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'DNA Repair, ' Volume 115 in the Advances in Protein Chemistry and Structural Biology series, provides an overview of current developments in mechanisms underlying DNA repair, their involvement in maintaining chromatin repair, the balance between chromosome breaks repair pathways, tumorigenesis, immune signaling and infection-induced inflammation. Specific chapters cover the Structure and function of the multi-subunit TFIIH with insights into nucleotide excision repair, Chromatin repair: how DNA packaging controls double-strand break repair, Controlling the balance between chromosome breaks repair pathways, The targeting of DNA repair pathways in the era of precision oncology, and much more. Key Features: Describes advances in our understanding on DNA repair mechanisms and the involvement of their dysregulation in promoting diseases; Presents data that is targeted to a very wide audience of specialists, researchers and students; Contains timely chapters written by well-renowned authorities in their field; Provides targeted information that is well supported by a number of high-quality illustrations, figures and tables. Readership: Protein chemists, biochemists, molecular biologists, cell biologists, immunologists, neuroscientists, structural biologists, medical doctors, pharmacologists, computational biochemists and other researchers working in this field. Articles published here would also be of a great benefit to medical, biology and pharmacology students specializing in this field. -- Provided by publisher.

Documentation and information --- Russian Federation --- Libraries --- Russia --- DNA repair. --- Deoxyribonucleic acid repair --- Repair, DNA --- Repair mechanisms in DNA --- Biochemical genetics --- Antimutagens --- DNA Repair.

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Tea, made from the leaves of the Camellia senenisis plant, is the second most consumed beverage worldwide after water. Accumulating evidence from cellular, animal, epidemiological and clinical studies have linked tea consumption to various health benefits, such as chemoprevention of cancers, chronic inflammation, heart and liver diseases, diabetes, neurodegenerative diseases, etc. Although such health benefits have not been consistently observed in some intervention trials, positive results from clinical trials have provided direct evidence supporting the cancer-protective effect of green tea. In addition, numerous mechanisms of action have been suggested to contribute to tea’s disease-preventive effects. Furthermore, effects of the processing and storage of tea, as well as additives on tea’s properties have been investigated.

polyphenols --- n/a --- cell cycle arrest and apoptosis --- neuroblastoma --- salivary ?-amylase activity --- cancer apoptosis --- yaupon holly --- bioaccessibility --- fracture --- p53 --- tea --- Liubao tea --- BE(2)-C --- matrix metalloproteinase-1 (MMP-1) --- catechin --- renal stone --- oxalate --- protein expression --- 67LR --- Alzheimer’s disease --- EGCG --- nutraceutical --- diseases --- anti-oxidant --- heme oxygenase-1 --- polyphenol --- anxiety --- matcha --- ERCC1/XPF --- neuro-sphere --- tea consumption --- theanine --- Rosmarinic acid --- yerba mate --- hypercalciuria --- gene expression --- microbiota --- cohort study --- histone deacetylase 2 (HDAC2) --- guayusa --- nuclear factor erythroid 2-related factor 2 (Nrf2) --- DNA repair --- mRNA expression --- caffeine --- chemoprevention --- cisplatin --- 6-OH-11-O-hydroxyphenanthrene --- adrenal hypertrophy --- hepatic damage --- anti-photoaging --- cell death --- green tea --- kudingcha --- suberoylanilide hydroxamic acid (SAHA) --- epigallocatechin gallate (EGCG) --- stress-reduction --- calcium oxalate monohydrate --- Camellia sinensis --- chemoresistance --- tea polyphenols --- green tea polyphenols --- green tea catechins --- N-MYC --- cancer --- epigallocatechin-gallate (EGCG) --- Parkinson’s disease --- Alzheimer's disease --- Parkinson's disease

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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.

Werner Syndrome --- n/a --- A549 cells --- epigenetic --- neurodegeneration --- Genome integrity --- adaptation --- cellular senescence --- genome instability --- Werner Syndrome Protein --- lipofuscin --- cell cycle checkpoints --- exonuclease 1 --- template-switching --- energy metabolism --- mutation frequency --- DNA replication --- fork regression --- motor neuron disease --- Microsatellites --- Alzheimer’s disease --- chromatin remodeler --- repair of DNA damage --- AP site analogue --- mutagens --- replication timing --- Thermococcus eurythermalis --- nucleolar stress --- gene expression --- mutations spectra --- origin firing --- Fanconi Anemia --- superfamily 2 ATPase --- DNA translocation --- DNA repair --- SSB signaling --- homologous recombination --- common fragile sites --- 8-chloro-adenosine --- replication --- genome stability --- mutagenicity --- fork reversal --- multiple sclerosis --- non-B DNA --- protein stability --- heterogeneity --- ubiquitin --- SenTraGorTM (GL13) --- replication restart --- EdU --- ?-arrestin --- NER --- aging --- SSB end resection --- oxidative stress --- ATR --- dormant origins --- R loops --- DNA damage response --- Difficult-to-Replicate Sequences --- DNA double-strand repair --- endonuclease IV --- ALS --- double strand break repair --- premature aging --- replication stress --- EXO1 --- POL? --- translesion synthesis --- strand displacements --- G2-arrest --- DNA replication pattern --- SSB repair --- genome integrity --- G protein-coupled receptor kinase interacting protein 2 (GIT2) --- MMR --- replicative stress --- senolytics --- spacer --- interactome --- ATR-Chk1 DDR pathway --- C9orf72 --- replication fork restart --- translesion DNA synthesis --- DNA damage --- mismatch repair --- DNA replication stress --- DNA helicase --- Polymerase kappa --- DNA fiber assay --- H1299 cells --- TLS --- APE2 --- ageing --- cell death --- chromosome --- TopBP1 --- barley --- clock proteins --- post-translational modification --- 8-oxoG --- S phase --- ataxia telangiectasia mutated (ATM) --- G protein-coupled receptor (GPCR) --- Polymerase eta --- cancer --- G protein-coupled receptor kinase (GRK) --- helicase --- genomic instability --- Parkinson’s disease --- nucleotide excision repair --- SupF --- Alzheimer's disease --- Parkinson's disease