ライフサイエンスコーパス: mispairing

1 formed in vivo (indicating initial disulfide mispairing).

2 bs without heavy/heavy and light/heavy chain mispairing.

3 on the helix destabilization associated with mispairing.

4 face collagen-like protein by slipped-strand mispairing.

5 primer/templates that are misaligned due to mispairing.

6 ions resulting in frequent T.dGTP and A.dGTP mispairing.

7 s playing a major role in the slipped-strand mispairing.

8 paired activity possibly caused by disulfide mispairing.

9 FAA is hypermutable, and that slipped-strand mispairing, a mutational mechanism recognized as importa

10 lyprotein can be modulated by slipped-strand mispairing across a pentanucleotide repeat, ACAGC, withi

11 E. coli AlaRS has an intrinsic capacity for mispairing alanine onto nonalanyl-tRNAs including tRNA(C

12 The results of undetectable mispairing and high biological activity have indicated t

13 rigin of the tandem repeat by slipped-strand mispairing and its subsequent turnover.

14 tify nucleoside analogs that mimic this base-mispairing and preferentially inhibit apicoplast DNA rep

15 tility is associated with meiotic chromosome mispairing, and is a likely consequence of recombining b

16 get recognition, as evidenced by lack of TCR mispairing, as well as preserved specificity.

17 ertion biases arise primarily from mRNA:tRNA mispairing at codon positions 1 and 3 and reflect, in pa

18 nto the DNA strand of an RNA.DNA hybrid, and mispairing at high frequency.

19 aspartic acid), probably arising by slipped mispairing between 2 copies of a direct repeat (GCGAGCAC

20 is delayed by misfolding of P3-P9, including mispairing between residues in P9 and the tRNA.

21 Mixed dimers, formed by mispairing between the endogenous and transgenic TCRs, m

22 However, in all mispairing cases, phosphodiester bond formation was inef

23 that (a) TRS instability is mediated by DNA mispairing caused by the accumulation of supercoiling wi

24 tion threshold are associated with increased mispairing caused by the optimal partitioning of writhe

25 This mispairing causes alterations in gene expression, and ce

26 in the presence of oxidants and their potent mispairing characteristics suggest that oxazolone may pl

27 O(6)-POB-dG is a strongly mispairing DNA lesion capable of inducing both G-->A and

28 d its reversion take place by slipped-strand mispairing during DNA replication and that swarming moti

29 e generated by a mechanism of slipped-strand mispairing during DNA replication.

30 those of others, we propose a model of slip mispairing during error-prone repair synthesis to explai

31 Slipped-strand mispairing during replication is likely to have generate

32 involve intramolecular or intermolecular DNA mispairing, even pairing across a replication fork.

33 es at a high frequency due to slipped-strand mispairing events that occur during DNA replication.

34 ck base pair with template dG and not during mispairing events.

35 hrough does not promote novel or alternative mispairing events; rather, readthrough effectors cause q

36 pendent pathway involves replication slipped mispairing, evoked from stalling at hairpin structures f

37 ent with a mutagenic mechanism involving T-G mispairing followed by a next-nucleotide effect involvin

38 e past, the methoxy groups do not facilitate mispairing, implying that they are not recognized by any

39 n, which was concomitant with slipped-strand mispairing in a poly(C) tract of the fucosyltransferase

40 56dupA and c.676dupC) in FERMT1, and slipped mispairing in direct nucleotide repeats was identified a

41 ess the effect of local DNA sequence on base mispairing in order to determine the mechanism of sequen

42 ow that chain termination is caused by tG:dG mispairing in the enzyme active site.

43 ach Hb receptor independently by slip-strand mispairing in the poly(G) tracts found in hpuA and hmbR.

44 ication/repair-related genes; slipped-strand mispairing is likely the mechanism responsible for the e

45 dence that this is subject to slipped-strand mispairing, leading to frameshifts that eliminate gene f

46 tudies indicate that oxazolone is a strongly mispairing lesion, inducing approximately 10-fold more m

47 us of the target genes by the strand-slipped mispairing mechanism, are often found in the genes encod

48 eats and likely originated through a slipped mispairing mechanism.

49 phase variation mediated by a slipped-strand mispairing mechanism; in each case the gene sequence con

50 f this mutation, consistent with the slipped mispairing model for the generation of short deletions d

51 t least 5-bp and may be explained by slipped-mispairing model of mutagenesis.

52 ethylG by human pol iota, in contrast to the mispairing modes observed previously for O(6)-methylG in

53 s that were consistent with a slipped-strand mispairing mutation model, as well as a smaller number o

54 evolved over several minutes, likely due to mispairing of a central helix junction.

55 Disulfide mispairing of a fraction of B9D, B10D, and B12E mutants

56 This may reflect mispairing of adenine with 8-oxoguanine in DNA attacked

57 Errors in protein synthesis due to mispairing of amino acids with tRNAs jeopardize cell via

58 Mispairing of dGTP and dTTP was similar and occurred wit

59 Mispairing of polymeric guanine (polyG) tracts within ea

60 ase switching appears to involve slip-strand mispairing of repeated dinucleotides in the pilus promot

61 Mispairing of the crossbone single-strand region and alt

62 , a major limitation to this approach is the mispairing of the introduced chains with the endogenous

63 This rearrangement could be explained by mispairing of the large inverted repeats, followed by do

64 However, mispairing of the therapeutic alphabeta chains with endo

65 ngement revealed a more common result of the mispairing of these large inverted repeats--recombinatio

66 on a "looped out" template strand instead of mispairing opposite a next available template base.

67 to repeat array expansion by slipped-strand mispairing or a similar mechanism.

68 ene family appears to reflect slipped-strand mispairing or domain duplication, allowing for redundanc

69 e form variation showed that slip strand DNA mispairing or unequal recombination resulted in gain or

70 likely tautomeric forms." Indeed, among many mispairing possibilities, either tautomerization or ioni

71 tion product analysis suggested that slipped mispairing, producing monomeric replicon products, may b

72 me length, we conclude that the twist in the mispairing region is similiar to that of completely pair

73 These include slipped strand mispairing, site-specific recombination and epigenetic r

74 Slipped-strand mispairing (SSM) has not been identified as a mechanism

75 We report a general strategy to prevent TCR mispairing: swapping constant domains between the alpha

76 Base mispairing, temperature and the presence of an interstra

77 Vsa tandem repeats occurs by slipped-strand mispairing, the ability of the mycoplasmas to form a bio

78 Light chain mispairing was circumvented by using an identical light

79 In addition, chromosome mispairing was seen in male meiosis.

80 These findings strongly suggest that slipped mispairing was the cause of this second-site mutation an

81 spiroiminodihydantoin (Sp) because of their mispairing with A or G.

82 By mispairing with adenine during replication, oxoG gives r

83 onably stable and strongly selective against mispairing with native bases.

84 mplating base, thereby competing against the mispairing with the templating base.

85 obably uses recombination and slipped-strand mispairing within repeats as mechanisms for antigenic va