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DNA Replication Controls

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ISBN: 9783038425724 9783038425731 Year: Volume: 2 Pages: X, 346 DOI: 10.3390/books978-3-03842-573-1 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology
Added to DOAB on : 2017-12-27 08:38:10
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The conditions for DNA replication are not ideal, owing to endogenous and exogenous replication stresses that lead to arrest of the replication fork. Arrested forks are among the most serious threats to genomic integrity because they can break or rearrange, leading to genomic instability, which is a hallmark of cancers and aging-related disorders. This title, “DNA Replication Controls”, presents series of new reviews and original research articles, providing a comprehensive guide to theoretical advancements in the field of DNA replication research in both prokaryotic and eukaryotic systems. The topics include DNA polymerases and helicases; replication initiation; replication timing; replication-associated DNA repair; and replication of difficult-to-replicate genomic regions, including telomeres, centromeres and highly-transcribed regions. This title also provides recent advancements in studies of cellular processes that are coordinated with DNA replication and how defects in the DNA replication program result in genetic disorders, including cancer. Written by leading experts in DNA replication regulation, this book will be an important resource for a wide variety of audiences, including junior graduate students and established investigators who have interests in DNA replication and genome maintenance mechanisms.

DNA Replication Controls

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ISBN: 9783038425687 9783038425694 Year: Volume: 1 Pages: X, 304 DOI: 10.3390/books978-3-03842-569-4 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology
Added to DOAB on : 2018-01-02 15:17:59
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Abstract

The conditions for DNA replication are not ideal, owing to endogenous and exogenous replication stresses that lead to arrest of the replication fork. Arrested forks are among the most serious threats to genomic integrity because they can break or rearrange, leading to genomic instability, which is a hallmark of cancers and aging-related disorders.

DNA Replication Stress

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ISBN: 9783039213894 9783039213900 Year: Pages: 368 DOI: 10.3390/books978-3-03921-390-0 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2019-12-09 16:10:12
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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.

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 --- ?-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 --- POL? --- 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

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