Erratum: “Impact of bulge loop size on DNA triplet repeat domains: Implications for DNA repair and expansion” Biopolymers 101(1), 1-12, (2014)

Biopolymers ◽  
2013 ◽  
Vol 101 (4) ◽  
pp. 439-439
Author(s):  
Jens Völker ◽  
G. Eric Plum ◽  
Vera Gindikin ◽  
Horst H. Klump ◽  
Kenneth J. Breslauer
Keyword(s):  
Dna Repair ◽  
Triplet Repeat ◽  
Loop Size ◽  
Bulge Loop

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

Biopolymers ◽  
2013 ◽  
Vol 101 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Jens Völker ◽  
G. Eric Plum ◽  
Vera Gindikin ◽  
Horst H. Klump ◽  
Kenneth J. Breslauer
Keyword(s):  
Dna Repair ◽  
Triplet Repeat ◽  
Loop Size ◽  
Bulge Loop

scholarly journals New developments in Huntington’s disease and other triplet repeat diseases: DNA repair turns to the dark side

2020 ◽  
Vol 4 (4) ◽  
Author(s):  
Robert S. Lahue
Keyword(s):  
Dna Repair ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Cag Repeat ◽  
Model Systems ◽  
Triplet Repeat ◽  
Maximal Effect ◽  
Huntingtin Protein ◽  
Dna Repair Proteins ◽  
Repeat Expansions

Abstract Huntington’s disease (HD) is a fatal, inherited neurodegenerative disease that causes neuronal death, particularly in medium spiny neurons. HD leads to serious and progressive motor, cognitive and psychiatric symptoms. Its genetic basis is an expansion of the CAG triplet repeat in the HTT gene, leading to extra glutamines in the huntingtin protein. HD is one of nine genetic diseases in this polyglutamine (polyQ) category, that also includes a number of inherited spinocerebellar ataxias (SCAs). Traditionally it has been assumed that HD age of onset and disease progression were solely the outcome of age-dependent exposure of neurons to toxic effects of the inherited mutant huntingtin protein. However, recent genome-wide association studies (GWAS) have revealed significant effects of genetic variants outside of HTT. Surprisingly, these variants turn out to be mostly in genes encoding DNA repair factors, suggesting that at least some disease modulation occurs at the level of the HTT DNA itself. These DNA repair proteins are known from model systems to promote ongoing somatic CAG repeat expansions in tissues affected by HD. Thus, for triplet repeats, some DNA repair proteins seem to abandon their normal genoprotective roles and, instead, drive expansions and accelerate disease. One attractive hypothesis—still to be proven rigorously—is that somatic HTT expansions augment the disease burden of the inherited allele. If so, therapeutic approaches that lower levels of huntingtin protein may need blending with additional therapies that reduce levels of somatic CAG repeat expansions to achieve maximal effect.

scholarly journals DNA Repair and DNA Triplet Repeat Expansion: The Impact of Abasic Lesions on Triplet Repeat DNA Energetics

2009 ◽  
Vol 131 (26) ◽  
pp. 9354-9360 ◽  
Author(s):  
Jens Völker ◽  
G. Eric Plum ◽  
Horst H. Klump ◽  
Kenneth J. Breslauer
Keyword(s):  
Dna Repair ◽  
Repeat Expansion ◽  
Triplet Repeat ◽  
Triplet Repeat Expansion ◽  
Repeat Dna ◽  
The Impact

scholarly journals Dynamic DNA Energy Landscapes and Substrate Complexity in Triplet Repeat Expansion and DNA Repair

Biomolecules ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. 709 ◽  
Author(s):  
Völker ◽  
Plum ◽  
Gindikin ◽  
Breslauer
Keyword(s):  
Dna Repair ◽  
Excision Repair ◽  
Repeat Expansion ◽  
Triplet Repeat ◽  
Energy Landscapes ◽  
Abasic Site ◽  
Triplet Repeat Expansion ◽  
Dna Repeat ◽  
Repeat Dna

DNA repeat domains implicated in DNA expansion diseases exhibit complex conformational and energy landscapes that impact biological outcomes. These landscapes include ensembles of entropically driven positional interchanges between isoenergetic, isomeric looped states referred to as rollamers. Here, we present evidence for the position-dependent impact on repeat DNA energy landscapes of an oxidative lesion (8oxodG) and of an abasic site analogue (tetrahydrofuran, F), the universal intermediate in base excision repair (BER). We demonstrate that these lesions modulate repeat bulge loop distributions within the wider dynamic rollamer triplet repeat landscapes. We showed that the presence of a lesion disrupts the energy degeneracy of the rollameric positional isomers. This lesion-induced disruption leads to the redistribution of loop isomers within the repeat loop rollamer ensemble, favoring those rollameric isomers where the lesion is positioned to be energetically least disruptive. These dynamic ensembles create a highly complex energy/conformational landscape of potential BER enzyme substrates to select for processing or to inhibit processing. We discuss the implications of such lesion-induced alterations in repeat DNA energy landscapes in the context of potential BER repair outcomes, thereby providing a biophysical basis for the intriguing in vivo observation of a linkage between pathogenic triplet repeat expansion and DNA repair.

259: Dna-Repair Genetic Polymorphisms and Prostate Cancer Risk

2005 ◽  
Vol 173 (4S) ◽  
pp. 71-71
Author(s):  
Peter E. Clark ◽  
M. Craig Hall ◽  
Kristin L. Lockett ◽  
Jianfeng Xu ◽  
Sigun L. Zheng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Repair ◽  
Cancer Risk ◽  
Genetic Polymorphisms ◽  
Prostate Cancer Risk

983: Bladder Cancer Predisposition: A Pathway-Based Approach to DNA Repair and Cell Cycle Control Genes

2006 ◽  
Vol 175 (4S) ◽  
pp. 317-317
Author(s):  
Xifeng Wu ◽  
Jian Gu ◽  
H. Barton Grossman ◽  
Christopher I. Amos ◽  
Carol Etzel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Dna Repair ◽  
Cell Cycle Control ◽  
Cancer Predisposition

Drugs Impair Keratinocyte DNA Repair in Culture

2005 ◽  
Vol 36 (7) ◽  
pp. 42
Author(s):  
PATRICE WENDLING
Keyword(s):  
Dna Repair
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