ライフサイエンスコーパス: tetranucleotide repeat

1 , using 14 new markers consisting of tri- or tetranucleotide repeats.

2 eotide repeats were higher than those of the tetranucleotide repeats.

3 l tumors previously analyzed with a panel of tetranucleotide repeats.

4 ates are highest in di-, then tri-, and then tetranucleotide repeats.

5 and 27 microsatellite loci of di-, tri-, or tetranucleotide repeats.

6 ed included dinucleotide, trinucleotide, and tetranucleotide repeats.

7 crease in stutter artifact on di-, tri-, and tetranucleotide repeats.

8 yped samples from three populations for five tetranucleotide repeats and an Alu insertion polymorphis

9 ns to investigate the mutation process at 14 tetranucleotide repeats and carry out an advanced multil

10 5' flanking region also contains two sets of tetranucleotide repeats and two short interspersed nucle

11 AAAG tetranucleotide repeats appear to be especially prone to

12 I) homologue increases the mutation rates of tetranucleotide repeats approximately 3-fold.

13 Most such microsatellites in Hi are tetranucleotide repeats, but an exception is the dinucle

14 btle changes, such as switching T for C in a tetranucleotide repeat, can have dramatic consequences o

15 A tetranucleotide repeat CATT((5-7)) beginning at nucleoti

16 acking interactions; analyses of 62 tri- and tetranucleotide repeat-containing genes associated with

17 Using lacZ fusions, we showed that these tetranucleotide repeats could mediate phase variation of

18 vated microsatellite alterations at selected tetranucleotide repeat (EMAST) tumors is still unknown.

19 vated microsatellite alterations at selected tetranucleotide repeats (EMAST) is the most common DNA m

20 vated microsatellite alterations at selected tetranucleotide repeats (EMAST), but little is known abo

21 vated microsatellite alterations at selected tetranucleotide repeats (EMAST)--where loci containing [

22 vated microsatellite instability at selected tetranucleotide repeats (EMAST).

23 ety of instability is best seen at selective tetranucleotide repeats (EMAST; elevated microsatellite

24 onica type 1 [DM1]), or an untranslated CCTG tetranucleotide repeat expansion in intron 1 of the ZNF9

25 on, e.g. the myotonic dystrophy type 2 (DM2) tetranucleotide repeat expansion site, more than one rep

26 We have identified a tetranucleotide repeat (fragment sizes from 324 to 464 b

27 with microsatellite alterations at selected tetranucleotide repeats have a high frequency of p53 mut

28 nomas, whereas studies with dinucleotide and tetranucleotide repeats have not.

29 Two novel tetranucleotide repeats (heterozygosity of 66 and 68%) a

30 the mutation rate differs in di-, tri-, and tetranucleotide repeats, how mutation rate distributes w

31 Highly polymorphic di- and tetranucleotide repeats in and around Npr3, a potential

32 vated microsatellite alterations at selected tetranucleotide repeats in approximately 60% that associ

33 nd use it to fit DNA data for di-, tri-, and tetranucleotide repeats in humans, mice, fruit flies, an

34 or BAT-40 was significantly associated with tetranucleotide repeat instability in sporadic adenomas

35 This tetranucleotide repeat is located in the first intron of

36 his variable expression involves slippage of tetranucleotide repeats located within the reading frame

37 y-five dinucleotide (dC.dA)n.(dG.dT)n and 18 tetranucleotide repeat loci were identified and genotype

38 The STSs include 18 (CA) repeat and one tetranucleotide repeat marker that detect polymorphism,

39 ite instability has been observed at certain tetranucleotide repeat markers (AAAGn) in lung, head and

40 Here we examine 236 mutations at 122 tetranucleotide repeat markers and find that the rate of

41 f MSI has been described that occurs only at tetranucleotide repeat markers.

42 ulted in a approximately 35-fold increase in tetranucleotide repeat-mediated PV rates.

43 Between three and six tri- and tetranucleotide repeat microsatellite loci were analyzed

44 ide sequences of 23 different alleles at one tetranucleotide repeat microsatellite locus in fin whale

45 Di-, tri- and tetranucleotide repeat microsatellite markers localized

46 In addition, a tetranucleotide repeat of variable length that may provi

47 sed as PCR templates with trinucleotide- and tetranucleotide-repeat polymorphic markers.

48 A previous linkage analysis, which used a tetranucleotide repeat polymorphism at the tyrosine hydr

49 The tetranucleotide repeat polymorphism is highly informativ

50 tified the start site of transcription and a tetranucleotide repeat polymorphism that locates at less

51 ion of human chromosome 17 were screened for tetranucleotide repeat polymorphisms by hybridizing shot

52 inucleotide repeat sequence [(CA)(17)] and a tetranucleotide repeat sequence [(GAAA)(17)] have been d

53 We have identified a tetranucleotide repeat sequence, (CAAA)(N), in the genom

54 esenting all previously reported LPS-related tetranucleotide repeat sequences in H. influenzae, were

55 Based on this, we hypothesized that tetranucleotide repeat sequences might be used to identi

56 comprising four primer pairs for polymorphic tetranucleotide repeat sequences on chromosome 21, four

57 We determined that the DM2 tetranucleotide repeats showed a lower thermodynamic sta

58 We analyze a set of data on tetranucleotide repeats that reveals the imbalance expec

59 instability was determined by a panel of 10 tetranucleotide repeats, the Bethesda consensus panel of

60 MSI was evaluated by a panel of 10 tetranucleotide repeats, the noncoding mononucleotide re

61 ion, we investigated the capacity of the DM2 tetranucleotide repeats to also expand during this proce

62 ion by human DNA polymerase beta, of several tetranucleotide repeat tracts in which the repeat units

63 ound upstream of most Haemophilus influenzae tetranucleotide repeat tracts, raising the possibility o

64 ragment processing destabilizes H.influenzae tetranucleotide repeat tracts.

65 he instabilities were greater for the longer tetranucleotide repeat tracts.

66 i containing tracts of six or more identical tetranucleotide repeat units.

67 ponse were observed between dinucleotide and tetranucleotide repeat units.

68 The distribution of the tetranucleotide repeats was bimodal, and there was stron

69 two cases indicating somatic expansion of a tetranucleotide repeat were found.

70 microsatellite loci including di-, tri-, and tetranucleotide repeats were evaluated.

71 Expansions of up to double the length of the tetranucleotide repeats were found.

72 bility results determined by the panel of 10 tetranucleotide repeats were highly significantly relate

73 The genetic instabilities of (CCTG.CAGG)(n) tetranucleotide repeats were investigated to evaluate th

74 TNRs showed no such preference, and di- and tetranucleotide repeats were most frequently found in no

75 eats (2 dinucleotide, 2 trinucleotide, and 1 tetranucleotide repeats) were analyzed by polymerase cha

76 A confounding factor is that tetranucleotide repeats within the lic2A, lgtC, and lex2