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DNA Replication Stress

Edited by
August 2019
368 pages
  • ISBN978-3-03921-389-4 (Paperback)
  • ISBN978-3-03921-390-0 (PDF)
https://doi.org/10.3390/books978-3-03921-390-0
Free download (PDF)

This book is a reprint of the Special Issue DNA Replication Stress that was published in

Biology & Life Sciences
Chemistry & Materials Science
Medicine & Pharmacology
Summary

This Special Issue of International Journal of Molecular Sciences (IJMS) is dedicated to the mechanisms mediated at the molecular and cellular levels in response to adverse genomic perturbations and DNA replication stress. The relevant proteins and processes play paramount roles in nucleic acid transactions to maintain genomic stability and cellular homeostasis. A total of 18 articles are presented which encompass a broad range of highly relevant topics in genome biology. These include replication fork dynamics, DNA repair processes, DNA damage signaling and cell cycle control, cancer biology, epigenetics, cellular senescence, neurodegeneration, and aging.

As Guest Editor for this IJMS Special Issue, I am very pleased to offer this collection of riveting articles centered on the theme of DNA replication stress. The blend of articles builds upon a theme that DNA damage has profound consequences for genomic stability and cellular homeostasis that affect tissue function, disease, cancer, and aging at multiple levels and through unique mechanisms. I thank the authors for their excellent contributions, which provide new insight into this fascinating and highly relevant area of genome biology.
Format
  • Paperback
License
© 2019 by the authors; CC BY-NC-ND license
Keywords
barley; chromosome; DNA replication pattern; EdU; mutagens; DNA replication; DNA damage; DNA repair; genome integrity; A549 cells; H1299 cells; heterogeneity; DNA damage response; 8-chloro-adenosine; DNA replication; S phase; origin firing; TopBP1; ATR; DNA fiber assay; APE2; ATR-Chk1 DDR pathway; Genome integrity; SSB end resection; SSB repair; SSB signaling; DNA replication stress; genome stability; ubiquitin; replication fork restart; translesion synthesis; template-switching; homologous recombination; Fanconi Anemia; G protein-coupled receptor (GPCR); aging; DNA damage; β-arrestin; G protein-coupled receptor kinase (GRK); interactome; G protein-coupled receptor kinase interacting protein 2 (GIT2); ataxia telangiectasia mutated (ATM); clock proteins; energy metabolism; neurodegeneration; cellular senescence; ageing; Alzheimer’s disease; multiple sclerosis; Parkinson’s disease; lipofuscin; SenTraGorTM (GL13); senolytics; DNA replication; DNA repair; DNA damage response; DNA translocation; DNA helicase; superfamily 2 ATPase; replication restart; fork reversal; fork regression; chromatin remodeler; C9orf72; ALS; motor neuron disease; R loops, nucleolar stress; neurodegeneration; Difficult-to-Replicate Sequences; replication stress; non-B DNA; Polymerase eta; Polymerase kappa; genome instability; common fragile sites; Microsatellites; cancer; DNA double-strand repair; premature aging; post-translational modification; protein stability; replication stress; Werner Syndrome; Werner Syndrome Protein; dormant origins; replicative stress; replication timing; DNA damage; genome instability; cancer; Thermococcus eurythermalis; endonuclease IV; AP site analogue; spacer; DNA repair; DNA repair; double strand break repair; exonuclease 1; EXO1; mismatch repair; MMR; NER; nucleotide excision repair; strand displacements; TLS; translesion DNA synthesis; POLζ; mutation frequency; mutations spectra; SupF; mutagenicity; oxidative stress; DNA damage; DNA repair; replication; 8-oxoG; epigenetic; gene expression; helicase; cell cycle checkpoints; genomic instability; G2-arrest; cell death; repair of DNA damage; adaptation; n/a