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1 eotide repeats were higher than those of the tetranucleotide repeats.
2 l tumors previously analyzed with a panel of tetranucleotide repeats.
3 ates are highest in di-, then tri-, and then tetranucleotide repeats.
4  and 27 microsatellite loci of di-, tri-, or tetranucleotide repeats.
5 , using 14 new markers consisting of tri- or tetranucleotide repeats.
6 ed included dinucleotide, trinucleotide, and tetranucleotide repeats.
7 crease in stutter artifact on di-, tri-, and tetranucleotide repeats.
8 ith those with the D allele, particularly at tetranucleotide repeats.
9 yped samples from three populations for five tetranucleotide repeats and an Alu insertion polymorphis
10 ns to investigate the mutation process at 14 tetranucleotide repeats and carry out an advanced multil
11 5' flanking region also contains two sets of tetranucleotide repeats and two short interspersed nucle
12                                         AAAG tetranucleotide repeats appear to be especially prone to
13 I) homologue increases the mutation rates of tetranucleotide repeats approximately 3-fold.
14                           A polymorphic CATT tetranucleotide repeat at position 794 of the human macr
15          Most such microsatellites in Hi are tetranucleotide repeats, but an exception is the dinucle
16 ing process-induced artifacts, validated for tetranucleotide repeats by use of synthetic constructs o
17 btle changes, such as switching T for C in a tetranucleotide repeat, can have dramatic consequences o
18                                            A tetranucleotide repeat CATT((5-7)) beginning at nucleoti
19 acking interactions; analyses of 62 tri- and tetranucleotide repeat-containing genes associated with
20     Using lacZ fusions, we showed that these tetranucleotide repeats could mediate phase variation of
21 vated microsatellite alterations at selected tetranucleotide repeat (EMAST) tumors is still unknown.
22 vated microsatellite alterations at selected tetranucleotide repeats (EMAST) is the most common DNA m
23 vated microsatellite alterations at selected tetranucleotide repeats (EMAST) show reduced nuclear Mut
24 vated microsatellite alterations at selected tetranucleotide repeats (EMAST), but little is known abo
25 vated microsatellite alterations at selected tetranucleotide repeats (EMAST)--where loci containing [
26 vated microsatellite instability at selected tetranucleotide repeats (EMAST).
27 ety of instability is best seen at selective tetranucleotide repeats (EMAST; elevated microsatellite
28 onica type 1 [DM1]), or an untranslated CCTG tetranucleotide repeat expansion in intron 1 of the ZNF9
29 on, e.g. the myotonic dystrophy type 2 (DM2) tetranucleotide repeat expansion site, more than one rep
30                         We have identified a tetranucleotide repeat (fragment sizes from 324 to 464 b
31  with microsatellite alterations at selected tetranucleotide repeats have a high frequency of p53 mut
32 nomas, whereas studies with dinucleotide and tetranucleotide repeats have not.
33                                    Two novel tetranucleotide repeats (heterozygosity of 66 and 68%) a
34  the mutation rate differs in di-, tri-, and tetranucleotide repeats, how mutation rate distributes w
35                   Highly polymorphic di- and tetranucleotide repeats in and around Npr3, a potential
36 vated microsatellite alterations at selected tetranucleotide repeats in approximately 60% that associ
37 nd use it to fit DNA data for di-, tri-, and tetranucleotide repeats in humans, mice, fruit flies, an
38  or BAT-40 was significantly associated with tetranucleotide repeat instability in sporadic adenomas
39                                         This tetranucleotide repeat is located in the first intron of
40 his variable expression involves slippage of tetranucleotide repeats located within the reading frame
41 y-five dinucleotide (dC.dA)n.(dG.dT)n and 18 tetranucleotide repeat loci were identified and genotype
42      The STSs include 18 (CA) repeat and one tetranucleotide repeat marker that detect polymorphism,
43 ite instability has been observed at certain tetranucleotide repeat markers (AAAGn) in lung, head and
44         Here we examine 236 mutations at 122 tetranucleotide repeat markers and find that the rate of
45 f MSI has been described that occurs only at tetranucleotide repeat markers.
46 ulted in a approximately 35-fold increase in tetranucleotide repeat-mediated PV rates.
47               Between three and six tri- and tetranucleotide repeat microsatellite loci were analyzed
48 ide sequences of 23 different alleles at one tetranucleotide repeat microsatellite locus in fin whale
49                                Di-, tri- and tetranucleotide repeat microsatellite markers localized
50                               In addition, a tetranucleotide repeat of variable length that may provi
51 sed as PCR templates with trinucleotide- and tetranucleotide-repeat polymorphic markers.
52    A previous linkage analysis, which used a tetranucleotide repeat polymorphism at the tyrosine hydr
53                                          The tetranucleotide repeat polymorphism is highly informativ
54 tified the start site of transcription and a tetranucleotide repeat polymorphism that locates at less
55 ion of human chromosome 17 were screened for tetranucleotide repeat polymorphisms by hybridizing shot
56 inucleotide repeat sequence [(CA)(17)] and a tetranucleotide repeat sequence [(GAAA)(17)] have been d
57                         We have identified a tetranucleotide repeat sequence, (CAAA)(N), in the genom
58 esenting all previously reported LPS-related tetranucleotide repeat sequences in H. influenzae, were
59          Based on this, we hypothesized that tetranucleotide repeat sequences might be used to identi
60 comprising four primer pairs for polymorphic tetranucleotide repeat sequences on chromosome 21, four
61                   We determined that the DM2 tetranucleotide repeats showed a lower thermodynamic sta
62                  We analyze a set of data on tetranucleotide repeats that reveals the imbalance expec
63  instability was determined by a panel of 10 tetranucleotide repeats, the Bethesda consensus panel of
64           MSI was evaluated by a panel of 10 tetranucleotide repeats, the noncoding mononucleotide re
65 ion, we investigated the capacity of the DM2 tetranucleotide repeats to also expand during this proce
66 ion by human DNA polymerase beta, of several tetranucleotide repeat tracts in which the repeat units
67 ound upstream of most Haemophilus influenzae tetranucleotide repeat tracts, raising the possibility o
68 ragment processing destabilizes H.influenzae tetranucleotide repeat tracts.
69 he instabilities were greater for the longer tetranucleotide repeat tracts.
70 i containing tracts of six or more identical tetranucleotide repeat units.
71 ponse were observed between dinucleotide and tetranucleotide repeat units.
72                      The distribution of the tetranucleotide repeats was bimodal, and there was stron
73  two cases indicating somatic expansion of a tetranucleotide repeat were found.
74 microsatellite loci including di-, tri-, and tetranucleotide repeats were evaluated.
75 Expansions of up to double the length of the tetranucleotide repeats were found.
76 bility results determined by the panel of 10 tetranucleotide repeats were highly significantly relate
77  The genetic instabilities of (CCTG.CAGG)(n) tetranucleotide repeats were investigated to evaluate th
78  TNRs showed no such preference, and di- and tetranucleotide repeats were most frequently found in no
79 eats (2 dinucleotide, 2 trinucleotide, and 1 tetranucleotide repeats) were analyzed by polymerase cha
80                 A confounding factor is that tetranucleotide repeats within the lic2A, lgtC, and lex2