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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

Mitochondria --- Aging --- age-related disease --- Lysosome --- Endoplasmic Reticulum

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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

Science: general issues --- Biology, life sciences --- Mitochondria --- Aging --- age-related disease --- Lysosome --- Endoplasmic Reticulum

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This book is a collection of articles from the Cells Special Issue on “Ubiquitin and Autophagy”. It contains an Editorial and 13 articles at the intersection of ubiquitin- and autophagy-related processes. Ubiquitin is a small protein modifier that is widely used to tag proteins, organelles, and pathogens for their degradation by the ubiquitin–proteasome system and/or autophagy–lysosomal pathway. Interestingly, several ubiquitin-like proteins are at a core of the autophagy mechanism. This book dedicates a lot of attention to the crosstalk between the ubiquitin–proteasome system and autophagy and serves as a good starting point for the readers interested in the current state of the knowledge on ubiquitin and autophagy.

PSMD14 --- ubiquitin --- retrograde --- trafficking --- APP --- autophagy --- Cx43 --- GABARAP --- gap junction --- MAPLC3 --- leukodystrophies --- globoid cell leukodystrophy --- psychosine --- p62 --- proteasome --- toll-like receptor 4 --- TRAF6 --- BECN1 --- ATG12~5/16 complex --- Dictyostelium --- ubiquitin-like protein --- phagocytosis --- pinocytosis --- UPS --- ubiquitin–proteasome system --- crosstalk --- tissue specificity --- C. elegans --- NFAT5 --- autophagy initiation --- islet --- FIP200 --- unfolded protein response --- UPR --- Atg8 --- LC3 --- LIR motif --- SAR --- UBL --- neurodegenerative diseases --- autophagy–lysosome pathway --- lysosome --- selective autophagy --- ubiquitination --- degradation --- the ubiquitin-proteasome system --- plants --- mitophagy --- aggrephagy --- lysophagy --- xenophagy --- lipophagy --- nucleophagy --- ER-phagy --- cargo receptors --- sorting nexins --- retromer --- endosome --- n/a --- ubiquitin-proteasome system --- autophagy-lysosome pathway

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The secretions of the exocrine pancreas provide for digestion of a meal into components that are then available for processing and absorption by the intestinal epithelium. Without the exocrine pancreas, malabsorption and malnutrition result. This chapter describes the cellular participants responsible for the secretion of digestive enzymes and fluid that in combination provide a pancreatic secretion that accomplishes the digestive functions of the gland. Key cellular participants, the acinar cell and the duct cell, are responsible for digestive enzyme and fluid secretion, respectively, of the exocrine pancreas. This chapter describes the neurohumoral pathways that mediate the pancreatic response to a meal as well as details of the cellular mechanisms that are necessary for the organ responses, including protein synthesis and transport and ion transports, and the regulation of these responses by intracellular signaling systems. Examples of pancreatic diseases resulting from dysfunction in cellular mechanisms provide emphasis of the importance of the normal physiologic mechanisms.

Pancreas. --- Pancreatic acinar cells. --- Pancreas, Exocrine. --- Pancreas --- Secretion --- Digestive enzymes --- Acinar cell --- Duct cell --- Digestion --- Centroacinar cell --- Cholecystokinin --- Secretin --- Endoplasmic reticulum --- Zymogens --- Zymogen granule --- Condensing vacuole --- Lysosome --- Unfolded protein response --- Cystic fibrosis --- Trypsinogen --- Lipase --- Amylase

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Despite the efficiency of current cancer treatments, cancer is still a deadly disease for too many. In 2008, 7.6 million people died of cancer; with the current development, it is estimated that the annual cancer death number will grow to 13 million by 2030. There is clearly a need for not only more research but also more innovative and out of the mainstream scientific ideas to discover and develop even better cancer treatments. This book presents the collective works published in the recent Special Issue entitled “Killing Cancer: Discovery and Selection of New Target Molecules”. These articles comprise a selection of studies, ideas, and opinions that aim to facilitate knowledge, thoughts, and discussion about which biological and molecular mechanisms in cancer we should target and how we should target them.

ferlin --- myoferlin --- dysferlin --- otoferlin --- C2 domain --- plasma membrane --- sulconazole --- NF-κB --- IL-8 --- mammosphere --- breast cancer stem cells --- AF1Q --- MLLT11 --- WNT --- STAT --- esophageal cancer --- prognosis --- mTORC1 --- mTORC2 --- metabolism --- rapalogs --- mTOR inhibitors --- cancer metabolism --- mTOR in immunotherapy --- nutrient metabolism --- kinase inhibitors --- mTOR signaling --- MAPK kinase --- ERK1 --- ERK2 --- CD domain --- Rolled --- SCH772984 --- VRT-11E --- sevenmaker --- cancer therapy --- EMT --- lysosome --- lysosome-mediated invasion --- MZF1 --- phosphorylation --- PAK4 --- SUMOylation --- transcription factor --- zinc finger --- glucocorticoids --- 3D growth --- nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB) --- epithelial–mesenchymal transition --- anoikis --- proliferation --- targeted cancer therapy --- disulfiram --- NPL4 --- replication stress --- DNA damage --- BRCA1 --- BRCA2 --- ATR pathway --- PDAC --- TCIRG1 --- ATP6V0a3 --- invasion --- migration --- matrix degradation --- pH-regulation --- autophagy --- multidrug resistance in cancer --- drug efflux pumps --- ATP-binding cassette transporter --- breast cancer resistance protein (BCRP) --- ABCG2 --- pyrazolo-pyrimidine derivative --- SCO-201 --- colorectal cancer --- immunotherapy --- inflammation --- microsatellite instability --- oncofetal chondroitin sulfate --- chondroitin sulfate --- cancer --- solid tumors --- target --- pediatric cancer --- VAR2 --- dexamethasone --- thyroid cancer --- microgravity --- space environment --- n/a --- epithelial-mesenchymal transition