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1 loid relatives; a trend seen particularly in low-copy repeats.
2 ous recombination between the MAPT family of low-copy repeats.
3 icated, truncated copies that comprise these low-copy repeats.
4 elic homologous recombination events between low-copy repeats, also known as segmental duplications.
5 22q11.21 inversion appears to be mediated by low copy repeats, and is presumed to have taken place pr
6 region 1q21.1 contains extensive and complex low-copy repeats, and copy number variants (CNVs) in thi
7 at the p13.3 genomic region lacks extensive low-copy repeat architecture; however, it is highly enri
8 tutional translocations at the same 22q11.21 low copy repeat B (LCR-B) breakpoint involved in the rec
10 everal large genomic duplications, and these low-copy repeats can cause genome instability in this re
11 homologous recombination between two of four low copy repeat clusters on chromosome 22q11.2 (LCR22s).
12 eakpoints occurred in an interval containing low-copy repeats, distal to RANBP1 and proximal to ZNF74
13 ed and analyzed directly oriented paralogous low-copy repeats (DP-LCRs) in the most recent version of
14 Recombination between chromosome-specific low-copy repeats (duplicons) is an underlying mechanism
16 trovirus elements within the large, flanking low-copy repeats; experimental validation of this breakp
18 regulated recombination between the abundant low-copy repeats in the human genome may prove to be an
20 ce of all three approximately 200-kb SMS-REP low-copy repeats in the mouse and indicates that the evo
21 by large (usually >10 kb), highly homologous low copy repeat (LCR) structures that can act as recombi
23 y unequal homologous recombination involving low copy repeats (LCR) that are found clustered in the r
24 pproximately 359-kb and approximately 215-kb low-copy repeat (LCR) clusters, respectively, by aCGH an
25 y is positively associated with the flanking low-copy repeat (LCR) length and inversely influenced by
27 his region contains both direct and inverted low-copy repeat (LCR) sequences; this same region underg
35 romosome 22-specific duplicated sequences or low copy repeats (LCRs) near the end-points of the 3 Mb
36 ayed by the genomic architecture, especially low copy repeats (LCRs) or segmental duplications (SDs).
38 y of dispersed breakpoints are in regions of low copy repeats (LCRs), indicating a possible role for
40 gous recombination (NAHR), occurring between low-copy repeats (LCRs) >10 kb in size and sharing >97%
41 cilitated by the presence of region-specific low-copy repeats (LCRs) and result from nonallelic homol
43 to 6% of the human genome, and the resulting low-copy repeats (LCRs) are known to be associated with
44 , and highly homologous ( approximately 98%) low-copy repeats (LCRs) are located inside or flanking t
45 homologous recombination utilizing flanking low-copy repeats (LCRs) as substrates, generating a comm
48 The human genome is particularly rich in low-copy repeats (LCRs) or segmental duplications (5%-10
50 c region on 5q35 revealed two complex mosaic low-copy repeats (LCRs) that are centromeric and telomer
52 genomic region is flanked by large, complex low-copy repeats (LCRs) with directly oriented subunits
53 y 38-49 kb), inverted and directly oriented, low-copy repeats (LCRs), known as REPA and REPB that app
55 ecurrent rearrangements mediated by flanking low-copy repeats (LCRs), NF1 intragenic rearrangements v
56 11.2) syndrome, is flanked by large, complex low-copy repeats (LCRs), termed proximal and distal SMS-
63 d that many deletion breakpoints occurred in low-copy repeats (LCRs); 13 were associated with novel l
64 SDs) in the reference sequence revealed many low-copy repeats, most of which overlap predicted coding
65 2, separated by 20 kb and located within the low-copy repeats NF1-REPa and NF1-REPc, which flank the
69 nonallelic homologous recombination between low-copy repeats on the normal and inverted region of ch
74 higher order genomic architecture involving low-copy repeats resulting from genomic duplication play
75 CNVs) are common because of an enrichment of low-copy repeat sequences that precipitate a high freque
76 he distal breakpoints were embedded in novel low-copy repeats, suggesting the potential involvement o
77 logous recombination events between flanking low copy repeats termed LCR22A and LCR22D, resulting in
78 ion breakpoint to a region on 22q11 within a low-copy repeat termed "LCR22" and within an AT-rich rep
80 qual crossing-over events between two 240-kb low-copy repeats termed LCR22 (LCR22-2 and LCR22-4) on C
82 the DGCR6 gene to chromosome 22q11 within a low copy repeat, termed sc11.1a, and identified a second
83 map immediately adjacent and internal to the low copy repeats, termed LCR22, that mediate the deletio
85 ion breakpoint to a region on 22q11 within a low-copy repeat, termed "LCR22." To define the breakpoin
86 s recombination hotspot motif is enriched in low copy repeats that mediate recurrent deletion at this
87 ions observed in other chromosomes harboring low copy repeats, this 22q11.2 inversion has not been ob
88 ) genes and that is flanked by large complex low-copy repeats, we identified sites for nonallelic hom
89 reakpoint on 22q11 within the 22q11-specific low-copy repeat where the breakpoints of the constitutio