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Highly emotional events tend to be well remembered. The adaptive value in this is clear – those events that have a bearing on survival should be stored for future use as long-term memories whereas memories of inconsequential events would not as likely contribute to future survival. Enduring changes in the structure and function of synapses, neural circuitry, and ultimately behavior, can be modulated by highly aversive or rewarding experiences. In the last decade, the convergence of cellular, molecular, and systems neuroscience has produced new insights into the biological mechanisms that determine whether a memory will be stored for the long-term or lost forever. This Research Topic brings together leading experts, who work at multiple levels of analysis, to reveal recent discoveries and concepts regarding the synaptic mechanisms of consolidation and extinction of emotionally arousing memories.

Synapses. --- Neurology --- Memory, Long-Term --- Synapses --- Research. --- physiology. --- Brain Stimulation --- Amygdala --- BDNF --- PDE4 --- reconsolidation --- Fear conditioning --- posttraumatic stress disorder --- ubiquitin-proteasome system --- CREB --- extinction --- Sleep --- gamma oscillations

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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.

Research & information: general --- Biology, life sciences --- 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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Ubiquitination is a biological process mediated by ubiquitin itself, the E1 ubiquitin-activating enzyme, E2 ubiquitin-conjugating enzyme, E3 ubiquitin ligase, and deubiquitinating enzyme, respectively. Currently, these multiple biological steps are revealed to participate in various life phenomena, such as cell proliferation, regulation of cell surface proteins expression, and mitochondrial function, which are profoundly related to human health and diseases. Although clinical applications targeting ubiquitination are still limited compared to those directed toward kinase systems such as tyrosine kinases, multiple enzymatic consequences should be future therapeutic implications. This Special Issue of IJMS entitled “Ubiquitination in Health and Disease” successfully published15 distinguished manuscripts, with a total of 66 international authors and. This book provides the latest and most useful information for researchers and scientists in this field.

Humanities --- Social interaction --- deubiquitinase --- degradation --- therapeutic target --- cancer --- hematopoiesis --- hematopoietic stem cells --- immune response --- regulation of gene expression --- ubiquitin system --- genetic diseases --- ubiquitin ligase --- deubiquitinases --- monoubiquitin signaling --- vesicular trafficking --- protein complex formation --- inflammation --- inhibitor --- innate immune --- interferon --- LUBAC --- NF-κB --- ubiquitin --- Parkinson’s disease --- dopa-responsive dystonia --- tyrosine hydroxylase --- α-synuclein --- fatty acid-binding protein 3 --- ubiquitination --- proteasomal degradation --- ubiquitin-proteasome system --- mitochondria --- E3 ubiquitin ligase --- MITOL/MARCH5 --- salt-sensitive hypertension --- Nedd4L/Nedd4-2 --- epithelial sodium channel --- aldosterone sensitive distal nephron --- excitation-transcription coupling --- RNF183 --- RNF186 --- RNF182 --- RNF152 --- RING finger --- mTOR --- endoplasmic reticulum stress --- osmotic stress --- ubiquitin code --- virus infection --- virus-host interaction --- tau protein --- semisynthesis --- disulfide-coupling --- polyubiquitin --- fibrils --- aggregation --- neurodegeneration --- deubiquitination --- inhibitors --- protein quality control --- proteolysis --- protein stabilization --- regulatory T cells --- mesenchymal stem cell --- cortical bone derived stem cell --- myocardial infarction --- blood pressure --- renal salt reabsorption --- vascular function --- ubiquitin proteasome system --- ubiquitin–proteasome pathway --- cilia --- ciliogenesis --- differentiation --- proliferation --- ciliopathy --- E3s --- DUBs --- UPS --- neurodegenerative disease --- immune-related diseases

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Ubiquitination is a biological process mediated by ubiquitin itself, the E1 ubiquitin-activating enzyme, E2 ubiquitin-conjugating enzyme, E3 ubiquitin ligase, and deubiquitinating enzyme, respectively. Currently, these multiple biological steps are revealed to participate in various life phenomena, such as cell proliferation, regulation of cell surface proteins expression, and mitochondrial function, which are profoundly related to human health and diseases. Although clinical applications targeting ubiquitination are still limited compared to those directed toward kinase systems such as tyrosine kinases, multiple enzymatic consequences should be future therapeutic implications. This Special Issue of IJMS entitled “Ubiquitination in Health and Disease” successfully published15 distinguished manuscripts, with a total of 66 international authors and. This book provides the latest and most useful information for researchers and scientists in this field.

deubiquitinase --- degradation --- therapeutic target --- cancer --- hematopoiesis --- hematopoietic stem cells --- immune response --- regulation of gene expression --- ubiquitin system --- genetic diseases --- ubiquitin ligase --- deubiquitinases --- monoubiquitin signaling --- vesicular trafficking --- protein complex formation --- inflammation --- inhibitor --- innate immune --- interferon --- LUBAC --- NF-κB --- ubiquitin --- Parkinson’s disease --- dopa-responsive dystonia --- tyrosine hydroxylase --- α-synuclein --- fatty acid-binding protein 3 --- ubiquitination --- proteasomal degradation --- ubiquitin-proteasome system --- mitochondria --- E3 ubiquitin ligase --- MITOL/MARCH5 --- salt-sensitive hypertension --- Nedd4L/Nedd4-2 --- epithelial sodium channel --- aldosterone sensitive distal nephron --- excitation-transcription coupling --- RNF183 --- RNF186 --- RNF182 --- RNF152 --- RING finger --- mTOR --- endoplasmic reticulum stress --- osmotic stress --- ubiquitin code --- virus infection --- virus-host interaction --- tau protein --- semisynthesis --- disulfide-coupling --- polyubiquitin --- fibrils --- aggregation --- neurodegeneration --- deubiquitination --- inhibitors --- protein quality control --- proteolysis --- protein stabilization --- regulatory T cells --- mesenchymal stem cell --- cortical bone derived stem cell --- myocardial infarction --- blood pressure --- renal salt reabsorption --- vascular function --- ubiquitin proteasome system --- ubiquitin–proteasome pathway --- cilia --- ciliogenesis --- differentiation --- proliferation --- ciliopathy --- E3s --- DUBs --- UPS --- neurodegenerative disease --- immune-related diseases

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Dear Readers, Understanding the pathological mechanisms involved in human diseases and their possible treatment has been historically based on comparative analysis of diverse animal species that share a similar genetic, physiological and behavioural composition. The ancient Greeks were the first to use animals as models for anatomy and physiology, and this was consequently adopted by other cultures and led to important discoveries. In recent years, there have been many efforts to understand and fight cancer through new revolutionary personalized treatments and wider screenings that help diagnose and treat cancer. A fundamental part of this effort is to develop suitable cancer animal models that simulate the different disease variants and their progression. Ranging from tumor-derived xenografts to genetically engineered models, a wide variety of systems are applied for this purpose, and many technological breakthroughs are changing the way cancer is studied and analyzed. In this Special Issue, we collected a set of research articles and reviews that focus on the generation of cancer animal models that are used for understanding the disease and contribute to designing and testing new drugs for cancer prevention or treatment. Vladimir Korinek Collection Editor

soy --- isoflavones --- mammary tumor prevention --- rodent models --- chemical carcinogens --- transgenic mice --- Zebrafish --- Drosophila --- rats --- mice --- NPM-1 --- FLT3 ITD --- ETO-1 --- IDH1/2 --- neural stem cells --- brain and nervous system cancers --- neurogenic niches --- radiotherapy --- sparing of neurogenic regions --- carcinoma --- consensus molecular subtypes --- intestine --- oncogenes --- signaling cascades --- tumor suppressors --- tumorigenesis --- MPN (myeloproliferative neoplasms) --- zebrafish --- iPSCs --- JAK2 --- MPL --- CALR --- thrombosis --- ubiquitin–proteasome system --- cancer --- mouse model --- gene inactivation --- colorectal cancer --- mouse models --- microbiota --- antitumor immunity --- melanoma --- mutation --- genetics --- animal model --- swine --- MeLiM --- progression --- spontaneous regression --- devitalization --- metaplasia --- Cdx --- animal models --- epigenetics --- xenotransplantation --- drug screen --- pre-clinical cancer model --- non-mouse models --- gene editing --- stem cells --- solid tumors --- hematologic malignancies