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The human genome, as with the genome of most organisms, is comprised of various types of mobile genetic element derived repeats. Mobile genetic elements that mobilize by an RNA intermediate, include both autonomous and non-autonomous retrotransposons, and mobilize by a “copy and paste” mechanism that relies of the presence of a functional reverse transcriptase activity. The extent to which these different types of elements are actively mobilizing varies among organisms, as revealed with the advent of Next Generation DNA sequencing (NGS).To understand the normal and aberrant mechanisms that impact the mobility of these elements requires a more extensive understanding of how these elements interact with molecular pathways of the cell, including DNA repair, recombination and chromatin. In addition, epigenetic based-mechanisms can also influence the mobility of these elements, likely by transcriptional activation or repression in certain cell types. Studies regarding how mobile genetic elements interface and evolve with these pathways will rely on genomic studies from various model organisms. In addition, the mechanistic details of how these elements are regulated will continue to be elucidated with the use of genetic, biochemical, molecular, cellular, and bioinformatic approaches. Remarkably, the current understanding regarding the biology of these elements in the human genome, suggests these elements may impact developmental biology, including cellular differentiation, neuronal development, and immune function. Thus, aberrant changes in these molecular pathways may also impact disease, including neuronal degeneration, autoimmunity, and cancer.
transposon --- genome stability --- model organisms --- reverse transcriptase --- Mobile DNA --- RNA-dependent DNA polymerase --- cellular differentiation --- retrotransposon --- DNA repair
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The human genome, as with the genome of most organisms, is comprised of various types of mobile genetic element derived repeats. Mobile genetic elements that mobilize by an RNA intermediate, include both autonomous and non-autonomous retrotransposons, and mobilize by a “copy and paste” mechanism that relies of the presence of a functional reverse transcriptase activity. The extent to which these different types of elements are actively mobilizing varies among organisms, as revealed with the advent of Next Generation DNA sequencing (NGS).To understand the normal and aberrant mechanisms that impact the mobility of these elements requires a more extensive understanding of how these elements interact with molecular pathways of the cell, including DNA repair, recombination and chromatin. In addition, epigenetic based-mechanisms can also influence the mobility of these elements, likely by transcriptional activation or repression in certain cell types. Studies regarding how mobile genetic elements interface and evolve with these pathways will rely on genomic studies from various model organisms. In addition, the mechanistic details of how these elements are regulated will continue to be elucidated with the use of genetic, biochemical, molecular, cellular, and bioinformatic approaches. Remarkably, the current understanding regarding the biology of these elements in the human genome, suggests these elements may impact developmental biology, including cellular differentiation, neuronal development, and immune function. Thus, aberrant changes in these molecular pathways may also impact disease, including neuronal degeneration, autoimmunity, and cancer.
transposon --- genome stability --- model organisms --- reverse transcriptase --- Mobile DNA --- RNA-dependent DNA polymerase --- cellular differentiation --- retrotransposon --- DNA repair
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The human genome, as with the genome of most organisms, is comprised of various types of mobile genetic element derived repeats. Mobile genetic elements that mobilize by an RNA intermediate, include both autonomous and non-autonomous retrotransposons, and mobilize by a “copy and paste” mechanism that relies of the presence of a functional reverse transcriptase activity. The extent to which these different types of elements are actively mobilizing varies among organisms, as revealed with the advent of Next Generation DNA sequencing (NGS).To understand the normal and aberrant mechanisms that impact the mobility of these elements requires a more extensive understanding of how these elements interact with molecular pathways of the cell, including DNA repair, recombination and chromatin. In addition, epigenetic based-mechanisms can also influence the mobility of these elements, likely by transcriptional activation or repression in certain cell types. Studies regarding how mobile genetic elements interface and evolve with these pathways will rely on genomic studies from various model organisms. In addition, the mechanistic details of how these elements are regulated will continue to be elucidated with the use of genetic, biochemical, molecular, cellular, and bioinformatic approaches. Remarkably, the current understanding regarding the biology of these elements in the human genome, suggests these elements may impact developmental biology, including cellular differentiation, neuronal development, and immune function. Thus, aberrant changes in these molecular pathways may also impact disease, including neuronal degeneration, autoimmunity, and cancer.
transposon --- genome stability --- model organisms --- reverse transcriptase --- Mobile DNA --- RNA-dependent DNA polymerase --- cellular differentiation --- retrotransposon --- DNA repair
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Cellular Responses to Stress brings together a group of scientists who work on different but interrelated aspects of cellular stress responses. The book provides state-of-the-art information on the wide spectrum of ways in which cells can respond to different forms of stress induced by chemicals, oxidants, and DNA-damaging agents. Mechanisms are described that involve altered uptake and efflux of chemical agents, intracellular detoxification, and DNA damage responses. Many of these changes trigger a cascade of reactions mediated by stress-activated signaling pathways, which have the capacity to determine whether a cell will survive or die. The spectrum of topics covered in this book aims to provide a broad overview of our current knowledge of the different forms of adaptive response systems.It is hoped that this text will stimulate further research to establish the relative cellular role of specific response pathways and will enable us to gain a deeper understanding of the mechanisms that allow cells to live or die. This book will be valued by university researchers at all levels, industrial scientists in the pharmaceutical and biotechnology industries, and clinical researchers.Originally published in 1999.The Princeton Legacy Library uses the latest print-on-demand technology to again make available previously out-of-print books from the distinguished backlist of Princeton University Press. These editions preserve the original texts of these important books while presenting them in durable paperback and hardcover editions. The goal of the Princeton Legacy Library is to vastly increase access to the rich scholarly heritage found in the thousands of books published by Princeton University Press since its founding in 1905.
Stress (Physiology) --- Cell metabolism --- Cellular control mechanisms --- Cells --- Metabolism --- Regulation --- AMPK. --- ASK1. --- Actin. --- Activation. --- Angiogenesis. --- Antibody. --- Antigen. --- Apoptosis. --- Autoimmunity. --- Autophosphorylation. --- C-Fos. --- C-Jun N-terminal kinases. --- C-terminus. --- Cell Cycle Arrest. --- Cell Line, Transformed. --- Cell cycle. --- Cell membrane. --- Cell migration. --- Cell surface receptor. --- Cellular differentiation. --- Cellular stress response. --- Conformational change. --- Cytochrome P450. --- Cytokine receptor. --- Cytokine. --- Cytotoxicity. --- DNA-PKcs. --- Drug metabolism. --- Ectopic expression. --- Effector (biology). --- Endonuclease. --- Enzyme. --- Epidermal growth factor receptor. --- Epidermal growth factor. --- Extracellular signal–regulated kinases. --- Fibroblast growth factor. --- Gene expression. --- Gene therapy. --- Gene. --- Germinal center. --- Glutathione S-transferase. --- HMG-CoA reductase. --- Heat shock. --- Histidine kinase. --- Hormone-sensitive lipase. --- Hsp27. --- Immortalised cell line. --- Immunodeficiency. --- Immunoglobulins. --- Immunoprecipitation. --- In vitro. --- Inducer. --- Inflammation. --- Jurkat cells. --- Kinase. --- Lymphotoxin. --- Macrophage colony-stimulating factor. --- Mechanism of action. --- Mechanistic target of rapamycin. --- Metabolism. --- Mitogen-activated protein kinase kinase. --- Mitogen-activated protein kinase. --- Mitogen. --- Mitosis. --- Model organism. --- Neuropeptide. --- Neurotoxin. --- Osmotic shock. --- Oxidative phosphorylation. --- Oxidative stress. --- P38 mitogen-activated protein kinases. --- Pathogenesis. --- Peptide. --- Peroxidase. --- Phosphatase. --- Phosphoinositide 3-kinase. --- Phosphorylation cascade. --- Phosphorylation. --- Post-translational modification. --- Protease. --- Protein kinase. --- Protein phosphorylation. --- Protein synthesis inhibitor. --- Protein. --- Proteolysis. --- RNA interference. --- Receptor (biochemistry). --- Receptor tyrosine kinase. --- Repressor. --- Response element. --- Signal transduction. --- Ternary Complex Factors. --- Thrombin. --- Transcription factor. --- Transcriptional regulation. --- Transfection. --- Transposable element. --- Tumor necrosis factor superfamily. --- Turgor pressure. --- Vascular endothelial growth factor.
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A major new theory of why human intelligence has not evolved in other speciesThe Human Evolutionary Transition offers a unified view of the evolution of intelligence, presenting a bold and provocative new account of how animals and humans have followed two powerful yet very different evolutionary paths to intelligence. This incisive book shows how animals rely on robust associative mechanisms that are guided by genetic information, which enable animals to sidestep complex problems in learning and decision making but ultimately limit what they can learn. Humans embody an evolutionary transition to a different kind of intelligence, one that relies on behavioral and mental flexibility. The book argues that flexibility is useless to most animals because they lack sufficient opportunities to learn new behavioral and mental skills. Humans find these opportunities in lengthy childhoods and through culture.Blending the latest findings in fields ranging from psychology to evolutionary anthropology, The Human Evolutionary Transition draws on computational analyses of the problems organisms face, extensive overviews of empirical data on animal and human learning, and mathematical modeling and computer simulations of hypotheses about intelligence. This compelling book demonstrates that animal and human intelligence evolved from similar selection pressures while identifying bottlenecks in evolution that may explain why human-like intelligence is so rare.
SCIENCE / Cognitive Science. --- Activation. --- Adaptation. --- Anatomically modern human. --- Animal cognition. --- Approach Behavior. --- Backtracking. --- Behavior. --- Behavioral modernity. --- Biology. --- Cellular differentiation. --- Cognition. --- Cognitive Psychology. --- Cognitive architecture. --- Cognitive revolution. --- Cognitive test. --- Combinatorial explosion. --- Comparative psychology. --- Computer. --- Conceptual framework. --- Cost-effectiveness analysis. --- Cultural evolution. --- Cultural history. --- Decision-making. --- Developmental psychology. --- Dimension. --- Dynamical system. --- Early childhood. --- Ecological niche. --- Emergence. --- Energy consumption. --- Episodic-like memory. --- Ethology. --- Evolution of human intelligence. --- Evolution. --- Evolutionary biology. --- Evolutionary dynamics. --- Evolutionary psychology. --- Explanatory power. --- Forward chaining. --- Genetic divergence. --- Genre. --- Gopnik. --- Governance. --- Hominidae. --- Human behavior. --- Human evolution (origins of society and culture). --- Human evolution. --- Implementation. --- Inference. --- Information processing. --- Institution. --- Invention. --- Jay. --- Language acquisition. --- Language. --- Learning curve. --- Learning. --- Life. --- Mass production. --- Mating. --- Mental process. --- Modern Studies. --- Observational learning. --- Obstacle. --- Order of acquisition. --- Organism. --- Outsourcing. --- Ownership (psychology). --- Perception. --- Perceptual learning. --- Philosophical theory. --- Planning. --- Population genetics. --- Probability. --- Programming language. --- Prokaryote. --- Reality. --- Reinforcement. --- Result. --- Sample Size. --- Scientific notation. --- Sensory processing. --- Skill. --- Social environment. --- Social intelligence. --- Social learning theory. --- Socialism. --- Sociocultural evolution. --- Stimulus (physiology). --- Suggestion. --- Summation. --- Supercomputer. --- Symbol. --- Symbolic language (engineering). --- Symbolic system. --- The Major Transitions in Evolution. --- Thought. --- Tool Use Behavior. --- Trait theory. --- Zone of proximal development. --- Neurosciences --- Research. --- Research --- Methodology. --- Neural sciences --- Neurological sciences --- Neuroscience --- Medical sciences --- Nervous system
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