Literature DB >> 11818139

Genome architecture, rearrangements and genomic disorders.

Paweł Stankiewicz1, James R Lupski.   

Abstract

An increasing number of human diseases are recognized to result from recurrent DNA rearrangements involving unstable genomic regions. These are termed genomic disorders, in which the clinical phenotype is a consequence of abnormal dosage of gene(s) located within the rearranged genomic fragments. Both inter- and intrachromosomal rearrangements are facilitated by the presence of region-specific low-copy repeats (LCRs) and result from nonallelic homologous recombination (NAHR) between paralogous genomic segments. LCRs usually span approximately 10-400 kb of genomic DNA, share >or= 97% sequence identity, and provide the substrates for homologous recombination, thus predisposing the region to rearrangements. Moreover, it has been suggested that higher order genomic architecture involving LCRs plays a significant role in karyotypic evolution accompanying primate speciation.

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Year:  2002        PMID: 11818139     DOI: 10.1016/s0168-9525(02)02592-1

Source DB:  PubMed          Journal:  Trends Genet        ISSN: 0168-9525            Impact factor:   11.639


  359 in total

1.  2002 Curt Stern Award Address. Genomic disorders recombination-based disease resulting from genomic architecture.

Authors:  James R Lupski
Journal:  Am J Hum Genet       Date:  2003-02       Impact factor: 11.025

Review 2.  Parental origin and timing of de novo Robertsonian translocation formation.

Authors:  Ruma Bandyopadhyay; Anita Heller; Cami Knox-DuBois; Christopher McCaskill; Sue Ann Berend; Scott L Page; Lisa G Shaffer
Journal:  Am J Hum Genet       Date:  2002-11-06       Impact factor: 11.025

3.  Gene content and function of the ancestral chromosome fusion site in human chromosome 2q13-2q14.1 and paralogous regions.

Authors:  Yuxin Fan; Tera Newman; Elena Linardopoulou; Barbara J Trask
Journal:  Genome Res       Date:  2002-11       Impact factor: 9.043

4.  Genetic proof of unequal meiotic crossovers in reciprocal deletion and duplication of 17p11.2.

Authors:  Christine J Shaw; Weimin Bi; James R Lupski
Journal:  Am J Hum Genet       Date:  2002-10-09       Impact factor: 11.025

5.  NSD1 mutations are the major cause of Sotos syndrome and occur in some cases of Weaver syndrome but are rare in other overgrowth phenotypes.

Authors:  Jenny Douglas; Sandra Hanks; I Karen Temple; Sally Davies; Alexandra Murray; Meena Upadhyaya; Susan Tomkins; Helen E Hughes; Trevor R P Cole; Nazneen Rahman
Journal:  Am J Hum Genet       Date:  2002-12-02       Impact factor: 11.025

Review 6.  Chromosomal translocations and palindromic AT-rich repeats.

Authors:  Takema Kato; Hiroki Kurahashi; Beverly S Emanuel
Journal:  Curr Opin Genet Dev       Date:  2012-03-06       Impact factor: 5.578

7.  Translocation breakpoint mapping and sequence analysis in three monosomy 1p36 subjects with der(1)t(1;1)(p36;q44) suggest mechanisms for telomere capture in stabilizing de novo terminal rearrangements.

Authors:  Blake C Ballif; Keiko Wakui; Marzena Gajecka; Lisa G Shaffer
Journal:  Hum Genet       Date:  2003-10-25       Impact factor: 4.132

8.  End-sequence profiling: sequence-based analysis of aberrant genomes.

Authors:  Stanislav Volik; Shaying Zhao; Koei Chin; John H Brebner; David R Herndon; Quanzhou Tao; David Kowbel; Guiqing Huang; Anna Lapuk; Wen-Lin Kuo; Gregg Magrane; Pieter De Jong; Joe W Gray; Colin Collins
Journal:  Proc Natl Acad Sci U S A       Date:  2003-06-04       Impact factor: 11.205

9.  2002 Curt Stern Award address. Introductory speech for James R. Lupski.

Authors:  Robert D Nicholls
Journal:  Am J Hum Genet       Date:  2003-02       Impact factor: 11.025

10.  Complex evolution of 7E olfactory receptor genes in segmental duplications.

Authors:  Tera Newman; Barbara J Trask
Journal:  Genome Res       Date:  2003-05       Impact factor: 9.043

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