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1 tRNA(Leu) charging decreased, but only small increases i
2 tRNALeu(UUR), an etiologic hot spot for such diseases, h
3 e complete initiator tRNA(Met) gene, metY; a tRNA(Leu) gene; the tpiA gene product; and the MrsA prot
4 es a single nucleotide in the anticodon of a tRNA(Leu) that changes its normal 5'CAG3' leucine antico
5 -proteobacteria, and the first instance of a tRNA(Leu)(UAA) group I intron to be found in a group of
6 thogenicity island (Pai) that is linked to a tRNA(Leu) gene found also in Pseudomonas aeruginosa but
10 itioning of G18 and G19 that is found in all tRNA(Leu); a base was inserted at position 47n between t
11 75%) reduction in the level of aminoacylated tRNA(Leu(UUR)) and a decrease in mitochondrial protein s
12 e if the decreased fraction of aminoacylated tRNA(Leu(UUR)) in A3243G mutant cells was due to a defec
14 showed that the alteration of aminoacylation tRNA(Leu(UUR)) caused by the A3243G mutation led to mito
15 c tRNA loci (e.g., the nuclear tRNA(Gly) and tRNA(Leu), the mitochondrial tRNA(Val) and tRNA(Pro)) we
17 c precursors containing the tRNA(1)(Ser) and tRNA(Leu) transcripts with a 59-nucleotide intergenic se
18 The substrate, composed of tRNA(Ser) and tRNA(Leu), is transcribed in tandem with a 59-nucleotide
19 8ph by mutant H3S28A repressed Brf1, TBP and tRNA(Leu) and 5S rRNA expression and decreased occupancy
20 process of charged and uncharged tRNALys and tRNALeu(UUR) has revealed that the separation of the two
21 nd secondary structural similarities between tRNA(Leu)UAA introns found in strains of the cyanobacter
23 cantly decreased use of codons recognized by tRNA(Leu(CUN)), likely due to selection to utilize the m
27 e II counterparts.A minimum of six conserved tRNA(Leu) nucleotides were required to change the amino
30 Reduction of Brf1 significantly decreased tRNA(Leu) and 5S rRNA transcription and repressed EGF-in
31 of tandem UAGA quadruplets by an engineered tRNA(Leu) with an eight-base anticodon loop, has been in
34 uggested that other tRNAs can substitute for tRNA(Leu) but that interactions in addition to pairing o
37 bstrate with a uridine at position 38 (human tRNA(Leu)), there was very slight formation of pseudouri
38 vivo and in vitro characteristics of type I tRNA(Leu) variants with their type II counterparts.A min
39 Experiments monitoring deacylation of Ile-tRNA(Leu) and misactivated adenylate turnover revealed t
40 quence changes, as significant levels of Ile-tRNA(Leu) are formed in the presence of high concentrati
41 In this way, a group I intron located in tRNA(Leu), which has been used extensively for phylogene
47 the substrate for the condensation with Leu-tRNA(Leu) catalyzed by the C-terminal domain of DhpH.
50 to characterize the determinants of the Leu-tRNALeu-4 acceptor stem recognized by the L/F-transferas
51 een L/F-transferase and either wild type Leu-tRNALeu-4 (UAA) or mutant Leu-tRNALeu-4 (CUA) are each 0
52 urnover, thus inhibiting synthesis of leucyl-tRNA(Leu) and consequentially blocking protein synthesis
59 pathogenetic mechanism of the mitochondrial tRNA(Leu(UUR)) A3243G transition associated with the mit
60 zes a mtDNA segment within the mitochondrial tRNA(Leu(UUR)) gene immediately adjacent to and downstre
61 3G and T3271C mutations in the mitochondrial tRNA(Leu(UUR)) gene on the aminoacylation of tRNA(Leu(UU
62 ease in steady-state levels of mitochondrial tRNALeu(UUR), and a partial impairment of mitochondrial
63 n at position 3256, within the mitochondrial tRNALeu(UUR) gene in a patient with a multisystem disord
64 ated mutations are known to affect the hs mt tRNA(Leu(UUR)) gene, and the molecular-level properties
65 f the D, TPsiC, and anticodon loops of hs mt tRNA(Leu(UUR)) in the structure and function of this mol
66 uences, indicating that this region of hs mt tRNA(Leu(UUR)) is not involved in recognition by LeuRS.
67 zed nucleotides in the loop regions of hs mt tRNA(Leu(UUR)), and tRNA variants that were aminoacylate
68 rs more structured than wild-type (WT) hs mt tRNA(Leu(UUR)), indicating that the entirely AU stem of
70 ially denatured for the wild type (WT) hs mt tRNALeu(UUR) and were significantly stabilized by mutati
71 as further elucidated with a mutant of hs mt tRNALeu(UUR) containing a stabilized D stem and a pathog
72 structure of the human mitochondrial (hs mt) tRNALeu(UUR) features several domains that are predicted
73 anscript of the A14G pathogenic mutant of mt-tRNA(Leu), which is known to dimerize, and find that the
74 high affinity wild-type and mutant human mt-tRNA(Leu(UUR)) and mt-tRNA(Lys), and stabilize mutant mt
75 ted either with the m.3243A>G mutation in mt-tRNA(Leu(UUR)) or with mutations in the mt-tRNA(Ile), bo
77 ino acid residue in the presence of a mutant tRNA(Leu) molecule containing the extra nucleotide, U, a
81 noacylation kinetics of wild-type and mutant tRNA(Leu(UUR)), using both native and in vitro transcrib
85 cer cells (MCF-7) decreases the induction of tRNA(Leu) and 5S rRNA genes by alcohol, whereas reductio
86 equence alters mitochondrial localization of tRNA(Leu), and in vivo studies also show a decrease in t
87 lation is facilitated by the misacylation of tRNA(Leu) with methionine by the methionyl-tRNA syntheta
90 st enough to completely block mischarging of tRNA(Leu), resulting in codon ambiguity and statistical
95 ate levels and the aminoacylated fraction of tRNA(Leu(UUR)) are likely to contribute to the decreases
96 rase-dependent increase in the proportion of tRNA(Leu(CAA)) containing m(5)C at the wobble position,
97 ichia coli LeuRS abolished aminoacylation of tRNALeu and also amino acid editing of mischarged tRNA m
98 Mutations in the anticodon and extra arm of tRNALeu-1 do not measurably effect its ability to serve
99 es of tRNASer genes, 7 from five families of tRNALeu genes, and 3 from three families of tRNAAla gene
100 leucine occurs through misaminoacylation of tRNALeu, similar to the misincorporation of norleucine f
102 n in the occupancy of all TFIIIB subunits on tRNA(Leu) genes, whereas prolonged PTEN expression resul
108 cyl-tRNA synthetase by formation of a stable tRNA(Leu)-AN2690 adduct in the editing site of the enzym
110 aled differences in the contributions of the tRNA(Leu) acceptor stem base-pairs to tRNA(Leu) function
112 found to interrupt the anticodon loop of the tRNA(Leu)(UAA) gene in a bacterium belonging to the gamm
115 ions of the mutation at position 3243 in the tRNA(Leu(UUR)) gene associated with the MELAS encephalom
116 ue, the levels of three point mutations, the tRNA(Leu(UUA)) 3243 mutation causing mitochondrial encep
123 ing analysis of the mtDNA segment within the tRNA(Leu(UUR)) gene that binds the transcription termina
124 ription termination region (TERM) within the tRNA(Leu(UUR)) gene was consistently and strongly protec
125 limiting C-terminal domain accessibility to tRNA(Leu) facilitates its role in protein synthesis and
126 of the tRNA(Leu) acceptor stem base-pairs to tRNA(Leu) function: in the type I, but not the type II f
130 n pattern was observed between the wild-type tRNALeu(UUR)and its counterpart carrying the A3243G muta
131 and processing of the genes tRNA(Thr)(UGU), tRNA(Leu)(UAA), and tRNA(Phe) (GAA) therefore attributes
132 induce H3S28ph, which, in turn, upregulates tRNA(Leu) and 5S rRNA transcription through Brf1 and TBP
134 .5-7.3 kb of dissimilar intervening DNA with tRNA(Leu)-queA-tgt sequences that are also found in Pseu
135 hat the association of BRF1 and pol III with tRNA(Leu) genes in cells decreases when ERK is inactivat
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