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Unfolded protein response (UPR) is a cellular adaptive response for restoring endoplasmic reticulum (ER) homeostasis in response to ER stress. Perturbation of the UPR and failure to restore ER homeostasis inevitably leads to diseases. It has now become evident that perturbation of the UPR is the cause of many important human diseases such as neurodegenerative diseases, cystic fibrosis, diabetes and cancer. It has recently emerged that virus infections can trigger the UPR but the relationship between virus infections and host UPR is intriguing. On one hand, UPR is harmful to the virus and virus has developed means to subvert the UPR. On the other hand, virus exploits the host UPR to assist in its own infection, gene expression, establishment of persistence, reactivation from latency and to evade the immune response. When this delicate balance of virus-host UPR interaction is broken down, it may cause diseases. This is particularly challenging for viruses that establish a chronic infection to maintain this balance. Each virus interacts with the host UPR in a different way to suit their life style and how the virus interacts with the host UPR can define the characteristic of a particular virus infection. Understanding how a particular virus interacts with the host UPR may pave the way to the design of a new class of anti-viral that targets this particular pathway to skew the response towards anti-virus. This knowledge can also be translated into the clinics to help re-design oncolytic virotherapy and gene therapy. In this research topic we aimed to compile a collection of focused review articles, original research articles, commentary, opinion, hypothesis and methods to highlight the current advances in this burgeoning area of research, in an attempt to provide an in-depth understanding of how viruses interact with the host UPR, which may be beneficial to the future combat of viral and human diseases.
Virus diseases. --- Viruses. --- ERAD --- virus-host interaction --- innate immunity --- Gene Therapy --- Pathogenesis --- Endoplasmic Reticulum Stress --- Unfolded Protein Response --- Autophagy
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The endoplasmic reticulum (ER) is an organelle crucial to many cellular functions and processes, including the mounting of T-cell immune responses. Indeed, the ER has a well-established central role in anti-tumor immunity. Perhaps best characterized is the role of the ER in the processing of antigen peptides and the subsequent peptide assembly into MHC class I and II molecules. Such MHC/tumor-derived peptide complexes are pivotal for the correct recognition of altered self or viral peptides and the subsequent clonal expansion of tumor-reactive T-cells. In line with the role of the ER in immunity, tumor-associated mutations in ER proteins, as well as ER protein content and localization can have both deleterious and advantageous effects on anti-tumor immune responses. For instance, loss of function of ER-aminopeptidases, that trim peptides to size for MHC, alter the MHC class I - peptide repertoire thereby critically and negatively affecting T-cell recognition. On the other hand, altered localization of ER proteins can have immune-promoting effects. Specifically, translocation of certain ER proteins to the cell surface has been shown to promote anti-tumor T-cell immunity by directing uptake of apoptotic tumor cells to professional antigen presenting cells, thereby facilitating anti-tumor T-cell immunity. These selected examples highlight a diverse and multi-faceted role of the ER in anti-tumor immunity. Molecular biological insights from the past decade have uncovered that ER components may affect tumor immunity and have invoked a variety of follow-up questions. For instance, how and why are ER proteins over-expressed in tumors? How do nucleotide and somatic mutations in ER chaperones/processing machinery affect the MHC/peptide complex and tumor cell immunogenicity? How do ER-proteins translocate to the cell surface? What if any is the potential role of extracellular ER protein in tumor immunotherapy/vaccines, and can they be delivered to the tumor cell surface by photodynamic therapy, anthracyclines or by other means? In this special research topics issue, we welcome basic and clinical research reports covering all aspects of ER proteins in cancer recognition by the immune system, therapy and drug development. We also welcome reports describing new insights into ER stress, signalling and homeostasis in immunogenic cell death in cancer, the effect of parasitic ER proteins on tumour growth, ER protein regulation of angiogenesis. Submission of original research articles, perspective, reviews and topical comments is encouraged. We aim to provide a comprehensive series of articles that will aid our understanding in a new and exiting avenue of tumour immunology and therapeutic development, exploiting a collection of proteins within the ER that are not obvious candidates for immunity to tumors.
Endoplasmic reticulum. --- Tumors --- Immunology. --- Oncology. --- Endoplasmic Reticulum Stress. --- Immunological aspects. --- Autoimmunity --- Angiogenesis --- T-cell receptors --- genome damage --- phage display --- Aminopeptidases --- Grp170 --- Oxidoreductases --- Vaccines --- chaperones
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The endoplasmic reticulum (ER) is a manufacturing unit in eukaryotic cells required for the synthesis of proteins, lipids, metabolites and hormones. Besides supporting cellular signalling networks by its anabolic function, the ER on its own or in communication with other organelles directly initiates signalling processes of physiological significance. Based on the intimate and immediate involvement in stress signalling the ER is considered as sensory organelle on which cells strongly rely to effectively translate environmental cues into adaptive stress responses. The transcellular distribution of the ER providing comprehensive cell-to-cell connections in multicellular organisms probably allows a concerted action of cell alliances and tissue areas towards environmental constraints. At the cellular level, stress adaptation correlates with the capability of the ER machinery to synthesise proteins participating in stress signalling as well as in the activation of ER membrane localised proteins to start cell-protective signalling processes. Importantly, depending on the stress insult, the ER either supports protective strategies or initiates cell death programmes. Recent, genetic, molecular and cell biological studies have drawn an initial picture of underlying signalling events activated by ER membrane localised proteins. In this Research Topic, we will provide a platform for articles describing research on ER morphology and metabolism with a focus on stress translation. The Research Topic will be sub-divided into the following sections: 1. ER in stress signalling and adaptation; 2. ER structure and biosynthetic functions; 3. Regulation of protein processing; 4. Regulation of programmed cell death.
Endoplasmic reticulum. --- Botany. --- Endoplasmic Reticulum Stress. --- Stress, Endoplasmic Reticulum --- Endoplasmic Reticulum Stresses --- Reticulum Stress, Endoplasmic --- Reticulum Stresses, Endoplasmic --- Stresses, Endoplasmic Reticulum --- Unfolded Protein Response --- Endoplasmic Reticulum-Associated Degradation --- Botanical science --- Floristic botany --- Phytobiology --- Phytography --- Phytology --- Plant biology --- Plant science --- Biology --- Natural history --- Plants --- Cell organelles --- Myosins --- cysteine endopeptidase --- ER associated degradation --- ER bodies --- programmed cell death --- bZIP transcription factors --- caspase
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The Special Issue “Marine Anti-Inflammatory and Antioxidants Agents 2021” collected the latest research, both in vitro and in vivo, on natural compounds from a variety of deep-sea organisms with anti-inflammatory and/or antioxidant properties as potential candidates for new drug discovery, and more generally for the field of marine biotechnology. The research presented here discusses the potential benefits of certain peptides and proteins derived from oysters, blue mussels, and cyanobacteria, as well as the carotenoid pigment astaxanthin, which is found in a variety of marine organisms. This Special Issue has carved out an important space for crude extracts from marine products, such as microalgae and green algae, highlighting their potential benefits to human health. Finally, the Special Issue includes a review of the benefits of some natural compounds derived from the algal biome against inflammatory bowel diseases, as well as a research article identifying the presence of the OvoA gene in arthropods for the first time. Through an excursus of high-quality research, this Special Issue provides the entire scientific community with new tools and insights to catch a molecular treasure for human health from the sea.
algal biome --- polysaccharides --- bioactive entities --- engineered cues --- therapeutic attributes --- inflammatory bowel disease --- microalgae --- Tisochrysis lutea --- fucoxanthin --- inflammation --- RAW 264.7 --- microRNA --- astaxanthin --- dendritic cells --- sepsis --- immune dysfunction --- lipopolysaccharide --- oxidative stress --- Ulva lactuca --- polysaccharide --- D-galactose --- kidney --- oyster peptides --- spermatogenesis --- apoptosis --- hormone --- testis --- C-phycoerythrin --- Phormidium persicinum --- acute kidney injury --- mercury --- endoplasmic reticulum stress --- bioactive peptide --- cytoprotective --- endothelial dysfunction --- blue mussel --- acute liver injury --- ferroptosis --- oyster --- peptide --- pyroptosis --- zooplankton --- natural products --- antioxidant --- transcriptome mining --- n/a
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This book provides a resource for the scientist or medical professional interested in the topic of insulin resistance. With a mix of review and primary data articles, emerging paradigms in insulin resistance are highlighted. The topics are succinctly presented, and distinct viewpoints are represented. An introduction to the Special Issue that provides summaries of the studies included, is provided by the Guest Editor, Dr. Susan Burke, and her colleague at the Pennington Biomedical Research Center, Dr. Jason Collier.
Research & information: general --- Biology, life sciences --- epicardial adipose tissue --- hypertrophy of adipocytes --- CAD severity --- adipokines --- insulin resistance --- insulin-degrading enzyme --- pancreas --- liver --- insulin receptor --- glucose transporters --- acute intermittent porphyria --- carbohydrate loading therapy --- hyperinsulinemia --- fast-acting insulin --- experimental liver-targeted insulin --- hyperinsulinaemia --- osteocalcin --- beta-hydroxybutyrate --- phenotype --- stages --- serotonin --- glucagon-like peptide-1 --- glucagon --- type 2 diabetes --- hyperglycaemia --- apoptosis --- endoplasmic reticulum stress --- glucosamine --- pancreatic β-cell dysfunction --- ovariectomy --- raloxifene --- Negr1 --- obesity --- metabolic disease --- metabolomics --- glucose intolerance --- genetic models --- beta hydroxybutyrate --- osteoporosis --- fragility fractures --- bone mineral density --- osteocalin --- vitamin D --- collagen --- hydroxyapatite --- diabetes --- inflammation --- thiazolidinedione --- n/a
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ROS were long considered one of the key players in tissue injury. Indeed, overproduction of ROS results in oxidative stress, a process leading to the development of many pathological conditions. For the treatment of these conditions, the use of antioxidants was proposed. Over time, it was shown that ROS at low concentrations act as signaling molecules, leading to the regulation of physiological functions. Moreover, several interventions that increase ROS generation activate stress-adaptive responses that extend the lifespan. It was also shown that excessive use of antioxidants can counter the beneficial effects of ROS. Currently, much progress has been made in understanding the role of ROS in human diseases and aging, as well as in the regulation of physiological functions, and in identifying the signaling pathways involved in ROS. However, much remains to be understood about the mutual interactions among signaling pathways underlying organisms’ adaptive responses, their modifications (which occur during aging), and some disease states. The aim of this Special Issue is to underline the effects of ROS production and antioxidant treatment in living organisms, focusing on their impact on health, disease, and aging.
CTCL --- apoptosis --- cell viability --- c-FLIP --- XIAP --- artemisinin --- SH-SY5Y cells --- hippocampal neurons --- H2O2 --- AMPK pathway --- atherosclerosis --- sphingomyelin synthase 2 --- endothelial dysfunction --- endoplasmic reticulum stress --- β-catenin --- insulin resistance --- cancer --- cardiovascular disease --- neurodegenerative disorders --- exercise --- mitochondria --- oxidative stress --- PGC-1 --- Nrf2 --- UCPs --- ROS --- light --- DNA damage --- evolution --- D-box --- cavefish --- Spalax --- trimethylamine N-oxide --- cardiomyocytes --- cardiotoxicity --- mitochondrial membrane potential --- CORM-2 --- NADPH oxidase --- AP-1 --- HO-1 --- Renal cell carcinoma (RCC) --- reactive oxygen species (ROS) --- glutathione (GSH) metabolism --- cancer therapy --- clear cell RCC --- papillary RCC --- chromophobe RCC --- sarcopenia --- reactive oxygen species --- redox signaling --- antioxidant supplementation --- protein aggregation --- redox --- proteinopathy --- peroxiredoxins --- tumorigenesis --- ROS scavengers --- n/a
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The book “Protective and Detrimental Role of Heme Oxygenase-1”, includes a selection of original research papers and reviews aimed at understanding the dual role (protective and detrimental) of HO-1 and the involved signaling pathways. Original research papers and reviews aimed at the identification of natural molecules or new synthetic compounds able to modulate HO-1 activity/expression help make HO-1 a potential therapeutic target for the amelioration of various diseases.
coronary artery disease --- n/a --- glucocorticoid receptor --- antigen presentation --- analgesia --- chemotherapy --- locus coeruleus --- Sirtuin 1 --- thiol groups --- Heme Oxygenase-1 --- Betula etnensis Raf. --- heme oxygenase 1 --- tolerance --- heme oxygenase --- atherosclerosis --- nitric oxide --- caloric restriction --- liver --- carbon monoxide --- ER stress --- heme oxygenase-1 --- mineralocorticoid receptor --- Type 1 diabetes mellitus (T1D) --- Gamma-Glutamyl-Cysteine Ligase (GGCL) --- angiotensin II --- bilirubin --- Heme oxygenase-1 (HO-1) inducers --- Inducible nitric oxide synthase (iNOS) --- HO-1 activity inhibitor --- ferroptosis --- Myristica fragrans kernels --- glutathione --- high-pressure gas --- apoptosis --- HO-1 --- diabetes mellitus --- Caffeic acid phenethyl ester (CAPE) --- carotid plaque --- ischemia–reperfusion injury --- ANTIGEN presenting cell --- LPS --- endoplasmic reticulum stress --- hemoglobin --- Pancreatic oxidative damage --- Colon cancer --- inflammation --- reactive oxygen species --- inflammatory pain --- paracetamol --- cardiomyopathy --- heme oxigenase-1 --- adipocytes --- sirtuin 1 --- peripheral artery disease --- PGC-1? --- heme --- Reactive oxygen species (ROS) --- metformin --- GR --- prostate cancer --- NF-?B --- hyperbilirubinemia --- iron --- Tet-ON system --- lung preservation --- oxidative stress --- Gunn rats --- Dimethylarginine dimethylaminohydrolase-1 (DDAH-1) --- ischemia-reperfusion injury
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Blindness and visual impairment impact significantly on an individual’s physical and mental well-being. Loss of vision is a global health problem, with approximately 250 million of the world’s population currently living with vision loss, of which 36 million are classified as blind. Visual impairment is more frequent in the elderly, with cataract and age-related macular degeneration (AMD) accounting for over 50% of cases globally. Oxidative stress has been strongly implicated in the pathogenesis of both conditions, and consequently the role of nutritional factors, in particular carotenoids and micronutrient antioxidants, have been investigated as possible preventative or therapeutic strategies. Dry eye syndrome (DES) is one of the most common ophthalmic conditions in the world. DES occurs where the eye does not produce enough tears and/or the tears evaporate too quicklyleading to discomfort and varying degrees of visual disturbance. There has recently been a great deal of interest in the potential for oral or topical supplementation with essential fatty acids (EFAs), specifically omega-3 and omega-6 fatty acids, as an adjunct to conventional treatments for DES. The objective of this Special Issue on ‘Nutrition and Eye Health’ is to publish papers describing the role of nutrition in maintaining eye health and the use of nutritional interventions to prevent or treat ocular disease. A particular (but not exclusive) emphasis will be on papers (reviews and/or clinical or experimental studies) relating to cataract, AMD and DES.
polyphenols --- n/a --- crocin --- chyrsin --- glaucoma --- dietary assessment --- photoreceptor degeneration --- dry eye --- RR-zeaxanthin --- nutritional supplements --- drug discovery --- corneal neovascularization (CNV) --- AMD --- dietary antioxidants --- micronutrients --- age-related macular degeneration --- preclinical models --- lenses --- microvascular lesions --- cyclooxigenase-2 (COX-2) --- angiogenesis --- fish oil --- macrophage --- anti-oxidant --- vascular endothelial growth factor (VEGF) --- rosmarinic acid --- visual cycle --- diabetic retinopathy --- lutein --- gut-retina axis --- light damage --- crocetin --- supplements --- clinical practice guidelines --- nutrition --- light --- eye disease --- dietary habits --- flavonoids --- phytoconstituents --- saffron --- carotenoids --- fatty acid --- electroretinography --- lens --- advanced glycation end products --- interleukin-1? (IL-1?) --- mesozeaxanthin (RS zeaxanthin) --- endoplasmic reticulum stress --- omega-3 polyunsaturated fatty acids --- clinical survey --- corneal chemical burn --- reduced glutathione --- omega-3 --- AGREE II --- retina --- inflammation --- anti-inflammatory --- retinal pigment epithelium --- diet --- Lactobacillus paracasei KW3110 --- Crocus Sativus L. --- saponins --- cataract --- CODS --- neoangiogenesis --- estrogen-deficient rats --- food frequency questionnaire --- gut microbiota --- antioxidant supplements --- sinapic acid --- personalised medicine --- systematic reviews --- nuclear factor-kappaB (NF-?B) --- diabetes --- Cucurbita argyrosperma --- oxidative stress --- endoplasmic reticulum
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Dear Colleagues, A rare disease, also known as an orphan disease, is any disease that affects a small percentage of the population. Although definitions vary from continent to continent, according to the European Union, rare diseases are those with a prevalence of less than 1 in 2000 people. Rare diseases are, in general, chronic, debilitating diseases, which in many cases threaten patients’ lives. It is estimated that 1–2 million people in the European Union are affected by a rare respiratory disease, which is a public health problem. Due to the low prevalence and severity of many of these diseases, whose symptoms often initially manifest in childhood, combined efforts are needed to improve our knowledge of the pathophysiology of these diseases that will lead to the development of new, more effective treatments. Therefore, since rare respiratory diseases represent an important field in medicine, we propose this Special Issue to promote the dissemination of the latest advances in basic and clinical research in these diseases. Prof. Dr. Francisco Dasí Guest Editor
standard diagnosis --- reference centres --- clinical presentation --- cilia --- primary ciliary dyskinesia --- alpha-1 antitrypsin deficiency --- rare respiratory diseases --- Mycobacterium avium --- Mycobacterium intracellulare --- nodular bronchiectasis --- non-tuberculous mycobacteria --- pulmonary aspergillosis --- rare pulmonary disease --- miRNA expression --- exhaled breath condensate --- sputum --- severity --- pulmonary exacerbation --- alpha1 antitrypsin deficiency --- augmentation therapy --- replacement therapy --- rare diseases --- gene therapy --- alpha-1-antitrypsin deficit --- cystic fibrosis --- neonatal respiratory distress --- laterality defect --- orphan diseases --- PCD --- immunofluorescence --- antibody --- ALI culture --- bio-resource --- primary nasal epithelium --- diagnostics --- Alpha-1 antitrypsin deficiency --- liver disease --- glutamate-oxaloacetate transaminase --- glutamate-pyruvate transaminase --- gamma-glutamyl transpeptidase --- resilience --- active lifestyle --- stress levels --- infection control measure --- self-quarantine --- flow cytometry --- nasal epithelium --- oxidative stress --- reactive oxygen species --- endoplasmic reticulum stress --- antioxidant therapies --- idiopathic pulmonary fibrosis --- chronic obstructive pulmonary disease --- bronchiectasis --- asthma --- emphysema --- alpha1-antitrypsin deficiency --- transient elastography --- n/a
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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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