus, our experiments indicate that RIP(HER) neurons inhibit anorexigenic neurons in the PVN

251 These results reveal that RIP kinase-mediated necrosis strongly contributes to con

252 These findings suggest that RIP specifically inhibits the interaction between RPM-1

253 n of the genome and methylome suggested that RIP and DNA methylation combinatorially maintain G. sine

254 The RIP kinases (RIPKs) play an essential role in inflammato

255 We propose that caspase-8 and the RIP kinases are key regulators of macrophage cell death,

256 t assays (RNA-EMSA) were used to confirm the RIP results and demonstrate that the TZF domain of AtC3H

257 onstructs encoding a region encompassing the RIP-RIP domain or a region spanning the RRM domain of OR

258 imply that the induction of diabetes in the RIP-B7.1 model is critically dependent on TLR3 and MyD88

259 In the RIP-DTA mouse model of beta cell ablation, WS6 normalize

260 decline in functional beta cell mass in the RIP-DTR mouse, a model of hyperglycemia resulting from d

261 The enrichment of the RIP-II family of plant proteins, such as ricin, abrin, v

262 The galactose affinity of the RIP-II proteins enabled their selective enrichment from

263 herited retinal degeneration, suggesting the RIP kinase pathway as a potential target to protect cone

264 Here we show that the RIP homotypic interaction motif (RHIM) in RIPK1 prevents

265 Here, we report that the RIP homotypic interaction motifs (RHIMs) of RIP1 and RIP

266 Second, light inhibits pumping through the RIP-I1-MC neuron polysynaptic circuit, in which an inhib

267 x manifested this function by binding to the RIP homotypic interaction motif (RHIM) domains of TRIF a

268 contain a motif with some resemblance to the RIP Homotypic Interaction Motif (RHIM), a domain found i

269 trans-cMRF pathway connecting the SC to the RIP is present.

270 courage its incorporation, together with the RIP competition assay, into existing target prediction a

271 ics currently exist to protect against these RIPs.

272 Thus, RIP kinase-mediated programmed necrosis is a redundant m

273 ncreased death associated with increased TNF-RIP-mediated necrosis.

274 ation in Irbp(-/-) mice, implicating the TNF-RIP pathway as a potential therapeutic target to prevent

275 SRF activated RIP II, and SRF binding to RIP II and the exon 5-encoded 64-aa subdomain of SRF was

276 concentration down-regulated SRF binding to RIP II SRE, and this down-regulation was associated with

277 In contrast to RIP-independent classical Fas-induced cell death trigger

278 iew is to illuminate the pathways leading to RIP that have been identified and proposed.

279 ngle-copy MgDNMT gene made it susceptible to RIP, resulting in complete loss of cytosine methylation

280 Type 2 ribosome-inactivating protein toxins (RIP-II toxins) were enriched and purified prior to enzym

281 unique complex that not only contains TRAF2, RIP, and IKKalpha/beta/gamma but also CARMA1, MALT1, BCL

282 Defects caused by transgenic RIP were suppressed by loss of function in the dlk-1 MAP

283 R and EGFR, respectively, were used to treat RIP-Tag2 transgenic mice bearing advanced multifocal PNE

284 ied a gene that contains a pair of truncated RIP domains (RIP-RIP).

285 use model of pancreatic neuroendocrine tumor RIP-Tag2.

286 sis, but little is known about how these two RIP kinases mediate this process, although reactive oxyg

287 factor-88 (MyD88), and most of the wild-type RIP-B7.1 mice housed under normal conditions remained di

288 A mice, a situation phenocopied in wild-type RIP-mOVA mice treated with the selective Syk inhibitor R

289 prolonged accumulation of K63-ubiquitinated RIP within the TNFR1 signaling complex.

290 ndent recognition of homology that underlies RIP and, potentially, other processes where sequence-spe

291 efensive symbiont and suggests an underlying RIP-dependent mechanism in Spiroplasma-mediated defense.

292 or transgene was specifically expressed upon RIP-specific Cre recombination using a RIP-Cre line firs

293 Using RIP-seq, we identified a subset of lncRNAs that interact

294 oimmune destruction of islet isografts using RIP-LCMV mice expressing a lymphocytic choriomeningitis

295 into the structural changes that occur when RIP kinases are triggered to execute different signaling

296 d type 2 RIPs, consisting of an A chain with RIP properties covalently linked to a B chain with lecti

297 signal of rRNA depurination consistent with RIP-dependent modification and large decreases in the pr

298 Recipient BALB/c mice transplanted with RIP.B7-H4 islets established euglycemia for 42.3+/-18.4

299 in the pancreatic beta-cells (arf-bp1(FL/Y)/RIP-cre) were viable and displayed no obvious abnormalit

300 ficantly extended (p53(LFL/FL)/arf-bp1(FL/Y)/RIP-cre).