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In contrast to the situation in heterotrophic organisms, plant genomes code for a significantly larger number of oxidoreductases such as thioredoxins (TRXs) and glutaredoxins (GRXs). These proteins provide a biochemical mechanism that allows the rapid and reversible activation or deactivation of protein functions in response to changing environmental conditions, as oxidative conditions caused by excessive photosynthesis. Indeed, owing to the fact that cysteines are sensitive to oxidation, TRXs and GRXs play an essential role in controlling the redox state of protein thiol groups. These redox-dependent post-translational modifications have proven to be critical for many cellular functions constituting regulatory, signalling or protective mechanisms. The articles contained in this Research Topic provide timely overviews and new insights into thiol-dependent redox regulation mechanisms with a focus on TRX- and GRX-based reduction systems in plants. The different contexts discussed take into account physiological, developmental and environmental conditions.
Homeostasis. --- Thioredoxin. --- Botany. --- redox signaling --- redox regulation --- thioredoxin --- Plants --- glutaredoxin --- Glutathione
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This volume of Methods in Enzymology is a companion to Volume 347 and addresses direct sensing of reactive oxygen species and related free radicals by thiol enzymes and proteins.
Proteins. --- Active oxygen --- Enzymes --- Proteins --- Active oxygen. --- Oxidation-reduction reaction. --- Thioredoxin. --- Thiols.
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Bacterial Proteins --- Thioredoxins --- Mycobacterium tuberculosis --- Thioredoxin-Disulfide Reductase --- Genes, Bacterial --- Genome, Bacterial --- analysis --- genetics
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This Special Issue features recent data concerning thioredoxins and glutaredoxins from various biological systems, including bacteria, mammals, and plants. Four of the sixteen articles are review papers that deal with the regulation of development of the effect of hydrogen peroxide and the interactions between oxidants and reductants, the description of methionine sulfoxide reductases, detoxification enzymes that require thioredoxin or glutaredoxin, and the response of plants to cold stress, respectively. This is followed by eleven research articles that focus on a reductant of thioredoxin in bacteria, a thioredoxin reductase, and a variety of plant and bacterial thioredoxins, including the m, f, o, and h isoforms and their targets. Various parameters are studied, including genetic, structural, and physiological properties of these systems. The redox regulation of monodehydroascorbate reductase, aminolevulinic acid dehydratase, and cytosolic isocitrate dehydrogenase could have very important consequences in plant metabolism. Also, the properties of the mitochondrial o-type thioredoxins and their unexpected capacity to bind iron–sulfur center (ISC) structures open new developments concerning the redox mitochondrial function and possibly ISC assembly in mitochondria. The final paper discusses interesting biotechnological applications of thioredoxin for breadmaking.
n/a --- regeneration --- posttranslational modification --- H2O2 --- chilling stress --- thioredoxin reductase --- X-ray crystallography --- photosynthesis --- Chlamydomonas reinhardtii --- protein --- monodehydroascorbate reductase --- methionine sulfoxide --- cysteine reactivity --- symbiosis --- plant --- MALDI-TOF mass spectrometry --- thioredoxins --- redox homeostasis --- methionine sulfoxide reductases --- redox --- redox signalling --- chloroplast --- protein-protein recognition --- cyanobacteria --- specificity --- wheat --- methanoarchaea --- stress --- redox regulation --- dough rheology --- methionine sulfoxide reductase --- electrostatic surface --- Calvin cycle --- ALAD --- metazoan --- Arabidopsis thaliana --- baking --- cold temperature --- macromolecular crystallography --- protein oxidation --- function --- methionine oxidation --- development --- iron–sulfur cluster --- tetrapyrrole biosynthesis --- legume plant --- glutathionylation --- Calvin-Benson cycle --- adult stem cells --- carbon fixation --- plastidial --- methionine --- redox active site --- ROS --- water stress --- NADPH --- repair --- physiological function --- signaling --- thioredoxin --- antioxidants --- glutathione --- glutaredoxin --- flavin --- Isocitrate dehydrogenase --- thiol redox network --- ageing --- disulfide --- mitochondria --- chlorophyll --- proteomic --- cysteine alkylation --- ferredoxin-thioredoxin reductase --- SAXS --- regulation --- oxidized protein repair --- ascorbate --- redox control --- nitrosylation --- iron-sulfur cluster
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The peroxiredoxin family was discovered approximately 30 years ago and is now recognized as one of the most important families of enzymes related to antioxidant defense and cellular signaling. Peroxiredoxin 6 shares the basic enzymatic functions that characterize this family, but also exhibits several unique and crucial activities. These include the ability to reduce phospholipid hydroperoxides, phospholipase A2 activity, and an acyl transferase activity that is important in phospholipid remodeling. This book describes the available models for investigating the unique functions of PRDX6 and its role in normal physiological function, as well its roles in the pathophysiology of diseases including cancer, diseases of the eye, and male fertility.
n/a --- NADPH (nicotinamide adenine dinucleotide phosphate) oxidase --- sperm capacitation --- phospholipid hydroperoxide --- cornea --- peroxidase --- phospholipase A2 --- 1-Cys Prdx --- knock-in mouse --- drug delivery --- antioxidant activity --- sulfinic acid --- radioprotection --- spermatozoa --- peroxiredoxin 6 --- mass spectroscopic analysis --- knockout mouse --- phospholipase A2 activity --- liposomes --- mitochondrial membrane potential --- lipid peroxidation --- PLA2 activity --- ionizing radiation --- glutathione peroxidase --- Peroxiredoxin --- Prdx6 structure --- membrane repair --- substrate binding --- inflammation --- reactive oxygen species --- Prdx6 --- sulfonic/sulfinic acid --- Fuchs’ endothelial corneal dystrophy --- endothelium --- fertilization --- peroxidatic cysteine --- thioredoxin fold --- redox balance --- surfactant protein A --- diabetes --- oxidative stress --- Fuchs' endothelial corneal dystrophy
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This Special Issue examines state-of-the-art in-cell NMR spectroscopy as it relates to biological systems of increasing complexity. The compendia of research and recent innovations from prominent laboratories in the field of solid state and solution in-cell NMR spectroscopy, metabolomics and technology development are presented. The work establishes in-cell NMR spectroscopy as the premier method for determining the structures and interaction capabilities of biological molecules at high resolution within the delicately intricate interior of living cells, and the means of utilizing cells as living laboratories to directly assess the effects of exogenous and endogenous stimuli on cell physiology.]
protein NMR --- time-resolved NMR --- Ribosome --- structural calculation 4 --- crystalline and amorphous starch --- in-cell NMR --- protein dynamics --- DNP --- protein modification --- Tau --- spectrum reconstruction 3 --- mRNA --- Thioredoxin --- protein structure --- protein interactions --- drug discovery --- protein structure determination 1 --- review --- enzyme activity --- MARK2 phosphorylation --- post-translational modifications --- Dihydrofolate reductase --- mammalian cells --- target engagement --- non-uniform sampling 2 --- paramagnetic effects --- protein structure-function --- cross-correlated relaxation --- structure function --- rRNA --- 2D INADEQUATE --- lipid membrane --- Thymidylate synthase --- whole cell NMR --- enzyme kinetics --- magic-angle spinning --- live cell --- solid-state NMR --- Adenylate kinase --- DNA --- in-situ NMR --- antimicrobial peptide --- NMR spectroscopy --- intrinsically disordered proteins
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The trace mineral selenium is still regarded as one of the most interesting and health-beneficial elements. In addition to the Editorial containing a dedication to Dr. Leopold Flohé, this Special Issue contains 13 research articles and 8 reviews, with over 120 different contributors covering many of the most important subjects concerning the study of selenium. The articles address both selenium as well as selenoproteins and their molecular roles, providing important considerations regarding this trace element’s impact on human and animal health and disease.
Research & information: general --- Biology, life sciences --- selenoproteome --- selenoprotein hierarchy --- nonradioactive isotopes --- SEC-ICP MS --- glutathione peroxidase --- thioredoxin reductase --- SECIS --- translation regulation --- autoimmune thyroid disease --- diabetes mellitus --- Graves' disease --- Hashimoto thyroiditis --- infection --- inflammation --- long-COVID --- rheumatoid arthritis --- selenoprotein P --- sepsis --- selenoprotein W --- thioredoxin --- 14-3-3 --- Akt --- cell death --- Selenof --- selenium --- selenoprotein --- colon cancer --- barrier integrity --- cardiovascular --- heart --- selenoproteins --- Keshan's Disease --- bacteria --- selenite --- selenium delivery system --- Trsp --- hypothalamus --- Agrp neuron --- sex differences --- diet-induced obesity --- leptin resistance --- macrophage --- differentiation --- redox signaling --- NRF2 --- NF-κB --- lipid mediators --- seleocysteine --- autoimmunity --- lymphocyte --- cadmium cytotoxicity --- cancer therapy --- cisplatin --- ICP-MS --- nonsynonymous mutation --- selenium homeostasis --- ZIP8 --- Trit1 --- isopentenylation --- tRNA[Ser]Sec --- selenocysteine --- genetic variance --- human disease --- selenophosphate synthetase --- endothelial cell --- reactive oxygen species --- cell growth --- angiogenesis --- SEPHS1 --- early embryogenesis --- embryonic lethality --- prostate --- cancer --- tumor suppressor --- selenoprotein deficiency --- SECISBP2 --- Sec-tRNA[Ser]Sec --- SEPSECS --- antioxidative defense --- autoantibody --- Hashimoto's thyroiditis --- trace element --- recoding --- SECIS-binding protein --- translation termination --- nonsense-mediated decay --- ribosome rescue --- health --- mouse models --- selenocysteine (Sec) --- virus --- viral --- antioxidant --- HIV --- HCV --- HBV --- coxsackie virus --- influenza --- HIV-1 --- viral infection --- SELENOS --- SELENOO --- primary T cells --- Jurkat --- SupT1 --- translational control --- selenoproteome --- selenoprotein hierarchy --- nonradioactive isotopes --- SEC-ICP MS --- glutathione peroxidase --- thioredoxin reductase --- SECIS --- translation regulation --- autoimmune thyroid disease --- diabetes mellitus --- Graves' disease --- Hashimoto thyroiditis --- infection --- inflammation --- long-COVID --- rheumatoid arthritis --- selenoprotein P --- sepsis --- selenoprotein W --- thioredoxin --- 14-3-3 --- Akt --- cell death --- Selenof --- selenium --- selenoprotein --- colon cancer --- barrier integrity --- cardiovascular --- heart --- selenoproteins --- Keshan's Disease --- bacteria --- selenite --- selenium delivery system --- Trsp --- hypothalamus --- Agrp neuron --- sex differences --- diet-induced obesity --- leptin resistance --- macrophage --- differentiation --- redox signaling --- NRF2 --- NF-κB --- lipid mediators --- seleocysteine --- autoimmunity --- lymphocyte --- cadmium cytotoxicity --- cancer therapy --- cisplatin --- ICP-MS --- nonsynonymous mutation --- selenium homeostasis --- ZIP8 --- Trit1 --- isopentenylation --- tRNA[Ser]Sec --- selenocysteine --- genetic variance --- human disease --- selenophosphate synthetase --- endothelial cell --- reactive oxygen species --- cell growth --- angiogenesis --- SEPHS1 --- early embryogenesis --- embryonic lethality --- prostate --- cancer --- tumor suppressor --- selenoprotein deficiency --- SECISBP2 --- Sec-tRNA[Ser]Sec --- SEPSECS --- antioxidative defense --- autoantibody --- Hashimoto's thyroiditis --- trace element --- recoding --- SECIS-binding protein --- translation termination --- nonsense-mediated decay --- ribosome rescue --- health --- mouse models --- selenocysteine (Sec) --- virus --- viral --- antioxidant --- HIV --- HCV --- HBV --- coxsackie virus --- influenza --- HIV-1 --- viral infection --- SELENOS --- SELENOO --- primary T cells --- Jurkat --- SupT1 --- translational control
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The trace mineral selenium is still regarded as one of the most interesting and health-beneficial elements. In addition to the Editorial containing a dedication to Dr. Leopold Flohé, this Special Issue contains 13 research articles and 8 reviews, with over 120 different contributors covering many of the most important subjects concerning the study of selenium. The articles address both selenium as well as selenoproteins and their molecular roles, providing important considerations regarding this trace element’s impact on human and animal health and disease.
selenoproteome --- selenoprotein hierarchy --- nonradioactive isotopes --- SEC-ICP MS --- glutathione peroxidase --- thioredoxin reductase --- SECIS --- translation regulation --- autoimmune thyroid disease --- diabetes mellitus --- Graves’ disease --- Hashimoto thyroiditis --- infection --- inflammation --- long-COVID --- rheumatoid arthritis --- selenoprotein P --- sepsis --- selenoprotein W --- thioredoxin --- 14-3-3 --- Akt --- cell death --- Selenof --- selenium --- selenoprotein --- colon cancer --- barrier integrity --- cardiovascular --- heart --- selenoproteins --- Keshan’s Disease --- bacteria --- selenite --- selenium delivery system --- Trsp --- hypothalamus --- Agrp neuron --- sex differences --- diet-induced obesity --- leptin resistance --- macrophage --- differentiation --- redox signaling --- NRF2 --- NF-κB --- lipid mediators --- seleocysteine --- autoimmunity --- lymphocyte --- cadmium cytotoxicity --- cancer therapy --- cisplatin --- ICP-MS --- nonsynonymous mutation --- selenium homeostasis --- ZIP8 --- Trit1 --- isopentenylation --- tRNA[Ser]Sec --- selenocysteine --- genetic variance --- human disease --- selenophosphate synthetase --- endothelial cell --- reactive oxygen species --- cell growth --- angiogenesis --- SEPHS1 --- early embryogenesis --- embryonic lethality --- prostate --- cancer --- tumor suppressor --- selenoprotein deficiency --- SECISBP2 --- Sec-tRNA[Ser]Sec --- SEPSECS --- antioxidative defense --- autoantibody --- Hashimoto’s thyroiditis --- trace element --- recoding --- SECIS-binding protein --- translation termination --- nonsense-mediated decay --- ribosome rescue --- health --- mouse models --- selenocysteine (Sec) --- virus --- viral --- antioxidant --- HIV --- HCV --- HBV --- coxsackie virus --- influenza --- n/a --- HIV-1 --- viral infection --- SELENOS --- SELENOO --- primary T cells --- Jurkat --- SupT1 --- translational control --- Graves' disease --- Keshan's Disease --- Hashimoto's thyroiditis
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The combination of an increasing prevalence of diabetes and the aging of populations enables the appearance of a greater number of associated complications such as diabetic retinopathy. Diabetic retinopathy is the leading cause of preventable vision loss in working-age adults. The objective of this Special Issue is to highlight the existing evidence regarding the relationship between oxidative stress and low-grade chronic inflammation induced by hyperglycemia with the development and progression of diabetic retinopathy, with an emphasis on the importance of early diagnosis and the use of antioxidant and anti-inflammatory approaches to prevent or delay the harmful effects of diabetes on retinal tissue.
Medicine --- eicosanoids --- oxidative stress --- diabetic retinopathy --- cyclooxygenase --- lipoxygenase --- Cytochrome P450 --- HDAC6 --- tubastatin A --- retinal endothelial cells --- retinal endothelial cell senescence --- db/db mice --- Cinnamomi Ramulus --- Paeoniae Radix --- CPA4-1 --- blood-retinal barrier --- occludin --- human retina --- epiretinal membrane --- internal limiting membrane --- vitreoretinal surgery --- macular hole --- proliferative diabetic retinopathy --- antioxidants --- diabetes mellitus --- free radicals --- high-mobility group box 1 (HMGB1) --- inflammatory pathways --- novel therapies --- diabetic retinopathy (DR) --- inflammation --- angiogenesis --- extracellular vesicles --- miRNA --- biomarkers --- apoptosis --- fenofibrate --- thioredoxin --- hyperglycemia --- astaxanthin --- carotenoid --- reactive oxygen species --- photoreceptor cells --- PI3K --- Nrf2 --- eicosapentaenoic acid (EPA) --- docosahexaenoic acid (DHA) --- retinal pigment epithelium --- antioxidant --- ascorbic acid --- retinal disease --- vitamin D --- GLP-1 --- superoxide dismutase --- biomarkers of diabetic retinopathy --- metabolic memory --- tear film --- aqueous humor --- vitreous humor --- mitochondria --- redox --- photoreceptor --- glycation --- aging --- glyoxalase --- eicosanoids --- oxidative stress --- diabetic retinopathy --- cyclooxygenase --- lipoxygenase --- Cytochrome P450 --- HDAC6 --- tubastatin A --- retinal endothelial cells --- retinal endothelial cell senescence --- db/db mice --- Cinnamomi Ramulus --- Paeoniae Radix --- CPA4-1 --- blood-retinal barrier --- occludin --- human retina --- epiretinal membrane --- internal limiting membrane --- vitreoretinal surgery --- macular hole --- proliferative diabetic retinopathy --- antioxidants --- diabetes mellitus --- free radicals --- high-mobility group box 1 (HMGB1) --- inflammatory pathways --- novel therapies --- diabetic retinopathy (DR) --- inflammation --- angiogenesis --- extracellular vesicles --- miRNA --- biomarkers --- apoptosis --- fenofibrate --- thioredoxin --- hyperglycemia --- astaxanthin --- carotenoid --- reactive oxygen species --- photoreceptor cells --- PI3K --- Nrf2 --- eicosapentaenoic acid (EPA) --- docosahexaenoic acid (DHA) --- retinal pigment epithelium --- antioxidant --- ascorbic acid --- retinal disease --- vitamin D --- GLP-1 --- superoxide dismutase --- biomarkers of diabetic retinopathy --- metabolic memory --- tear film --- aqueous humor --- vitreous humor --- mitochondria --- redox --- photoreceptor --- glycation --- aging --- glyoxalase
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MicroRNAs (miRNAs) are small noncoding RNAs that are 19–24 nucleotides in length, following maturation. Recent evidence has demonstrated their key role as post-transcriptional regulators of gene expression through the binding of specific sequences within target messenger RNA (mRNA). miRNAs are involved in the synthesis of a very large number of proteins, and it is speculated that they could regulate up to 30% of the human genome. They control virtually every cellular process and are essential for animal development, cell differentiation, and homeostasis. Altered miRNA expression has been linked to such pathological events as inflammatory, degenerative, or autoimmune processes and have been associated with several diseases, including cancer, cardiovascular diseases, diabetes mellitus, and rheumatic and neurological disorders. Recently, miRNAs have been found in many different biological fluids, and this observation suggests the potential of miRNAs as new candidate biomarkers for diagnosis, classification, prognosis, and responsiveness in the treatment of different pathological conditions. Furthermore, the development of therapeutic strategies that involve either restoring or repressing miRNAs expression and activity has attracted much attention. Significant progress has been made in the systems for delivery of miRNAs, even if substantial improvements in this area are still necessary. Although they have been extensively studied, a number of interesting questions regarding the physiological and pathological role of miRNAs have been postulated, and their potential diagnostic and therapeutic role remain yet unanswered. Reactive oxygen species (ROS) are free radical-containing oxygen molecules derived from cellular oxidative metabolism, including enzyme activities and mitochondrial respiration, and play a pivotal role in many cellular functions. Whereas ROS are essential for normal cellular processes, their aberrant production, or failure of the capacity to scavenge excessive ROS, induces an altered redox status with excessive synthesis of free radicals, leading to an imbalance in the redox environment of the cell. The loss of normal ROS levels causes lipid, protein, and DNA damage, which contribute to the development of various pathologies including neurological disorders, rheumatic and cardiovascular diseases, diabetes, and cancer. Increasing evidence highlights that there is crosstalk between miRNAs and components of redox signaling, even if this complex and the characteristics of mutual interaction need to be amply elucidated. Hence, both miRNAs and oxidative stress are involved in the multifactorial development and progression of acute and chronic diseases by influencing numerous signaling and metabolic pathways. The Special Issue entitled "Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology" of the International Journal of Molecular Sciences includes original articles and reviews that provide new insights into the interaction between miRNAs and oxidative stress under normal and pathological conditions which can assist in the development of new therapeutic strategies. Finally, I would like to thank all the authors for their excellent contribution. I hope this Special Issue will provide readers with updated knowledge about the role of miRNAs and oxidative stress in physiology and pathology.
Medicine --- miR-27a-5p --- acute myocardial infarction --- autophagy --- apoptosis --- hypoxia --- MicroRNA (miRNA) --- miR526b --- miR655 --- oxidative stress --- reactive oxygen species (ROS) --- superoxide (SO) --- Thioredoxin Reductase 1 (TXNRD1) --- breast cancer --- nucleic acid medicine --- pancreatic cancer --- clinical trial --- siRNA --- antisense oligonucleotide --- MicroRNA --- signal transduction --- therapeutic target --- miRNAs --- ROS --- noncoding RNA --- microRNA --- long noncoding RNA --- mitochondrial dysfunction --- nitrosative stress. exosome --- cross-talk --- systemic lupus erythematosus --- visfatin --- resistin --- osteoarthritis --- synovial fibroblasts --- synovitis --- NF-κB --- thyroid hormone --- liver cancer --- metabolism --- physiology --- ASH --- NAFLD --- NASH --- HCC --- HCV --- HBV --- endometriosis --- high-grade serous ovarian cancer --- endometriosis-associated ovarian cancer --- epithelial-to-mesenchymal transition --- chemoresistance --- antioxidants --- miRNA --- cancer --- diabetes --- beta cells --- microRNAs --- translation regulation --- neurodegeneration --- Alzheimer's disease --- Parkinson's disease --- Huntington's disease --- ALS --- reactive oxygen species --- redox signaling --- therapeutic tolerance --- therapeutic resistance --- miR-27a-5p --- acute myocardial infarction --- autophagy --- apoptosis --- hypoxia --- MicroRNA (miRNA) --- miR526b --- miR655 --- oxidative stress --- reactive oxygen species (ROS) --- superoxide (SO) --- Thioredoxin Reductase 1 (TXNRD1) --- breast cancer --- nucleic acid medicine --- pancreatic cancer --- clinical trial --- siRNA --- antisense oligonucleotide --- MicroRNA --- signal transduction --- therapeutic target --- miRNAs --- ROS --- noncoding RNA --- microRNA --- long noncoding RNA --- mitochondrial dysfunction --- nitrosative stress. exosome --- cross-talk --- systemic lupus erythematosus --- visfatin --- resistin --- osteoarthritis --- synovial fibroblasts --- synovitis --- NF-κB --- thyroid hormone --- liver cancer --- metabolism --- physiology --- ASH --- NAFLD --- NASH --- HCC --- HCV --- HBV --- endometriosis --- high-grade serous ovarian cancer --- endometriosis-associated ovarian cancer --- epithelial-to-mesenchymal transition --- chemoresistance --- antioxidants --- miRNA --- cancer --- diabetes --- beta cells --- microRNAs --- translation regulation --- neurodegeneration --- Alzheimer's disease --- Parkinson's disease --- Huntington's disease --- ALS --- reactive oxygen species --- redox signaling --- therapeutic tolerance --- therapeutic resistance
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