ライフサイエンスコーパス: RIP

1 RIP and esophageal manometry can objectively identify su

2 RIP enables a protein fragment of a transmembrane precur

3 RIP is conserved from bacteria to humans and governs man

4 RIP limits radiation dosage, interrupts treatment, and l

5 RIP measures work of breathing (WOB) indices including p

6 RIP mediated by site-1 protease (S1P) and site-2 proteas

7 RIP mutations are, however, relatively rare in coding se

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

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

10 RIP-LCMV islets express CXCL10 after isolation and maint

11 RIP-qPCR confirmed TTP binding to both sites, with a hig

12 RIP-seq and eCLIP analysis characterised the SND1 bindin

13 RIP-seq revealed that these proteins are bound primarily

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 hat were identified by HUMMR as containing a RIP domain.

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

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

35 rat insulin promoter and diphtheria toxin A (RIP-DTA) mice.

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

37 ported for their protection of cells 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 dentified sets of deregulated miRNAs by Ago2-RIP-seq.

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

43 owed by high-throughput RNA sequencing (Ago2-RIP-seq) to capture functionally active microRNAs (miRNA

44 een SSEA3/SSEA4/Globo-H and the FAK/CAV1/AKT/RIP complex in tumor progression and apoptosis and sugge

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

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

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

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

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

57 queries, bioinformatic analyses, as well as RIP and RNA pull-down assays, we discovered and validate

58 of RIP, the mutational burden appears to be RIP-associated but not directly caused by RIP.

59 ely rare in coding sequence, in part because RIP preferentially attacks GC-poor long duplicates that

60 ral organism, with 93-98% of mutations being RIP-associated.

61 plex virus 1 (HSV1) UL39-encoded ICP6 blocks RIP homotypic interacting motif (RHIM) signal transducti

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

63 focusing on CREB3L1 activation through both RIP and RAT, and discuss current open questions about th

64 be RIP-associated but not directly caused by RIP.

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

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

67 In resting cells, RIP of CREB3L1 is blocked by transmembrane 4 L6 family m

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

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

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

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

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

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

74 e substrates through a spatially coordinated RIP mechanism.

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

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

77 of poorly characterized ER stress-dependent RIP.

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

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

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

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

82 ion, and correlated this information with DO-RIP-Seq-identified DND1 direct targets.

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

84 complex that provides sequential, efficient RIP processing of full-length substrates to final produc

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

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

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

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

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

90 ver, the detailed mechanisms responsible for RIP of the transcription factors, including the precise

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

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

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

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

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

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

97 d cells, xenograft, and spontaneous genetic (RIP-Tag2) mouse models of PanNETs revealed that UPR sign

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

99 TRIF, the four mammalian proteins harboring RIP homotypic interaction motif (RHIM) domains, are key

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

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

102 RNA immunoprecipitation (RIP) and mRNA-decay assays reveal that QKI-7 binds and p

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

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

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

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

107 iferase experiment, RNA immunoprecipitation (RIP), and mRNA stability analysis, we evaluated the pote

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

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

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

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

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

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

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

115 Remarkably, ceramide-induced RIP of cAMP response element-binding protein 3-like 1 (C

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

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

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

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

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

121 Here, I review recent insights into RIP of membrane-bound transcription factors, focusing on

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

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

124 RIPK1 deficiency, or mutation of its RIP homotypic interaction motif (RHIM), triggers ZBP1-de

125 with pentatricopeptide transfactors via its RIP-RIP domain.

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

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

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

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

130 AKT and receptor-interacting protein kinase (RIP), respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

144 Nonetheless, RIP-deficient strains have over an order of magnitude fe

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

146 he high rate is largely due to the action of RIP, the mutational burden appears to be RIP-associated

147 TM4SF20 from an inhibitor to an activator of RIP of CREB3L1.

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

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

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

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

152 nd induces apoptosis through dissociation of RIP from the complex to interact with the Fas death doma

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

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

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

160 tions appear not to be the direct product of RIP being mostly in non-duplicate sequence and predomina

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

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

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

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

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

166 This study demonstrated the utility of RIP as a rapid, noninvasive approach for evaluating trea

167 hia treatment, consistent with the action of RIPs.

168 s of intracellular retrograde trafficking of RIPs.

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

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

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

172 munoprecipitation and RNA sequencing (8-oxoG RIP-seq) to identify 343 RNA transcripts heavily enriche

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

174 ive site of JIP60 are conserved in 815 plant RIPs in the Pfam database that were identified by HUMMR

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

176 Respiratory inductance plethysmography (RIP) provides a noninvasive method of PFT requiring mini

177 Repeat-induced point (RIP) mutation in Neurospora crassa degrades transposable

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

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

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

181 3-dihydroquinazolin-4(1H)-one as a promising RIP inhibitor and for chemical characterization of drug

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

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

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

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

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

187 oin, a type 1 ribosome-inactivating protein (RIP) contained in quinoa seeds.

188 (JIP60) is a ribosome-inactivating protein (RIP) from barley (Hordeum vulgare) and is involved in th

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

190 , a notorious ribosome inactivating protein (RIP).

191 isms for each 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 lated to RHIM [receptor-interacting protein (RIP) homotypic interaction motif], an amyloid motif regu

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

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

201 Receptor-interacting protein (RIP) kinase 3 (RIPK3)-dependent necroptosis directs infl

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

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

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

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

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

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

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

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

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

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

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

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

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

215 activity of Ribosome Inactivating Proteins (RIPs) encoded by Spiroplasma poulsonii.

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 eins by regulated intramembrane proteolysis (RIP) and regulated alternative translocation (RAT).

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

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

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

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

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

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

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

228 through regulated intramembrane proteolysis (RIP), to increase intracellular cholesterol and facilita

229 called regulated intramembrane proteolysis (RIP).

230 nown as regulated intramembrane proteolysis (RIP).

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

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

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

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

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

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

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

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

239 how by RNA coimmunoprecipitation sequencing (RIP-seq) that artificial PPR proteins designed to bind t

240 oprecipitation coupled with deep sequencing (RIP-seq) revealed that CDK12 regulates release of 4E-BP1

241 noprecipitation followed by deep sequencing (RIP-seq) reveals that cytoplasmic CBFB binds to hundreds

242 oprecipitation coupled with deep sequencing (RIP-Seq); and that PUMPKIN can bind RNA efficiently in v

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

244 e, using RNA immunoprecipitation-sequencing (RIP-seq), we identified the Polycomb-group histone methy

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

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

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

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

249 ay analysis of the RISC-bound miRNA targets (RIP-Chip) to evaluate the relative enrichment or depleti

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

251 mutations outside of duplicated domains than RIP-proficient strains.

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

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

254 This result supports a recent report that RIP-induced damage contributes to male embryo death.

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

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

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

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

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

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

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

262 Caspase-6 facilitated the RIP homotypic interaction motif (RHIM)-dependent binding

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

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

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

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

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

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

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

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

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

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

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

274 opmental Cell, Michael et al. (2019) use the RIP-Tag mouse model to show that pro-apoptotic signals m

275 ies perinatal lethality in mice in which the RIP homotypic interaction motif domain of RIPK1 has been

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

277 ng on the structural differences between the RIPs.

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

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

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

281 r transcription factors and are subjected to RIP by site-1 protease (S1P) and site-2 protease (S2P) s

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

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

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

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

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

291 Here, we used RIP-seq (RNA immunoprecipitation followed by high-throug

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

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

294 23-5p in GCB-DLBCL cells were verified using RIP-Northern blotting.

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

296 Whether RIP affects core genomic sequence in important ways is u

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

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

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

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