Literature DB >> 16807140

The involvement of non-B DNA structures in gross chromosomal rearrangements.

Albino Bacolla1, Marzena Wojciechowska, Beata Kosmider, Jacquelynn E Larson, Robert D Wells.   

Abstract

Non-B DNA conformations adopted by certain types of DNA sequences promote genetic instabilities, especially gross rearrangements including translocations. We conclude the following: (a) slipped (hairpin) structures, cruciforms, triplexes, tetraplexes and i-motifs, and left-handed Z-DNA are formed in chromosomes and elicit profound genetic consequences via recombination-repair, (b) repeating sequences, probably in their non-B conformations, cause gross genomic rearrangements (translocations, deletions, insertions, inversions, and duplications), and (c) these rearrangements are the genetic basis for numerous human diseases including polycystic kidney disease, adrenoleukodystrophy, follicular lymphomas, and spermatogenic failure.

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Year:  2006        PMID: 16807140     DOI: 10.1016/j.dnarep.2006.05.032

Source DB:  PubMed          Journal:  DNA Repair (Amst)        ISSN: 1568-7856


  42 in total

Review 1.  The constitutional t(11;22): implications for a novel mechanism responsible for gross chromosomal rearrangements.

Authors:  H Kurahashi; H Inagaki; T Ohye; H Kogo; M Tsutsumi; T Kato; M Tong; B S Emanuel
Journal:  Clin Genet       Date:  2010-10       Impact factor: 4.438

2.  Discovery of the role of non-B DNA structures in mutagenesis and human genomic disorders.

Authors:  Robert D Wells
Journal:  J Biol Chem       Date:  2008-12-03       Impact factor: 5.157

3.  DNA energy landscapes via calorimetric detection of microstate ensembles of metastable macrostates and triplet repeat diseases.

Authors:  Jens Völker; Horst H Klump; Kenneth J Breslauer
Journal:  Proc Natl Acad Sci U S A       Date:  2008-11-17       Impact factor: 11.205

4.  Guanine repeat-containing sequences confer transcription-dependent instability in an orientation-specific manner in yeast.

Authors:  Nayun Kim; Sue Jinks-Robertson
Journal:  DNA Repair (Amst)       Date:  2011-08-02

Review 5.  Non-B DNA structure-induced genetic instability and evolution.

Authors:  Junhua Zhao; Albino Bacolla; Guliang Wang; Karen M Vasquez
Journal:  Cell Mol Life Sci       Date:  2009-09-01       Impact factor: 9.261

6.  Hereditary Hemorrhagic Telangiectasia: Breakpoint Characterization of a Novel Large Deletion in ACVRL1 Suggests the Causing Mechanism.

Authors:  Laura Boeri; Orietta Radi; Cecilia Canzonieri; Elisabetta Buscarini; Agnese Scatigno; Antonella Minelli; Federica Ornati; Fabio Pagella; Cesare Danesino; Carla Olivieri
Journal:  Mol Syndromol       Date:  2013-02-28

Review 7.  Histone methylation and V(D)J recombination.

Authors:  Noriko Shimazaki; Michael R Lieber
Journal:  Int J Hematol       Date:  2014-07-25       Impact factor: 2.490

8.  Type 2 NF1 deletions are highly unusual by virtue of the absence of nonallelic homologous recombination hotspots and an apparent preference for female mitotic recombination.

Authors:  Katharina Steinmann; David N Cooper; Lan Kluwe; Nadia A Chuzhanova; Cornelia Senger; Eduard Serra; Conxi Lazaro; Montserrat Gilaberte; Katharina Wimmer; Viktor-Felix Mautner; Hildegard Kehrer-Sawatzki
Journal:  Am J Hum Genet       Date:  2007-10-31       Impact factor: 11.025

9.  Analysis of the t(3;8) of hereditary renal cell carcinoma: a palindrome-mediated translocation.

Authors:  Takema Kato; Colleen P Franconi; Molly B Sheridan; April M Hacker; Hidehito Inagakai; Thomas W Glover; Martin F Arlt; Harry A Drabkin; Robert M Gemmill; Hiroki Kurahashi; Beverly S Emanuel
Journal:  Cancer Genet       Date:  2014-03-18

10.  Impact of bulge loop size on DNA triplet repeat domains: Implications for DNA repair and expansion.

Authors:  Jens Völker; G Eric Plum; Vera Gindikin; Horst H Klump; Kenneth J Breslauer
Journal:  Biopolymers       Date:  2014-01       Impact factor: 2.505

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