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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

chemotaxis --- chemokine --- atypical chemokine receptor --- G protein-coupled receptor --- signaling --- arrestin --- GPCR

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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.

proliferation and differentiation --- metastasis --- vitamin D --- G protein-coupled receptor (GPCR) --- crystal structure --- parathyroid hormone (PTH) --- cancer --- Alzheimer

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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.

proliferation and differentiation --- metastasis --- vitamin D --- G protein-coupled receptor (GPCR) --- crystal structure --- parathyroid hormone (PTH) --- cancer --- Alzheimer

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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

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The Hippo pathway is a highly dynamic cellular signaling nexus that plays central roles in multiple cell types and regulates regeneration, metabolism, and development. The Hippo pathway integrates mechanotransduction, cell polarity, inflammation, and numerous types of paracrine signaling. If not tightly regulated, dysregulated Hippo pathway signaling drives the onset and progression of a range of diseases, including fibrosis and cancer. The molecular understanding of the Hippo pathway is rapidly evolving. This Special Issue contains ten articles contributed by established and up-and-coming Hippo pathway experts that, as a whole, provides an up-to-date overview of how dysregulated Hippo pathway activity is a common driver of specific diseases. The articles have a particular focus on the underlying molecular and cellular mechanisms that cause the Hippo pathway to go awry, and especially how this drives disease. The articles analyze disease-specific as well as common themes, which provides valuable insights into the fundamental molecular mechanisms in the dysfunctioning Hippo pathway, and thereby offer practical insights into potential future therapeutic intervention strategies.

STRIPAK --- skin cancer --- n/a --- Lats2 --- transcription --- myofibroblast --- epigenetic --- Hippo --- cancer immunity --- TAZ --- Taz --- TAZ (transcriptional co-activator with PDZ-binding motif) --- adaptive immunity --- fibroblasts --- innate immunity --- LATS --- MST (mammalian STE20-like protein kinase) --- phosphorylation --- stem cells --- wound healing --- signal transduction --- angiogenesis --- LATS1/2 --- EMT --- protein-protein interactions --- structure biology --- Hippo pathway --- hippo pathway --- autoimmunity --- Mps one binder --- YAP/TAZ --- GPCR --- fibrosis --- MST1/2 --- YAP (yes-associated protein) --- YAP --- Yap --- protein kinase --- LATS (large tumor suppressor kinase) --- peripheral nerve sheath tumor --- signal cross-talk --- stem cell --- skin development --- STK38 --- tumorigenesis --- NDR --- schwannoma --- G protein-coupled receptor --- anti-cancer therapy --- feedback loops --- vascular mimicry --- castration resistance --- chromatin --- Hippo signalling --- ECM --- MST --- prostate cancer --- TEAD --- cancer --- zebrafish