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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
CRISPR/Cas9 --- genome edited plants --- biosafety --- agriculture --- policy and legislation
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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
Trypanosoma cruzi --- Chagas disease --- parasite-host interaction --- gene function --- CRISPR/Cas9 technique
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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 --- Long non-coding RNAs --- RNA interference --- Neurodegenerative diseases --- CRISPR/Cas9 --- Neurodegeneration --- Gene editing --- Antisense oligonucleotides --- Neuroinflammation --- iPS cells
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RNA interference (RNAi) is a widely used technology for gene silencing and has become a key tool in a myriad of research and lead discoveries. In recent years, the mechanism of RNAi agents has been well investigated, and the technique has been optimized for better effectiveness and safety. On the other hand, the clustered regularly interspaced short palindromic repeats (CRISPR)-associated Cas9/gRNA system is a recent, novel, targeted genome-editing technique derived from the bacterial immune system. Recent advances in gene-editing research and technologies have enabled the CRISPR Cas9 system to become a popular tool for sequence-specific gene editing to correct and modify eukaryotic systems. In this book, we will focus on the mechanisms, applications, regulations (their pros and cons), and various ways in which RNAi-based methods and CRIPSR-Cas9 technology have stimulated the modulation of gene expression, thereby making them a promising therapeutic tool to treat and prevent complex diseases and disorders.
CRISPR-associated protein 9. --- Cas9 (CRISPR-associated protein 9) --- CRISPR/Cas9 --- Endonucleases --- Gene editing --- Life Sciences --- Molecular Genetics --- Genetics and Molecular Biology --- Genomics --- Biochemistry
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Would you change your genes if you could? As we confront the 'industrial revolution of the genome', the recent discoveries of Crispr-Cas9 technologies are offering, for the first time, cheap and effective methods for editing the human genome. This opens up startling new opportunities as well as significant ethical uncertainty. Tracing events across a fifty-year period, from the first gene splicing techniques to the present day, this is the story of gene editing - the science, the impact and the potential. Kozubek weaves together the fascinating stories of many of the scientists involved in the development of gene editing technology. Along the way, he demystifies how the technology really works and provides vivid and thought-provoking reflections on the continuing ethical debate. Ultimately, Kozubek places the debate in its historical and scientific context to consider both what drives scientific discovery and the implications of the 'commodification' of life.
Gene targeting. --- Genomes. --- CRISPR-associated protein 9. --- Cas9 (CRISPR-associated protein 9) --- CRISPR/Cas9 --- Endonucleases --- Gene editing --- Genetics --- Genomics --- Haploidy --- Targeting, Gene --- Genetic engineering
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Genetic engineering. --- CRISPR-associated protein 9. --- Cas9 (CRISPR-associated protein 9) --- CRISPR/Cas9 --- Endonucleases --- Gene editing --- Designed genetic change --- Engineering, Genetic --- Gene splicing --- Genetic intervention --- Genetic surgery --- Genetic recombination --- Biotechnology --- Transgenic organisms
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Genome Editing: A Practical Guide to Research and Clinical Applications is geared towards investigators interested in learning how to use CRISPR-Cas9-based technologies, with a focus on cardiovascular research and clinical applications. Covering a range of topics from the basics of genome editing to design considerations, to assessments and applications, this reference allows readers to get started and establish a full workflow from the beginning of the project to its full completion. With worked examples drawn from real-life experiments, as well as troubleshooting and pitfalls to avoid, the book serves as an essential reference for researchers and investigators in both cardiovascular and biomedical research.
Gene editing. --- CRISPR-associated protein 9. --- CRISPR (Genetics). --- Cardiovascular system --- Diseases --- Genetic aspects. --- Circulatory system --- Vascular system --- Blood --- Clustered Regularly Interspaced Short Palindromic Repeats (Genetics) --- Immunogenetics --- Nucleotide sequence --- Cas9 (CRISPR-associated protein 9) --- CRISPR/Cas9 --- Endonucleases --- Gene editing --- Editing, Gene --- Editing, Genome --- Genome editing --- Genetic engineering --- Circulation --- Methodology.
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Apomixis is the consequence of a concerted mechanism that harnesses the sexual machinery and coordinates developmental steps in the ovule to produce an asexual (clonal) seed. Altered sexual developments involve widely characterized functional and anatomical changes in meiosis, gametogenesis, and embryo and endosperm formation. The ovules of apomictic plants skip meiosis and form unreduced female gametophytes whose egg cells develop into a parthenogenetic embryo, and the central cells may or may not fuse to a sperm to develop the seed endosperm. Thus, functional apomixis involves at least three components, apomeiosis, parthenogenesis, and endosperm development, modified from sexual reproduction that must be coordinated at the molecular level to progress through the developmental steps and form a clonal seed. Despite recent progress uncovering specific genes related to apomixis-like phenotypes and the formation of clonal seeds, the molecular basis and regulatorynetwork of apomixis is still unknown. This is a central problem underlying the current limitations of apomixis breeding. This book collates twelve publications addressing different topics around the molecular basis of apomixis, illustrating recent discoveries and advances toward understanding the genetic regulation of the trait, discussing the possible origins of apomixis and the remaining challenges for its commercial deployment in plants.
apomixis --- evolution --- germline --- gene regulation --- sporogenesis --- plant reproduction --- ribosome --- RNA helicase --- sexual development --- stress response --- apomeiosis --- clonal seeds --- endosperm --- heterosis capture --- molecular breeding --- parthenogenesis --- differentially expressed genes --- hybridization --- microarrays --- polyploidy --- Ranunculus --- sexuality --- character segregation --- crop biotechnology --- heterosis --- meiosis --- recombination --- agamospermy --- basal angiosperms (ANA-grade) --- sporocyteless --- polycomb-group proteins --- reproductive systems --- apomixis evolution --- APOSTART --- Poa pratensis --- diplospory --- autonomous endosperm --- genetics --- Taraxacum --- dandelion --- weeping lovegrass --- drought stress --- RNA-seq --- plant breeding --- plant development --- Hieracium piloselloides --- CRISPR/Cas9 --- PHYTOENE DESATURASE (PDS) --- amplicon sequencing --- genome editing --- tissue culture --- haploid progeny --- dicotyledon --- PsASGR-BBML --- pseudogamy --- 5-azacytidine --- abscisic acid --- apospory --- expression profiling --- fluridone --- metabolic homeostasis --- oxidative stress --- sucrose non-fermenting-related protein kinase --- n/a
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Nerve sheath tumors can be a significant cause of morbidity for many patients. These include benign tumors such as schwannomas, diffuse and plexiform neurofibromas, and atypical neurofibromas, as well as the aggressive soft tissue sarcoma known as the malignant peripheral nerve sheath tumor (MPNST). Nerve sheath tumors occur sporadically and in the context of the clinical neuro-genetic tumor predisposition syndromes neurofibromatosis type 1 (NF1) and type 2 (NF2). Historically, the mainstay of treatment for nerve sheath tumors has been surgery. However, for both benign and malignant nerve sheath tumors, there is a high recurrence rate, highlighting the pressing need for novel therapies. As we have entered the genomic era, the hope is that an improved understanding of the genetics, and therefore the biology, of these tumors will ultimately lead to therapies that result in better outcomes. In this Special Issue, we include both review articles and original research related to the genomic understanding and modeling of schwannomas, plexiform and diffuse neurofibromas, atypical neurofibromas, and malignant peripheral nerve sheath tumors as well as genomic methods being developed and applied to advance our understanding of these tumors.
neurofibromatosis type 1 --- nerve sheath tumor --- cancer --- latent variables --- machine learning --- supervised learning --- transfer learning --- random forest --- metaVIPER --- tumor deconvolution --- neurofibromatosis --- malignant peripheral nerve sheath tumor --- MPNST --- polycomb repressive complex --- PRC2 --- NF1 --- kinase --- kinome adaptation --- kinome reprogramming --- MET --- MEK --- doxorubicin --- capmatinib --- tram --- genomics --- tumor evolution --- pathology --- next generation sequencing --- clinical genetics --- malignant peripheral nerve sheath tumors --- plexiform neurofibromas --- Schwann cells --- neurofibromatosis type 1 syndrome --- neurofibromin 1 --- genetically engineered mouse models --- heterogeneity --- CRISPR/Cas9 --- mouse models --- sarcoma --- tumor microenvironment --- neurofibromatosis 1 (NF1) --- mebendazole (MBZ) --- COX-2 inhibitor --- malignancy --- chemoprevention --- nerve sheath tumors
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