ライフサイエンスコーパス: nonsense codon

1 p also enhances translation termination at a nonsense codon.

2 itution in the mutant gene, which produced a nonsense codon.

3 enerates three missense codons followed by a nonsense codon.

4 nduce skipping of the exon that contains the nonsense codon.

5 e isomerization of uridine to Psi within the nonsense codon.

6 etase (aaRS)/tRNA pair that reads a distinct nonsense codon.

7 ulline (SM60) into proteins in response to a nonsense codon.

8 n in mammalian cells in response to an amber nonsense codon.

9 two base changes, one of which formed a TGA nonsense codon.

10 he third, it results from homozygosity for a nonsense codon.

11 in Escherichia coli in response to the amber nonsense codon.

12 nslational fidelity in response to the amber nonsense codon.

13 acid into proteins in response to the amber nonsense codon.

14 denylation regardless of the position of the nonsense codon.

15 anslation termination process at a premature nonsense codon.

16 n inactive form because of the presence of a nonsense codon.

17 yrosine into protein in response to an amber nonsense codon.

18 geting the most common human disease-causing nonsense codons.

19 selectively stabilize mRNAs harboring early nonsense codons.

20 ion-independent decapping triggered by early nonsense codons.

21 = any base) with the remaining codons being nonsense codons.

22 ng mRNA decay and translation termination at nonsense codons.

23 es govern the decay of CFTR mRNAs containing nonsense codons.

24 1% of human genomes, was unable to translate nonsense codons.

25 vivo and translational recoding of lysine at nonsense codons.

26 acids at specific sites designated by amber nonsense codons.

27 two A-site-specific drugs and on suppression nonsense codons.

28 d involved [PSI(+)]-mediated read-through of nonsense codons.

29 eukaryotic cells to degrade mRNAs containing nonsense codons.

30 ory elements identified that act upstream of nonsense codons.

31 zipper [ZIP]) domains by either deletions or nonsense codons.

32 s the offending mutations that generate such nonsense codons.

33 wn mammalian gene transcripts in response to nonsense codons.

34 functions to degrade transcripts containing nonsense codons.

35 rades mRNAs harboring premature termination (nonsense) codons.

36 e, resulting in translation termination at a nonsense codon 138 nucleotides downstream of the deletio

37 Transcripts with nonsense codons about 20, 40 or 60% of the way through t

38 s genetically encoded in E. coli by an amber nonsense codon and corresponding orthogonal tRNA/aminoac

39 n Saccharomyces cerevisiae by using an amber nonsense codon and corresponding orthogonal tRNA/aminoac

40 reduce the abundance of mRNAs that harbor a nonsense codon and prematurely terminate translation.

41 This mutation changes an AAG codon to a TAG nonsense codon and results in a null phenotype.

42 was previously shown to cause readthrough of nonsense codons and high temperature-conditional lethali

43 vidual amino acids was distinct for specific nonsense codons and readthrough-inducing agents.

44 te tRNAs could mispair at position 1 or 3 of nonsense codons and that, irrespective of whether readth

45 the efficiency of translation termination at nonsense codons and/or the process of programmed -1 ribo

46 tening, arrest of translation at a premature nonsense codon, and endonucleolytic cleavage.

47 trons that normally reside downstream of the nonsense codon are deleted so the nonsense codon is loca

48 rate that all evaluated CFTR mRNAs harboring nonsense codons are degraded by the SMG6-mediated endonu

49 mRNAs often contain premature-termination (nonsense) codons as a result of mutations and RNA splici

50 their activity in a FLuc reporter cell-based nonsense codon assay, with PTC124 emerging as the most p

51 unstable mRNAs, whereas a transcript with a nonsense codon at 80% was as stable as wild-type.

52 a protein encoded by a gene with an in-frame nonsense codon at an essential lysine can be expressed i

53 Here, we provide evidence that a nonsense codon at position 1, 2 or 10 reduces the abunda

54 Until now, a nonsense codon at position 23 has been the 5'-most nonse

55 CAT) gene that lacked an initiation codon, a nonsense codon at TPI position 1 or 2 allowed for the pr

56 produced by a nonsense-free gene, whereas a nonsense codon at TPI position 23 precluded the producti

57 ffect was evaluated by introducing premature nonsense codons at different distances from the PHA AUG

58 beta (TCRbeta) gene, which acquires in-frame nonsense codons at high frequency during normal lymphocy

59 rough efficiently suppresses premature CDKL5 nonsense codons, but the recoded kinase remained highly

60 pregulation of all evaluated CFTR mRNAs with nonsense codons by NMD pathway inhibition improves outco

61 ults are consistent with the notion that the nonsense codon can function in the cytoplasm by promotin

62 the particular mRNA and how it is produced, nonsense codons can mediate a reduction in mRNA abundanc

63 These nonsense codons cause rapid decay of the mRNAs that cont

64 markably, we also show that pseudouridylated nonsense codons code for amino acids with similar proper

65 All three translation termination codons, or nonsense codons, contain a uridine residue at the first

66 ng NMD factors to evaluate the regulation of nonsense codon-containing CFTR mRNAs by the NMD pathway.

67 eased levels of spliced RNA from the unusual nonsense codon-containing U22 host gene, which is a natu

68 1 is required in yeast for discrimination of nonsense-codon-containing mRNA from normal by NMD.

69 d in the stabilization of both wild-type and nonsense-codon-containing mRNAs in vivo.

70 pidly degrade certain transcripts with early nonsense codons could provide plant cells with a means t

71 ng in the substitution of glutamic acid by a nonsense codon, designated E133X.

72 s were replaced by new amino acids that used nonsense codons differing by one base change from the se

73 ide 1101 (epsilon 11O1insT) that generates a nonsense codon directly, and insertion of a guanine afte

74 In support of scanning, a nonsense codon does not elicit decay if some of the intr

75 Here we show that the nonsense codon effect results primarily from lowering th

76 The positional dependence of the nonsense codon effect was evaluated by introducing prema

77 While triplet nonsense codons, especially the amber codon, have been w

78 that a surveillance complex searches 3' of a nonsense codon for a downstream sequence element (DSE) a

79 We show that nonsense codons from variable (V) Igkappa exons promote

80 We observe that CFTR mRNAs with nonsense codons G542X, R1162X, and W1282X, but not Y122X

81 f mutation, the rate of reversion of the TAG nonsense codon has been determined for different motifs

82 s measured by translational suppression of a nonsense codon in a luciferase reporter gene.

83 A), which has been modified to translate the nonsense codon in mcd1-2.

84 he sasA1 mutant, which was found to encode a nonsense codon in the beginning of rfbA, produced less O

85 derivatives were used for suppression of the nonsense codons in a cell-free protein biosynthesizing s

86 cine was employed for the suppression of the nonsense codons in a cell-free protein biosynthesizing s

87 B1 induced readthrough at all three nonsense codons in cultured cancer cells with TP53 (tumo

88 ese hamster ovary (CHO) cell mutants bearing nonsense codons in four of the five exons of the adenine

89 lity of attempts at regulated suppression of nonsense codons in mammalian cells by regulating express

90 acids in response to three independent amber nonsense codons in sperm whale myoglobin or green fluore

91 nce regulator (CFTR) gene which can generate nonsense codons in the CFTR mRNA and subsequently activa

92 The present analysis of nonsense codons in the human alpha-globin mRNA illustrat

93 that they are down-regulated in response to nonsense codons in the nuclear fraction of cells.

94 amma2a heavy chain constructs containing TAG nonsense codons in their V regions that are part of eith

95 mulation of transcripts containing premature nonsense codons in transgenic plants.

96 cid residues, site-directed incorporation at nonsense codons in Xenopus laevis oocytes, and electroph

97 d: base substitutions leading to missense or nonsense codons, in-frame deletions or duplications with

98 repression or induction suggested that this nonsense codon-induced partitioning shift (NIPS) respons

99 cteristic of strain C57BL/6Jand introduces a nonsense codon into sodium channel modifier 1 (SCNM1), a

100 Following the introduction of nonsense codons into promoter-proximal genes, polarity i

101 uently added to the genetic code by changing nonsense codons into sense codons for these amino acids.

102 nd aberrant MLH1 transcript encompassing the nonsense codon is also produced.

103 eam of the nonsense codon are deleted so the nonsense codon is located (i) too far away from a downst

104 In vivo targeting of nonsense codons is accomplished by the expression of an

105 only well recognized entity that recognizes nonsense codons is the cytoplasmic translation apparatus

106 s, we demonstrated that the recognition of a nonsense codon led to a decrease in the translational ef

107 In-frame nonsense codons located at a minimum distance upstream o

108 human triosephosphate isomerase (TPI gene), nonsense codons located less than 50 to 55 bp upstream o

109 n-exon junction of product mRNA so that only nonsense codons located more than 50 to 55 nucleotides u

110 ormed cell lines demonstrated that premature nonsense codons markedly destabilized the mRNA.

111 A codon during mRNA translation augments the nonsense-codon-mediated decay of cytoplasmic Se-GPx1 mRN

112 very that 129-derived strains of mice have a nonsense codon mutation in exon 2 that abrogates product

113 1-2, had a single base change resulting in a nonsense codon near the N-terminus.

114 ominant RP1 alleles typically have premature nonsense codons occurring in the last exon of the gene a

115 e phenotypes examined include suppression of nonsense codons on different media and at different temp

116 on the suppression of altered start codons, nonsense codons or frameshift mutations in genes involve

117 region, alternative splicing that introduces nonsense codons or frameshifts, introns in the 3' untran

118 A) anticodon to CUA so as to translate amber nonsense codons permits tRNA (Trp)(CCA) to be aminoacyla

119 ORFs would function in a manner analogous to nonsense codons, promoting rapid degradation of the mRNA

120 nvestigated the therapeutic potential of the nonsense codon read-through-inducing drug, PTC124, in tr

121 strated ability of the [PSI+] prion to cause nonsense-codon read-through.

122 preexisting nonsense suppression facilitated nonsense codon reassignments and constitutes a novel mec

123 tion, we demonstrate a striking link between nonsense codon reassignments and the decoding properties

124 ppressor tRNAs provided the raw material for nonsense codon reassignments, implying that the properti

125 tRNA anticodon have dictated the identity of nonsense codon reassignments.

126 This anomaly depends on prior nonsense codon recognition and is eliminated in extracts

127 ediated mRNA decay (NMD) is a consequence of nonsense codon recognition during a pioneer round of tra

128 accordingly, NMD occurs as a consequence of nonsense codon recognition during a pioneer round of tra

129 e evidence that phospho-Upf1 functions after nonsense codon recognition during steps that involve the

130 Collectively, the results suggest that nonsense codon recognition may occur in the nucleus.

131 sed the effectiveness with which an upstream nonsense codon reduces mRNA abundance.

132 ation of TCR-beta transcripts in response to nonsense codons requires several features of translation

133 ed decay when inserted into exon 6 between a nonsense codon residing in exon 6 and intron 6.

134 the frameshift mutation or a closely located nonsense codon resulted in half the normal mRNA level.

135 can stimulate readthrough of disease-causing nonsense codons, resulting in high yields of full-length

136 uridine into pseudouridine (Psi), ref. 4) of nonsense codons suppresses translation termination both

137 se compounds, including PTC124, fail to show nonsense codon suppression activity when Renilla renifor

138 ntified in a cell-based FLuc assay as having nonsense codon suppression activity.

139 Using the in vivo nonsense codon suppression method for incorporating unna

140 A nonsense codon suppression technique was employed to inc

141 genetic defect, called 'exon skipping' and 'nonsense codon suppression'.

142 discovered in an FLuc-based assay targeting nonsense codon suppression, is an unusually potent FLuc-

143 effective therapy, including exon skipping, nonsense codon suppression, upregulation of surrogate ge

144 tus determines viability as a consequence of nonsense codon suppression.

145 from mutation-specific treatments, including nonsense codon suppressors and exon skipping, to gene th

146 modified amino acid in response to the amber nonsense codon TAG.

147 ly and with high fidelity in response to the nonsense codon TAG.

148 of the ecotin gene containing an engineered nonsense codon (TAG) at the positions of interest.

149 For example, the amber nonsense codon, TAG, together with orthogonal Methanococ

150 serts sulfotyrosine in response to the amber nonsense codon, TAG.

151 natural amino acids in response to the amber nonsense codon, TAG.

152 A) for the tryptophan codon (TGG) causing a nonsense codon (TGA) at residue 498 within the transmemb

153 o modify this pair to decode either the opal nonsense codon, TGA, or the four-base codon, AGGA, limit

154 se codon at position 23 has been the 5'-most nonsense codon that has been analyzed.

155 on 127ins5 and epsilon 553del 7) generates a nonsense codon that predicts truncation of the epsilon s

156 lls from the deleterious effects of in-frame nonsense codons that are generated by routine inefficien

157 of GPx1 mRNA positions the boundary between nonsense codons that do and do not elicit NMD, as has be

158 function in positioning the boundary between nonsense codons that do and do not mediate decay, the ef

159 Nonsense codons that prematurely terminate translation g

160 hibition (GINI), to identify genes harboring nonsense codons that underlie human diseases.

161 ns trigger faster rates of decapping than 3' nonsense codons, thereby providing a mechanistic basis f

162 drug, PTC124, was identified that suppresses nonsense codon translation termination.

163 These results suggest that nonsense codons trigger a decay pathway distinct from th

164 We also show that 5' nonsense codons trigger faster rates of decapping than 3

165 In this pathway, a nonsense codon triggers accelerated deadenylation that p

166 Nonsense codons upstream of and including position 192 o

167 d using reversion analysis of an Ig V region nonsense codon (Vn).

168 The nonsense codon was found in a conserved haplotype in the

169 The mutant allele contains a nonsense codon which truncates the 1,317-amino-acid prot

170 apid turnover of an mRNA containing an early nonsense codon, which is degraded by a deadenylation-ind

171 tants also enhance translational fidelity at nonsense codons, which correlates with a reduction in to

172 ncipal NMD factor, Upf1p, or by flanking the nonsense codon with a normal 3'-untranslated region (UTR

173 acylated amino acid in response to an amber nonsense codon with translational fidelity greater than

174 The new orthogonal pair suppresses amber nonsense codons with an efficiency roughly comparable to

175 anine (tfm-Phe) into proteins in vivo at TAG nonsense codons with high translational efficiency and f

176 Insertion of nonsense codons within the Fed-1 coding sequence disrupt

177 ion of near-cognate tRNAs at the site of the nonsense codon without apparent effects on transcription