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1 ll-length clone revealed only one unexpected silent mutation.
2 nt adenovirus containing a fiber gene with a silent mutation.
3 ields a phenotype equivalent to wild-type, a silent mutation.
4 and three clustered amino acid changes and a silent mutation.
5 ubstrates heteroallelic at 11 phenotypically silent mutations.
6 confirms the existence of fitness classes of silent mutations.
7 70V), Ile337atc-->Val337gtc (I337V), and two silent mutations.
8 nt leukemic clone carrying a mean of 1.3 non-silent mutations.
9 tional mutation group in comparison with the silent mutations.
10 an a background mutation rate estimated from silent mutations.
11  DCK cDNA was created by the introduction of silent mutations.
12 lation dynamics of conservative missense and silent mutations.
13 ften be interpreted as nonsense, missense or silent mutations.
14 tained an uninterrupted incorporation of the silent mutations.
15 ccumulated at a higher rate than synonymous (silent) mutations.
16  mutations (0.027), the ratio of missense to silent mutations (1.15), and the ratio of non-synonymous
17 ng a specific identifier: through additional silent mutations a restriction site is included or a pre
18  at low clonal levels (13%, 4%, and 4% for a silent mutation, a 180-base pair deletion in exon 3, and
19                                        These silent mutations also strongly affected the genotype of
20                                              Silent mutations and mutations associated with low-level
21 rimary SCLC tumors and metastases showed two silent mutations, and two apparent homozygous deletions.
22                           Disease-associated silent mutations are considered to affect the accurate p
23                                        These silent mutations are predicted to destabilize a stem loo
24  human polymorphic replacement mutations and silent mutations are randomly distributed across sites w
25 ide substitutions leading to translationally silent mutations as well as reciprocal amino acid substi
26 codons 109, 223, 343, 656 and 1019, one rare silent mutation at codon 986 and one novel alternatively
27 parent), both of which were in the L gene: a silent mutation at nucleotide position 8821 (amino acid
28 a rapidly evolving protein, accumulating non-silent mutations at a rate exceeding those of most other
29 s that the RNase 8 gene has incorporated non-silent mutations at an elevated rate (1.3 x 10(-9) subst
30  a glycine receptor (GlyR) with phenotypical silent mutations at KK385/386AA, we studied its cellular
31   Rare mutations were detected; 6 of 50 were silent mutations at the amino terminus of the peptide, w
32 se strain that expresses HBZ mRNA altered by silent mutations but encoding intact protein.
33                 We identified a heterozygous silent mutation, c.7464C>T, in exon 44 of the von Willeb
34 t a compelling analysis suggesting that such silent mutations can be oncogenic by altering transcript
35                  These results indicate that silent mutations can significantly contribute to adaptat
36 ely 2500 generations of PACE contains 20 non-silent mutations, cleaves human IL-23 at the target pept
37 on 5, codon 160 ATGmet-->GTGval) and another silent mutation (codon 182, TGCcys-->TGTcys).
38  containing this mutation and two additional silent mutations created in codons flanking the Lys-546
39 vo that carried mutant pvdhfr and additional silent mutations designed to confirm editing.
40 us was recovered from PV-AB RNA carrying 680 silent mutations, due to a reduction of genome translati
41            Under such an evolutionary model, silent mutations fall into two fitness categories: prefe
42  null mutations fell into domain B while the silent mutations fell outside domain B.
43 d amino acid substitutions were favored over silent mutations, findings indicative of antigen selecti
44     Interestingly, with the exception of two silent mutations, full viral genome sequencing showed id
45  indicate that single base substitution (the silent mutation giving rise to the Xho I site) and delet
46 ACG, TCG, GCG, and CCG to frequently undergo silent mutation in any gene due to the putative lack of
47      Neither a coding mutation in NS5A nor a silent mutation in E2 was adaptive, whereas coding mutat
48                     Here we describe a novel silent mutation in exon 10 of tau (N296N) in this famili
49  sequence analysis of human COX-2 revealed a silent mutation in exon 3 that was evenly distributed be
50                        TC PEC/Cowden has one silent mutation in its protease, two amino acid changes
51 n its protease, two amino acid changes and a silent mutation in its RNA polymerase, and five nucleoti
52 effects but when coupled to a phenotypically silent mutation in the TATA box gave rise to viruses wit
53  region of the GP Ib alpha transcript, and a silent mutation in the third base of the codon for Arg34
54       The ratios of replacement mutations to silent mutations in DNA1 and DNA4 suggest that their V g
55 pecies dynamics of preferred and unpreferred silent mutations in Drosophila simulans.
56 ions but did identify two lines with single, silent mutations in exon 1 and exon 2, respectively.
57  mutation, two mis-sense mutations and three silent mutations in five squamous cell carcinoma samples
58 tatistically analyzing ratios of missense to silent mutations in functional LtrA variants isolated fr
59 egions which code for more than one protein, silent mutations in one reading frame generally have a p
60 e PCR (RT-qPCR) were designed by identifying silent mutations in quail, duck, chicken, mouse and huma
61                             We observed that silent mutations in segment 13 (S13) (nucleotides [nt] 7
62  net increase in the ratio of replacement to silent mutations in the CDRs compared with that in the F
63 ng one in the promoter region (-213A/G), two silent mutations in the codons for Ala 97 (291C/T) and G
64 luding: (1) a higher ratio of replacement to silent mutations in the complementarity determining regi
65 ve broader implications for the relevance of silent mutations in the evolution and fitness of RNA vir
66                  Analysis of replacement and silent mutations in the framework and CDRs suggests that
67                 The ratios of replacement to silent mutations in the framework and complementarity de
68 an miR160-resistant form of ARF10, which has silent mutations in the miRNA target site (termed mARF10
69 xpressed plastid genes or by introduction of silent mutations in the N-terminal part of the coding re
70                               We report that silent mutations in the rbcL segment reduced NPTII accum
71                                              Silent mutations in the second signal abrogate function
72               Expression of DOCK5 cDNA, with silent mutations in the siRNA target region allowing exp
73 ssing engineered mutant apoE with introduced silent mutations in the siRNA target sequence.
74 ce; however, the selection of synonymous or 'silent' mutations in the HIV-1 genome with cART has been
75 ncy (false discovery rate (FDR)<0.05) of non-silent mutations include TP53 (47.1%), KRAS (7.8%) and E
76 ons was low (10%), whereas the likelihood of silent mutations increased disproportionately with the t
77  molecular pathological mechanism by which a silent mutation inhibits splicing and leads to intron re
78                             Introducing many silent mutations into a functional AAP coding region did
79 efficacy comparable to shRNAs, and introduce silent mutations into an ataxin 7 transgene such that it
80 n of the avian M segment or introducing five silent mutations into the human M segment was sufficient
81 us recombination, we introduced missense and silent mutations into the Rab38 gene, encoding a small G
82                                              Silent mutations introduced into a highly conserved nucl
83                                              Silent mutations make up approximately 3% of the total r
84 g, the 1B1 and SV8 proviruses possessed only silent mutations, making p140Axl overexpression the most
85                                              Silent mutations may be deleterious when they affect spl
86 lts indicate that transformants containing a silent mutation near the start of the protein-encoding s
87  All characterized doublets are allelic, and silent mutations occur rarely.
88 an HCII in Escherichia coli was optimized by silent mutation of 27 rare codons and five secondary Shi
89                                              Silent mutation of target sequences confirms the specifi
90 dominant genetic disease that is caused by a silent mutation of the LMNA gene encoding lamins A and C
91  A total of 52 null, six reversion, and five silent mutations of frr (the gene encoding for ribosome
92                   Detailed analysis revealed silent mutations of six amino acid residues within the e
93  less stringently conserved sites, including silent mutations of the last nucleotide of exons, mutati
94 ic fingerprinting to reveal the phenotype of silent mutations of yeast genes.
95                  Surprisingly, we found that silent mutations on average are not neutral; with the av
96 ent, we introduced point mutations to create silent mutations or amino acid substitutions in uORF4.
97       Due to the distribution effect of many silent mutations over large genome segments, codon-deopt
98                Additionally, we identified a silent mutation (P96P) in exon 5 of the PTEN/MMAC1 gene
99 aediatric tumours, with a median of 0.35 non-silent mutations per megabase.
100 the mutants that disrupted SRA function were silent mutations presumed not to alter deduced encoded a
101 have been defined as those for which the non-silent mutation rate is significantly greater than a bac
102                         The mean replacement/silent mutation ratio of systemic compartment IgD- B cel
103                                  Missense to silent mutations ratio and the persistence of potentiall
104             The CDRs and V(H) FR replacement/silent mutation ratios exceeded the ratio for a random m
105                   Analysis of replacement to silent mutation ratios indicated that the genes underwen
106 gh somatic mutation with high replacement-to-silent mutation ratios.
107                       Putatively "preferred" silent mutations segregate at higher frequencies and are
108 de new mechanistic insights into the role of silent mutations selected during antiretroviral therapy
109 at had a mutation in the coding region was a silent mutation, since it did not alter the amino acid s
110 ant pIHBoV1 infectious plasmids which harbor silent mutations (sm) smA1' and smD1' at the A1' and D1'
111                              Intronic and/or silent mutation SNPs within each gene were analyzed in 4
112 ement mutations at a higher rate relative to silent mutations than have their D. simulans orthologs.
113  and is also marked by the introduction of a silent mutation that created an XhoI restriction site in
114 inhibitors is to engineer in protein kinases silent mutations that allow selective inhibition while r
115  on concurrent expression of Scpep1 carrying silent mutations that evade knockdown.
116 c studies attempting to select catalytically silent mutations that reduce inhibitor binding may furth
117 t mutations in the transmembrane portion and silent mutations throughout tend to be neutral.
118    However, the basis for selection of these silent mutations under selective drug pressure is unknow
119 lection analyze the ratio of replacement and silent mutations using a binomial statistical analysis.
120                                    A fourth, silent mutation was introduced 654 bp downstream in the
121                                 Missense and silent mutations were found to destroy, create or change
122            To test this hypothesis, over 300 silent mutations were introduced into the genome of a se
123 nsfection with recombinant T3D muNS in which silent mutations were introduced into the sequence targe
124 rotein gene with synthetic versions in which silent mutations were introduced to replace wild-type co
125                                              Silent mutations were observed in exon 10 at positions 1
126  (GR(Qn)) with an expanded CAG track and two silent mutations, when compared with the sequence of oth
127       Three of the replacements proved to be silent mutations, while a single cysteine, Cys-207, was
128 t mutations generated an increased number of silent mutations within both the CDRs and FRs of the pro

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