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Physiology and Pathophysiology of the Extracellular Calcium-Sensing Receptor

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889455126 Year: Pages: 189 DOI: 10.3389/978-2-88945-512-6 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2019-01-23 14:53:42
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Abstract

Calcium is vital for human physiology; it mediates multiple signaling cascades, critical for cell survival, differentiation, or death both as first and as second messenger. The role of calcium as first messenger is mediated by the G-protein coupled receptor, the extracellular calcium-sensing receptor (CaSR). The CaSR is a multifaceted molecule that senses changes in the concentration of a wide variety of environmental factors including di- and trivalent cations, amino acids, polyamines, and pH. In calcitropic tissues with obvious roles in calcium homeostasis such as parathyroid, kidney, and bone it regulates circulating calcium concentrations. The germline mutations of the CaSR cause parathyroid disorders demonstrating the importance of the CaSR for the maintenance of serum calcium homeostasis. The CaSR has an important role also in a range of non-calcitropic tissues, such as the intestine, lungs, central and peripheral nervous system, breast, skin and reproductive system, where it regulates molecular and cellular processes such as gene expression, proliferation, differentiation and apoptosis; as well as regulating hormone secretion and lactation.This Research Topic is an overview of the CaSR and its molecular signaling properties together with the various organ systems where it plays an important role. The articles highlight the current knowledge regarding many aspects of the calcitropic and non-calcitropic physiology and pathophysiology of the CaSR.

DNA Replication Stress

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ISBN: 9783039213894 / 9783039213900 Year: Pages: 368 DOI: 10.3390/books978-3-03921-390-0 Language: eng
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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