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Epigenetics is a new field that explains gene expression at the chromatin structure and organization level. Three principal epigenetic mechanisms are known and hundreds of combinations among them can develop different phenotypic characteristics. DNA methylation, histone modifications and small RNAs have been identified, and their functions are being studied in order to understand the mechanisms of interaction and regulation among the different biological processes in plants. Although, fundamental epigenetic mechanisms in crop plants are beginning to be elucidated, the comprehension of the different epigenetic mechanisms, by which plant gene regulation and phenotype are modified, is a major topic to develop in the near future in order to increase crop productivity. Thus, the importance of epigenetics in improving crop productivity is undoubtedly growing. Current research on epigenetics suggest that DNA methylation, histone modifications and small RNAs are involved in almost every aspect of plant life including agronomically important traits such as flowering time, fruit development, responses to environmental factors, defense response and plant growth. The aim of this Research Topic is to explore the recent advances concerning the role of epigenetics in crop biotechnology, as well as to enhance and promote interactions among high quality researchers from different disciplines such as genetics, cell biology, pathology, microbiology, and evolutionary biology in order to join forces and decipher the epigenetic mechanisms in crop productivity.
crop --- epigenetics --- Biotechnology --- DNA Methylation --- Histone posttranslational modifications --- small non-coding RNAs
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Non-coding RNAs (ncRNAs), and in particular microRNAs are rapidly becoming the focus of research interest in numerous basic and translational fields, including brain research; and their importance for many aspects in brain functioning merits special discussion. The wide-scope, multi-targeted and highly efficient manner of ncRNA regulatory activities draws attention to this topic by many, but the available research and analysis tools and experimental protocols are still at their infancy, and calls for special discussion given their importance for many aspects in brain functioning. This eBook is correspondingly focused on the search for, identification and exploration of those non-coding RNAs whose activities modulate the multi-leveled functions of the eukaryotic brain. The different articles strive to cover novel approaches for identifying and establishing ncRNA-target relationships, provide state of the art reports of the affected neurotransmission pathways, describe inherited and acquired changes in ncRNA functioning and cover the use of ncRNA mimics and blockade tools for interference with their functions in health and disease of the brain. Non-coding RNAs are here to stay, and this exciting eBook provides a glimpse into their impact on our brain’s functioning at the physiology, cell biology, behavior and immune levels.
MicroRNAs --- long non-coding RNAs --- Central Nervous System --- cholinergic signaling --- Schizophrenia --- Epilepsy --- ischemic stroke --- Alzheimer
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Neurodegenerative diseases (NDs) are a heterogeneous group of disorders affecting the central nervous system. Despite significant differences in their causes, neuropathological abnormalities, and clinical outcomes, some similarities can be found among them, as for example: 1) frequent aggregation and deposition of misfolded proteins, 2) common molecular mechanisms leading to neurodegeneration, and 3) certain overlap in symptoms and clinical features. To date, there is no cure that could stop or delay the progression of these diseases. The advent of advanced gene therapy techniques such as gene silencing and gene editing opened a new avenue for the development of therapeutic strategies for NDs.The discovery of the RNA interference (RNAi) mechanism, in 1998, by Andrew Fire and Craig Mello allowed an important boost to the gene therapy field, providing a potential therapeutic strategy to treat inherited dominant genetic disorders. The use of small RNA sequences to control the expression of disease-causing genes rapidly implemented in the preclinical studies for different diseases. In the field of NDs, several successful studies using this technology proved its potential as a therapeutic option. However, issues like the type of delivery system (non-viral versus viral) or the potential toxicity of the small RNA molecules, made the translation of gene silencing therapeutics to human application very slow and difficult.Recently, a new hope in the gene therapy field emerged with the development of gene editing techniques like TALENs or CRISPR/Cas9 systems. The opportunity of editing or deleting gene sequences drove the scientific community euphoric, with an enormous increase in the number of published studies using this type of techniques. Recently, the first clinical trial using one of these systems was approved in China. For NDs, gene-editing technology also represents an important therapeutic option, and the first preclinical studies are now being published, showing the potential accomplishment for this technology.
Gene silencing --- Gene editing --- Neurodegenerative diseases --- Antisense oligonucleotides --- CRISPR/Cas9 --- Neuroinflammation --- iPS cells --- Long non-coding RNAs --- RNA interference --- Neurodegeneration
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The epithelial-to-mesenchymal transition (EMT) is a highly dynamic process with multiple transitional states, by which epithelial cells can convert into a mesenchymal phenotype. This process involves loss of cellular adhesion and cellular polarity, and an improvement in migratory and invasive properties. It occurs during normal embryonic development, tissue regeneration, organ fibrosis, and wound healing. It is also involved in tumor progression with metastatic expansion, and plays a major role in resistance to cancer treatment. In cancers, EMT inducers are hypoxia, cytokines and growth factors secreted by the tumor microenvironment, stroma crosstalk, metabolic changes, innate and adaptive immune responses, and treatment with antitumor drugs. Switch in gene expression from epithelial to mesenchymal phenotype is triggered by complex regulatory networks involving transcriptional control, non-coding RNAs, chromatin remodeling and epigenetic modifications, alternative splicing, post-translational regulation, protein stability and subcellular localization. Reversion of EMT, the mesenchymal-to-epithelial transition (MET), affects circulating cancer cells when they reach a desirable metastatic niche to develop secondary tumors. More knowledge and control of EMT to MET is necessary and will be beneficial for patients for cancer treatment. This current Special Issue entitled “Epithelial to Mesenchymal Transition in Cancer” will address these questions.
Epithelial-to-mesenchymal transition (EMT) --- cancer --- metastasis --- chemoresistance --- cancer therapy, epigenetics --- non-coding RNAs --- TGF-beta --- PLK1 --- CK2, exosomes --- epithelial-to-pericyte transition (EPT)
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This Special Issue of Cancers (Basel) is mainly dedicated to selecting papers from the talks given during the first Joint Meeting on Lung Cancer (JMLC) between the MD Anderson Cancer Center (Houston, Texas USA) and the Hospital University Federation (HUF) OncoAge (University Côte d’Azur, Nice, France) (Nice, September 2018). The central theme of JMLC is to discuss new advances and exchange ideas regarding lung cancer. Notably, the talks covered different topics on new therapeutic strategies (targeted therapy and immuno-oncology), molecular and cellular biology, biomarkers, and the epidemiology of lung cancer. Special attention was also given to lung cancer in elderly patients. The articles published in this Special Issue covered subjects such as the assessment of new biomarkers and new approaches for the early detection of lung cancer, epidemiological data, and emphasized a place for the newly characterized cellular pathways in lung cancer, which opens room for therapeutic perspectives for lung cancer patients.
cancer --- older adults --- geriatric assessment --- geriatric interventions --- non-small cell lung cancer --- non-smoker --- tumor microenvironment --- targeted treatment --- lung cancer --- artificial intelligence --- screening --- lncRNA --- MALAT1 --- metastasis --- bioinformatics --- integrated approaches --- lung cancer --- rational therapy --- immune profiling --- cancer tissues --- multiplexed methodologies --- image analysis --- spatial analysis --- aging --- cancer --- optimization --- research --- education --- elderly --- well-being --- circulating tumor cells --- liquid biopsy --- lung cancer --- personal medicine --- techniques --- xenograft --- multiplexed --- brightfield --- chromogenic --- fluorescence --- molecular --- immune profiling --- immune-oncology --- digital --- lung cancer --- lung adenocarcinoma --- macrophage --- immunotherapy --- interleukin-1? and immunometabolism --- lung cancer --- EGFR mutations --- EGFR TKIs --- non-coding RNAs --- microRNAs --- long non-coding RNAs --- hormones --- hormone-like action --- non-small cell lung cancer --- immunotherapy --- PD-1/PD-L1 checkpoint blockade --- CD8 T Cells --- immune blockade --- NSCLC --- reversal of EMT --- tumor microenvironment --- tumor plasticity --- TNBC
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Repetitive DNA is ubiquitous in eukaryotic genomes, and, in many species, comprises the bulk of the genome. Repeats include transposable elements that can self-mobilize and disperse around the genome, and tandemly-repeated satellite DNAs that increase in copy number due to replication slippage and unequal crossing over. Despite their abundance, repetitive DNA is often ignored in genomic studies due to technical challenges in their identification, assembly, and quantification. New technologies and methods are now providing the unprecedented power to analyze repetitive DNAs across diverse taxa. Repetitive DNA is of particular interest because it can represent distinct modes of genome evolution. Some repetitive DNA forms essential genome structures, such as telomeres and centromeres, which are required for proper chromosome maintenance and segregation, whereas others form piRNA clusters that regulate transposable elements; thus, these elements are expected to evolve under purifying selection. In contrast, other repeats evolve selfishly and produce genetic conflicts with their host species that drive adaptive evolution of host defense systems. However, the majority of repeats likely accumulate in eukaryotes in the absence of selection due to mechanisms of transposition and unequal crossing over. Even these neutral repeats may indirectly influence genome evolution as they reach high abundance. In this Special Issue, the contributing authors explore these questions from a range of perspectives.
B chromosomes --- PSR (Paternal sex ratio) --- genome elimination --- ncRNAs (non coding RNAs) --- selfish elements --- super-Mendelian --- repeated elements --- endogenous retrovirus --- host genome --- evolution --- segregation --- drosophila --- retrotransposons --- transgene --- piRNA cluster --- insulator --- Su(Hw) --- Rhino --- germline --- transcription --- HeT-A and TART telomeric retrotransposons --- satellite --- transposable element --- repetitive DNA --- chromosome evolution --- centromere drive --- genetic conflict --- CENP-A --- centromeric transcription --- transposable elements --- gene duplication --- gene evolution --- epigenetics --- transposable elements --- transposons --- LTR retrotransposons --- ERV --- genome --- genome annotation --- karyotype --- estrildidae --- zebra finch --- Uraeginthus cyanocephalus --- transposable element --- horizontal transfer --- arms race --- LINE-1 --- Alu --- hobo --- I element --- transposable elements --- evolution --- arthropods --- genome size --- horizontal transfer --- database --- nuclear rDNA --- rRNA --- GC-content --- secondary structure --- nucleolus --- satellite DNA --- centromere --- sequence variation --- structural variation --- repeat --- alpha satellite --- human satellites --- genome assembly --- transposable elements --- population genetics --- selection --- drift --- coevolution --- repetitive DNA --- transposable element --- heterochromatin --- genome evolution --- genomic conflict
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Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of subsequent chronic kidney disease. Although the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function is urgently needed. The Special Issue covers research articles that investigated the molecular mechanisms of inflammation and injury during different renal pathologies, renal regeneration, diagnostics using new biomarkers, and the effects of different stimuli like medication or bacterial components on isolated renal cells or in vivo models. The Special Issue contains important reviews that consider the current knowledge of cell death and regeneration, inflammation, and the molecular mechanisms of kidney diseases. In addition, the potential of cell-based therapy approaches that use mesenchymal stromal/stem cells or their derivates is summarized. This edition is complemented by reviews that deal with the current data situation on other specific topics like diabetes and diabetic nephropathy or new therapeutic targets.
kidney injury --- alport syndrome --- modifier gene --- nephrin --- podocin --- glomerular basement membrane --- slit diaphragm --- focal segmental glomerulosclerosis --- inflammatory bowel disease (IBD) --- DSS-colitis --- glomerular filtration barrier (GFB) --- type IV collagen --- type I collagen --- type V collagen --- genotype --- IL-18 --- polymorphism --- renal cell carcinoma --- Taiwan --- mesenchymal stem cells --- acute and chronic kidney disease --- exosome --- natural products --- non-coding RNAs --- microRNAs --- long non-coding RNAs --- renal fibrosis --- biomarkers --- therapeutics targets --- rhabdomyolysis --- pigment nephropathy --- haem --- NLRP3 inflammasome --- acute kidney injury --- hypertension --- kidney --- molecular signaling --- hematuria --- inflammation --- oxidative stress --- tubular injury --- AKI --- chronic kidney disease (CKD) --- mesenchymal stromal cells --- extracellular vesicles --- acute kidney injury --- modified-MSCs --- microRNA --- mesenchymal stem cell --- mesodermal stem cell --- renal ischemia-reperfusion --- inflammation --- kidney transplantation --- microRNA --- extracellular vesicles --- exosomes --- B-cell attracting chemokine --- CXCL13 --- kidney transplantation --- allograft rejection --- T cell-mediated rejection --- diabetic nephropathy --- lysophosphatidic acid --- lysophosphatidic acid receptor --- chronic kidney injury --- kidney proximal tubule --- acute kidney failure --- signal transduction --- transcription --- CREB Regulated Transcriptional Coactivators (CRTC) --- cAMP Regulatory Element Binding Protein (CREB) --- Salt Inducible Kinase (SIK) --- Class IIa Histone Deacetylases (HDAC) --- lncRNA --- long non-coding RNA --- miRNA --- kidney --- glomerulus --- podocyte --- acute kidney injury --- AKI --- diabetic nephropathy --- diabetic kidney disease --- diabetic nephropathy --- inflammation --- signaling cascade --- ischemia-reperfusion --- acute kidney injury --- stem cell --- conditioned medium --- inflammation --- apoptosis --- necrosis --- regulated necrosis --- kidney injury --- tubular injury --- glomerular injury --- polyunsaturated fatty acids --- omega-3 fatty acid --- inflammatory maker --- C-reactive protein --- interleukin-6 --- LPS-binding protein --- fibrosis --- pericyte --- myofibroblast --- endotoxemia-induced oliguric kidney injury --- arachidonic acid --- cyclooxygenase --- lipoxygenase --- cytochrome P450 --- kidney inflammation --- therapeutic target --- obese kidney fibrosis --- endotoxemia --- ROS --- cPLA2 and COX-2 --- IgA nephropathy --- KIT assay --- KIT-IgA score --- noninvasive --- diagnostics --- prediction --- diabetic kidney diseases --- xanthine oxidase --- glomerular damage --- acute kidney injury --- chronic kidney disease --- renal progenitors --- polyploidization --- diabetic nephropathy --- diabetes mellitus --- GLP-1 receptor agonists --- SGLT2 inhibitors --- molecular mechanisms --- chemerin --- CmklR1 --- 2-kidney-1-clip --- 2k1c --- Thy1.1 nephritis --- renovascular hypertension --- renal inflammation --- renal injury --- renal fibrosis --- inflammation --- ischemia/reperfusion injury --- Farnesiferol B --- Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-?B) --- G-protein-coupled bile acid receptor (TGR5) --- renal stem cells --- differentiation --- scattered tubular cells --- papilla --- niches --- renal tubular cells --- epithelial cells --- proximal tubule --- cytotoxicity --- injury --- inflammation --- empagliflozin --- dapagliflozin --- kidney --- n/a
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Transcriptional regulation is a critical biological process involved in the response of a cell, a tissue or an organism to a variety of intra- and extra-cellular signals. Besides, it controls the establishment and maintenance of cell identity throughout developmental and differentiation programs. This highly complex and dynamic process is orchestrated by a huge number of molecules and protein networks and occurs through multiple temporal and functional steps. Of note, many human disorders are characterized by misregulation of global transcription since most of the signaling pathways ultimately target components of transcription machinery. This book includes a selection of papers that illustrate recent advances in our understanding of transcriptional regulation and focuses on many important topics, from cis-regulatory elements to transcription factors, chromatin regulators and non-coding RNAs, other than several transcriptome studies and computational analyses.
major depressive disorder --- glioblastoma --- differentially expressed genes --- transcriptomics --- common pathway --- mouse --- miR-25-3p --- Akt1 --- AP-2? --- promoter --- cell metabolism --- p57Kip2 --- CDKN1C --- epigenetics --- disease --- cell differentiation --- placenta --- long non-coding RNA (lncRNA) --- human --- pregnancy --- high-throughput RNA sequencing (RNA-Seq) --- transcriptome --- Rsh regulon --- Novosphingobium pentaromativorans US6-1 --- sphingomonads --- RNA-seq --- N-acyl-l-homoserine lactone --- ppGpp --- selenium --- selenocysteine --- selenoproteins --- selenocysteine insertion sequence --- nonsense-mediated decay --- G-quadruplex --- transcriptional regulation --- promoter --- CRISPR/Cas9 --- PRDM gene family --- TCGA data analysis --- somatic mutations --- transcriptome profiling --- human malignancies --- tristetraprolin (TTP) --- tumorigenesis --- posttranscriptional regulation --- adenosine and uridine-rich elements (AREs) --- circRNA-disease associations --- pathway --- heterogeneous network --- Patau Syndrome --- cytogenetics --- FOXO1 --- transcription factor --- molecular pathways --- bioinformatics --- molecular docking --- and drug design --- transcription regulation --- gene expression --- causal inference --- enhancer activity --- insect --- transcription factors --- structures and functions --- research methods --- progress and prospects --- Pax3 --- Pteria penguin (Röding, 1798) --- tyrosinase --- melanin --- RNA interference --- liquid chromatograph-tandem mass spectrometer (LC-MS/MS) --- epigenetics --- gene expression --- nutrition --- transcription --- disorders --- mechanisms --- Crassostrea gigas --- Pacific oyster --- pediveliger larvae --- bioadhesive --- transcriptome --- gene expression --- interactome --- microscopy --- fertilization --- self-incompatibility --- transcriptome --- tea --- long non-coding RNAs --- cancer --- acute leukemia --- therapeutic targets --- Adiponectin --- cancer --- Adiponectin receptors --- obesity --- inflammatory response --- inflammation --- nutritional status --- n/a
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