ライフサイエンスコーパス: NMD

1 NMD components, including smg-2/UPF1, are required to ac

2 NMD efficiency can be variable amongst individuals with

3 NMD in the nervous system of the animals is particularly

4 NMD inhibition with caffeine was shown to restore CHM mR

5 NMD is regulated in a tissue-specific and developmentall

6 NMD suppression by persistent DNA damage required the ac

7 NMD-elicit mutations in tumour suppressor genes (TSGs) a

8 NMD-escape fs-indels represent an attractive target for

9 NMD-escape mutations are additionally found to associate

10 rom January 2009 through March 2018 from 471 NMD facilities.

11 isense oligonucleotides circumvents aberrant NMD promoted by mutant SRSF2, restoring the expression o

12 Although NMD-induced loss-of-function has been shown to contribut

13 These results indicate that although NMD machinery is at work, efficiency is highly variable

14 Finally, after validating tranilast as an NMD-activating drug, we demonstrated the therapeutic pot

15 Activating transcription factor 3 (ATF3), an NMD target and a key stress-inducible transcription fact

16 f the 51 upregulated genes, 75% contained an NMD-targeting feature, thus identifying high-confidence

17 Moreover, we identified an NMD-regulated link between activation of the unfolded pr

18 ain KSHV transcription factor RTA, itself an NMD target.

19 lation of yars-2/tyrosyl-tRNA synthetase, an NMD target transcript, by daf-2 mutations contributes to

20 that neuron-specific disruption of UPF2, an NMD component, in adulthood attenuates learning, memory,

21 ay (NMD), and we found that both the EJC and NMD are antiviral and the EJC protein RBM8A directly bin

22 t expansion mutations and highlight eRF1 and NMD as therapeutic targets in C9orf72-associated ALS and

23 egulate p53beta in a synergistic manner, and NMD plays a critical role in the determination of the p5

24 gulated by Nonsense Mediated Decay (NMD) and NMD has been shown to be of variable efficiency in cance

25 on factor, was stabilized in a p38alpha- and NMD-dependent manner following persistent DNA damage.

26 echanistic relationship between splicing and NMD, we sought evidence for a specific role of mutant SR

27 ctional relationship between translation and NMD.

28 as effective as UPF1, expression of another NMD gene UPF2 also ameliorated the degenerative phenotyp

29 Hundreds of Arabidopsis NMD targets possess evident EJC footprints, validating t

30 nding of RNA surveillance mechanisms such as NMD and crucial for the development of therapeutic strat

31 dent mRNA translation, rapamycin can augment NMD of certain transcripts.

32 t yet been fully assessed, partially because NMD inactivation is lethal in many organisms.

33 cross multiple tumor types are controlled by NMD.

34 at leads to a frame shift and degradation by NMD.

35 rotects a subset of RNAs from degradation by NMD.

36 bserved for AS events that are detectable by NMD as well as for those that are not, which invalidates

37 apamycin modulates global RNA homeostasis by NMD.

38 Regulation of HR by NMD extends to multiple targets beyond RAD55, including

39 s observed in genes known to be regulated by NMD.

40 lternative distal 3'-UTR that is targeted by NMD, and (ii) RPS3 binding activates a poison 5'-splice

41 ode a transcript predicted to be targeted by NMD.

42 th 36 repeats (GR36) was sufficient to cause NMD inhibition.

43 ing transcripts, with UPF1 being the central NMD modulator.

44 Despite these global changes, NMD targets and mRNAs expressed at low levels with short

45 optive cell therapy treated melanoma cohort, NMD-escape mutation count is the most significant biomar

46 Across four independent melanoma cohorts, NMD-escape mutations are significantly associated with c

47 Surprisingly, however, some core NMD factors that are essential for NMD in simpler organi

48 Phosphorylation of the core NMD component UPF1 is critical for NMD and is regulated

49 Transcriptome-wide, the core NMD factor UPF1 preferentially recognizes long 3'UTR pro

50 quires the interaction of NBAS with the core NMD factor UPF1, which is partially localized at the ER

51 cted from the National Mammography Database (NMD).

52 graphy in the National Mammography Database (NMD).

53 tially regulated by Nonsense Mediated Decay (NMD) and NMD has been shown to be of variable efficiency

54 also contributes to nonsense-mediated decay (NMD) and xrn4 accumulates 3' fragments of select NMD tar

55 protect mRNAs from nonsense-mediated decay (NMD) by preventing the UPF1 RNA helicase from associatin

56 is dependent on the nonsense-mediated decay (NMD) component, Upf1, which promotes histone mRNA uridyl

57 Nonsense-mediated decay (NMD) degrades mRNAs containing a premature termination c

58 Nonsense-mediated decay (NMD) eliminates transcripts with premature termination c

59 mans, disruption of nonsense-mediated decay (NMD) has been associated with neurodevelopmental disorde

60 Nonsense-mediated decay (NMD) has been suggested to be responsible for the observ

61 Nonsense-mediated decay (NMD) is a eukaryotic mRNA surveillance system that selec

62 Nonsense-mediated decay (NMD) is a translation-dependent RNA quality control mech

63 Nonsense-mediated decay (NMD) is an important process that is best known for degr

64 likely mediated by nonsense-mediated decay (NMD) of splicing isoforms, with autism phenotypes usuall

65 INDEL that elicits nonsense-mediated decay (NMD) of the mutant mRNA.

66 egraded through the nonsense-mediated decay (NMD) pathway, we hypothesise that some fs-indels escape

67 licase required for nonsense-mediated decay (NMD) regulating mRNA stability in the cytoplasm.

68 he EJC has roles in nonsense-mediated decay (NMD), and we found that both the EJC and NMD are antivir

69 1 (UPF1), including nonsense-mediated decay (NMD), are inhibited in c9ALS/FTD brains and in cultured

70 not substrates for nonsense-mediated decay (NMD), even though they were detected in polysomes.

71 ty control process, nonsense-mediated decay (NMD), were found to genetically interact with rad55 phos

72 is subjected to the nonsense-mediated decay (NMD).

73 lele is degraded by nonsense-mediated decay (NMD).

74 ion termination and nonsense-mediated decay (NMD).

75 pts by antagonizing nonsense-mediated decay (NMD).

76 ipt degradation via nonsense-mediated decay (NMD).

77 with high levels of nonsense-mediated decay (NMD).

78 usion triggers nonsense-mediated mRNA decay (NMD) and unproductive translation of Bak1 transcripts (N

79 hat inhibiting nonsense-mediated mRNA decay (NMD) contributes to the pathogenesis of neurodevelopment

80 Nonsense-mediated mRNA decay (NMD) degrades EJC-bound mRNA, but the lack of suitable m

81 pletion of the nonsense-mediated mRNA decay (NMD) factor SMG7 or UPF1 significantly induced p53beta b

82 s required for nonsense-mediated mRNA decay (NMD) in eukaryotes, and the predominant view is that UPF

83 Nonsense-mediated mRNA decay (NMD) is a cellular surveillance pathway that recognizes

84 Nonsense-mediated mRNA decay (NMD) is a conserved translation-coupled quality control

85 Nonsense-mediated mRNA decay (NMD) is a eukaryotic mRNA quality control and regulatory

86 y machineries, nonsense-mediated mRNA decay (NMD) is a stress responsive cellular surveillance system

87 Nonsense-mediated mRNA decay (NMD) is a surveillance pathway that degrades aberrant mR

88 Nonsense-mediated mRNA decay (NMD) is an essential eukaryotic process regulating trans

89 Nonsense-mediated mRNA decay (NMD) is an evolutionarily conserved RNA decay mechanism

90 Nonsense-mediated mRNA decay (NMD) is the cell's natural surveillance mechanism that d

91 ase H prevents nonsense-mediated mRNA decay (NMD) of mRNAs.

92 d in mediating nonsense-mediated mRNA decay (NMD) of transcripts containing premature stop codons and

93 ediated by the nonsense-mediated mRNA decay (NMD) pathway and requires a conserved set of proteins in

94 rily conserved nonsense-mediated mRNA decay (NMD) pathway degrades aberrant mRNAs, but also functions

95 The nonsense-mediated mRNA decay (NMD) pathway degrades mRNAs containing long 3'UTRs to pe

96 The nonsense-mediated mRNA decay (NMD) pathway degrades some but not all mRNAs bearing pre

97 illnesses, the nonsense-mediated mRNA decay (NMD) pathway presents an unexplored regulatory mechanism

98 Nonsense-mediated mRNA decay (NMD) represents a eukaryotic quality control pathway tha

99 ass of cryptic nonsense-mediated mRNA decay (NMD) substrates with extended 3'UTRs that gene- or trans

100 athway, termed nonsense-mediated mRNA decay (NMD), by phosphorylating the NMD factor UPF1.

101 nisms, such as nonsense-mediated mRNA decay (NMD), which degrades both abnormal as well as some norma

102 ial targets of nonsense-mediated mRNA decay (NMD).

103 suppressor of nonsense-mediated mRNA decay (NMD).

104 e response and nonsense-mediated mRNA decay (NMD).

105 graded through nonsense-mediated mRNA decay (NMD).

106 degradation by nonsense-mediated mRNA decay (NMD).

107 on is known as nonsense-mediated mRNA decay (NMD).

108 egradation via nonsense-mediated mRNA decay (NMD).

109 onsense-mediated messenger RNA (mRNA) decay (NMD).

110 Nonsense-mediated RNA decay (NMD) is a highly conserved and selective RNA degradation

111 Nonsense-mediated RNA decay (NMD) is an RNA control mechanism that has also been impl

112 t branch of the nonsense-mediated RNA decay (NMD) pathway is critical for human cognition.

113 d and selective nonsense-mediated RNA decay (NMD) pathway remain murky.

114 ritical for the nonsense-mediated RNA decay (NMD) pathway, while its autosomal counterpart--UPF3A--en

115 damage inhibits nonsense-mediated RNA decay (NMD), an RNA surveillance and gene-regulatory pathway, i

116 rane of the ER and activates an ER-dedicated NMD pathway, thus providing an ER-protective function by

117 However, the mechanism by which deficient NMD leads to neurodevelopmental dysfunction remains unkn

118 ndings indicate that impaired UPF2-dependent NMD leads to neurodevelopmental dysfunction and suggest

119 known NDD genes, suggesting UPF3B-dependent NMD regulates gene networks critical for cognition and b

120 le computational approaches, UPF3B-dependent NMD target transcripts that are candidates to mediate th

121 ure, thus identifying high-confidence direct NMD targets.

122 ified UPF3B-regulated RNAs, including direct NMD target transcripts encoding proteins with known func

123 For many neuromuscular diseases (NMDs), cardiac disease represents a major cause of morbi

124 berrant p53beta expression and dysfunctional NMD are both implicated in cancers, our studies may prov

125 t beyond selecting for mutations that elicit NMD in tumor suppressors, tumor evolution may react to t

126 73 K mutations that are predicted to elicit NMD (NMD-elicit).

127 nts transgenic for TAV accumulate endogenous NMD-elicited mRNAs, while decay of AU-rich instability e

128 enerated by inflammation to globally enhance NMD through coordinated amplification and/or mutation.

129 Enhanced NMD activity also correlates with an enrichment of the n

130 We find that daf-2 mutants display enhanced NMD activity and reduced levels of potentially aberrant

131 This ER-NMD pathway requires the interaction of NBAS with the co

132 hed in genomic positions predicted to escape NMD, and associated with higher protein expression, cons

133 ression, consistent with degradation escape (NMD-escape).

134 ng to genetic buffering within the essential NMD pathway.

135 However, some PTC-containing mRNAs evade NMD, and might generate mutant proteins responsible for

136 rons, allowing these aberrant mRNAs to evade NMD and promoting BCL2 overexpression and neoplasia.

137 Finally, NMD burden also stratified patient survival in multivari

138 the core NMD component UPF1 is critical for NMD and is regulated in mammals by the SURF complex (UPF

139 on the 3'UTRs of mRNAs that are directed for NMD in the cytoplasm.

140 some core NMD factors that are essential for NMD in simpler organisms appear to be dispensable for ve

141 icase whose ATPase activity is essential for NMD.

142 UVBL1-RUVBL2 ATPase activity is required for NMD activation by an unknown mechanism.

143 Nevertheless, a role for NMD in genome regulation has not yet been fully assessed

144 r, our findings reveal a widespread role for NMD in shaping the outcomes of APA.

145 red systematic forward genetic screening for NMD factors in human cells.

146 s CRISPR-based forward genetic screening for NMD pathway defects in human cells.

147 he development of therapeutic strategies for NMD-related diseases.

148 l Prkag3 mRNA as a mechanistic substrate for NMD that contributes to the UPF2-mediated regulation of

149 30%) of PTC-containing mRNAs expressed from NMD-competent PTC-containing constructs were as stable a

150 wever, the production of EJC footprints from NMD but not microRNA targets requires the NMD factor SUP

151 ion of trace amounts of mutant proteins from NMD-competent PTC-containing constructs was not affected

152 fic retroviral and cellular transcripts from NMD.

153 role of RNA helicases in the transition from NMD complexes that recognize a PTC to those that promote

154 died how mutational changes influence global NMD and cytolytic immune responses.

155 ge, sex, race, and dialysis status), greater NMD associated with greater 6-week AVF blood flow rate a

156 However, it is unknown how NMD regulates the stability of RNAs translated at the en

157 conditionally lacking UPF3A exhibit "hyper" NMD and display defects in embryogenesis and gametogenes

158 high-throughput transcriptomics we identify NMD targets transcriptome-wide in PEL cells and identify

159 he forebrain (Upf2 fb-KO mice) show impaired NMD, memory deficits, abnormal long-term potentiation (L

160 ive for treatment of disorders with impaired NMD.

161 how different mutation and most importantly NMD burdens influence cytolytic activity using machine l

162 of polypyrimidine tract binding protein 1 in NMD evasion enables enhanced prediction of transcript su

163 We show that in both normal and in NMD-deficient cells, AS rates strongly decrease with inc

164 tive mRNA splicing and pronounced changes in NMD-sensitive isoforms.

165 a transcript, which was further confirmed in NMD reporter gene assays.

166 AVF diameter (per absolute 10% difference in NMD: change in blood flow rate =14.0%; 95% confidence in

167 Interestingly, these exons are enriched in NMD signals, and, accordingly, ZMAT3 broadly affects tar

168 hat NBAS fulfills an independent function in NMD.

169 significant overlap of upregulated genes in NMD-defective cells with those in the brain tissues, mic

170 n the NMD pathway, with a global increase in NMD efficiency in patients with NMD co-alterations.

171 dence for a specific role of mutant SRSF2 in NMD.

172 that 5'-3' mRNA decapping is a late step in NMD-related mRNA degradation in plants.

173 The management of cardiac disease in NMDs is made challenging by the broad clinical heterogen

174 rich C9orf72 dipeptide repeats could inhibit NMD activities by reducing the abundance of processing b

175 However, elevated SRSF7 levels inhibit NMD and promote translation of two protein halves, terme

176 short and long 3'UTR isoforms by inhibiting NMD, in addition to its previously described modulation

177 ting and tumor evolution, and how inhibiting NMD may be an effective strategy to increase the efficac

178 unteract this, flavivirus infection inhibits NMD and the capsid-PYM1 interaction interferes with EJC

179 Instead, NMD inhibition is primarily a result from global transla

180 Our data suggest that TAV can intercept NMD by targeting the decapping machinery through the sca

181 Overexpression of UPF1, but none of its NMD-deficient mutants, enhanced the survival of neurons

182 hitecture then favors the association of key NMD factors to elicit mRNA decay.

183 rks genetic screen identifies multiple known NMD factors and numerous human candidate genes, providin

184 confirming that a cytoplasmic mechanism like NMD indeed cannot be responsible for the observed reduct

185 Here, we identify a localized NMD pathway dedicated to ER-translated mRNAs.

186 linical heterogeneity that exists among many NMDs and by limited knowledge about disease-specific car

187 mutant retain fully functional UPF1-mediated NMD.

188 to IR also occurs when other genes mediating NMD are mutated.

189 urther show that hundreds of human and mouse NMD targets, especially RNA-binding proteins, encode pot

190 In upf1-deficient mutants, NMD-susceptible transcripts of ribosomal proteins that a

191 mutations that are predicted to elicit NMD (NMD-elicit).

192 olved in Golgi-to-ER trafficking, as a novel NMD factor.

193 At the same time, numerous NMD enhancers and suppressors have been identified in mu

194 s as genuine, preserving both the ability of NMD to accurately detect aberrant mRNAs and the capacity

195 may benefit from inhibition or activation of NMD.

196 veloped a method of in vivo amplification of NMD reporter fluorescence (Fireworks) that enables CRISP

197 s that gene- or transcript-level analyses of NMD often fail to detect.

198 Notably, this increased burden of NMD, INIT and splice variants was more pronounced in a s

199 ly proline-arginine, as the main culprits of NMD inhibition.

200 Indeed, loss or depletion of NMD factors have been shown to disrupt developmental eve

201 factors, efficient and accurate detection of NMD substrates involves proteins that safeguard normal m

202 ocess owing to expansion of the diversity of NMD-regulated transcripts, particularly during various d

203 involvement, highlighting unique features of NMD-associated myocardial disease that require clinician

204 insight into the neuron-specific function of NMD within the brain.

205 t are candidates to mediate the functions of NMD in mOSNs were identified in vivo.

206 esence of unique features - key hallmarks of NMD targets in the p53beta transcript, which was further

207 We also discuss the importance of NMD for gene editing and tumor evolution, and how inhibi

208 for a large RBP panel, shRNA inactivation of NMD pathway, and shRNA-depletion of RBPs followed by RNA

209 , stress granule formation is independent of NMD inhibition.

210 Here we report the inhibition of NMD by arginine-rich dipeptide repeats derived from C9or

211 sent the mechanistic basis for inhibition of NMD by PTBP1.

212 We observed that the inhibition of NMD does not normalize DMD gene expression in DMD.

213 tion, which contributed to the inhibition of NMD.

214 sed, most notably, rpl10a When the levels of NMD-susceptible rpl10a transcripts were artificially inc

215 While loss of NMD is tolerated, loss of hUPF1 induces a DNA damage res

216 d RAD57 Finally, we demonstrate that loss of NMD results in an increase in recombination rates and re

217 However, the majority of NMD factors were first discovered in model organisms and

218 Here, we will focus on the mechanism of NMD with an emphasis on the role of RNA helicases in the

219 have elucidated the molecular mechanisms of NMD.

220 Here, we report a gene-specific method of NMD inhibition using antisense oligonucleotides (ASOs) a

221 Despite the critical role of NMD at the cellular level, our knowledge about the conse

222 factory field and insights into the roles of NMD in vivo.

223 the importance of known and novel 'rules of NMD' to be tested and combined into methods that accurat

224 eat expansion, suggesting the suppression of NMD pathway in these patients.

225 , we derived novel patient-level metrics of 'NMD burden' and interrogated how different mutation and

226 indications exhibited varying dependence on NMD and mutation burden features.

227 tunities by targeting tumour dependencies on NMD-elicit mutations.

228 required to best inform future guidelines on NMD-specific cardiovascular health risks, treatments, an

229 found different impacts of these proteins on NMD and the Arabidopsis transcriptome, with UPF1 having

230 However, other NMD components are also implicated, distinguishing it fr

231 Since partial NMD attenuation can potentially enhance nonsense suppres

232 human nonsense-mediated mRNA decay pathway (NMD) performs quality control and regulatory functions w

233 overed that UPF3A acts primarily as a potent NMD inhibitor that stabilizes hundreds of transcripts.

234 ns control kinetic proofreading of potential NMD substrates, presenting a new model for RNA helicase

235 Here we develop an algorithm to predict NMD and apply it on somatic mutations reported in The Ca

236 This prohibited NMD, and the lack of a transmembrane region (DeltaTM) pr

237 el p38alpha-dependent pathway that regulates NMD activity in response to persistent DNA damage, which

238 show that DHX34, an RNA helicase regulating NMD initiation, directly interacts with RUVBL1-RUVBL2 in

239 lay between the virus and host in regulating NMD and the EJC.

240 and xrn4 accumulates 3' fragments of select NMD targets, despite the lack of the metazoan endoribonu

241 statement, we provide background on several NMDs in which there is cardiac involvement, highlighting

242 Indeed, slowing NMD by inhibiting late-acting factors triggers UPF1 hype

243 We discover cancer-specific NMD-elicit signatures in TSGs and cancer-associated gene

244 erapies, better definition of human-specific NMD is required.

245 radome and provide a new avenue for studying NMD and other mechanisms targeting EJC-bound mRNAs for d

246 Here, we demonstrate that NMD restricts KSHV lytic reactivation.

247 lytic gene expression, and demonstrates that NMD can function as a cell intrinsic restriction mechani

248 We find that NMD is a significant and independent predictor of immune

249 ipulating splicing components, we found that NMD activities are crucial to control p53beta levels und

250 ate specific DNA repair proteins and/or that NMD inactivation may lead to aberrant mRNAs leading to s

251 We propose that NMD-mediated RNA surveillance is a crucial quality contr

252 Here we show that NMD mediates longevity in C. elegans strains with mutati

253 known to induce DSBs, further supports that NMD pathway mutants are defective in DSB repair.

254 Overexpression of eRF1 and the NMD driver UPF1 ameliorate C9-HRE toxicity in vivo.

255 ent cause of human genetic diseases, and the NMD pathway is known to modulate disease severity.

256 hat is critical for both VCS binding and the NMD suppression effect.

257 ntified a functional interaction between the NMD machinery and terminating ribosomes based on 3' RNA

258 F3B is involved in the crosstalk between the NMD machinery and the PTC-bound ribosome, a central mech

259 en bound near a stop codon, PTBP1 blocks the NMD protein UPF1 from binding 3'UTRs.

260 gain variant predicted to be degraded by the NMD-pathway.

261 In humans, mutations in the NMD factor gene, UPF3B, cause intellectual disability (I

262 UPF3B is itself involved in the NMD mechanism which degrades both PTC-bearing mutant tra

263 ably, expression of UPF1, a core gene in the NMD pathway, efficiently blocked neurotoxicity caused by

264 ed significant co-alteration of genes in the NMD pathway, with a global increase in NMD efficiency in

265 icase regulation and target selection in the NMD pathway.

266 ing factors and their functional role in the NMD pathway.

267 assembly of factors required to initiate the NMD response.

268 s (Arabidopsis thaliana) mutants lacking the NMD-related proteins UPF3, UPF1, and SMG7.

269 Although some of the NMD machinery is conserved between kingdoms, little is k

270 upf1, encoding the central component of the NMD machinery.

271 enomics to determine the conservation of the NMD pathway across eukaryotic evolution.

272 our results suggested that activation of the NMD pathway could be a potential therapeutic strategy fo

273 is dependent on UPF3A and independent of the NMD pathway or the XRN1-CNOT pathway.

274 oducts could lead to the accumulation of the NMD substrates and identified arginine-rich dipeptide re

275 ted mRNA decay (NMD), by phosphorylating the NMD factor UPF1.

276 ted in vitro translation system to probe the NMD proteins for interaction with the termination appara

277 indicating that genetically reactivating the NMD pathway could suppress dipeptide repeat toxicity.

278 om NMD but not microRNA targets requires the NMD factor SUPPRESSOR WITH MORPHOLOGICAL EFFECT ON GENIT

279 Our results suggest the NMD as a possible mechanism for achieving the homozygosi

280 Our data demonstrate that the NMD and alternative splicing pathways regulate p53beta i

281 We report that the NMD pathway operates within dendrites to regulate Glutam

282 or pediatric heart failure guidelines to the NMD population problematic.

283 ere disease than the PKD2 group, whereas the NMD group had a PKD2-like phenotype.

284 re-mRNAs, their exons respond prominently to NMD pathway disruption, and that the responding exons ar

285 d prediction of transcript susceptibility to NMD.

286 the susceptibility of a given transcript to NMD can be modulated by its 3'UTR length and ability to

287 protective shift from protein translation to NMD-dependent mRNA degradation.

288 matic protein previously shown to have trace NMD activity.

289 , we found that FRY2/CPL1 interacts with two NMD factors, eIF4AIII and UPF3, and is involved in the d

290 d the intriguing possibility of undiscovered NMD regulatory pathways.

291 ysomes of upf1 mutants, indicating that UPF1/NMD suppresses the translation of aberrant RNAs.

292 The regulation of TNLs via UPF1/NMD-mediated mRNA stability and translational derepressi

293 These upregulated NMD targets included NIK mRNA, which encodes a potent ac

294 isms appear to be dispensable for vertebrate NMD.

295 , the available data suggest that vertebrate NMD is a complex, branched pathway wherein individual br

296 In vertebrates, NMD has become an essential process owing to expansion o

297 However, whether NMD is capable of restricting DNA viruses is not known.

298 stomach adenocarcinomas are associated with NMD-elicit mutations of the translation initiators LARP4

299 hnRNP L as a factor that protects mRNAs with NMD-inducing features including long 3'UTRs.

300 increase in NMD efficiency in patients with NMD co-alterations.