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Książki na temat „Molecular Modifications”

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Data publikacji: 6 września 2023

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1

Geological Survey (U.S.), red. Modifications of two palynological processing techniques: Ultrasonic processing and early-stage sieving. [Reston, VA]: Dept. of the Interior, U.S. Geological Survey, 1992.

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2

Overweg, Arian. The preparation, modification and characterization of some molecular sieve materials. Eindhoven: Eindhoven University, 1998.

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3

Henri, Grosjean, red. DNA and RNA modification enzymes: Structure, mechanism, function, and evolution. Austin, Tex: Landes Bioscience, 2009.

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4

Blair, Mary Elizabeth. Habitat modification and gene flow in Saimiri oerstedii: Landscape genetics, intraspecific molecular systematics, and conservation. [New York, N.Y.?]: [publisher not identified], 2011.

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5

Susanne, Brakmann, i Johnsson Kai, red. Directed molecular evolution of proteins: Or how to improve enzymes for biocatalysis. Weinheim: Wiley-VCH, 2002.

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6

Thor, G. Bioprocesses of biopharmaceuticals: The obligatory role of post translational modifications to create functional bioactive molecules. Westborough, MA: D&MD Publications, 2005.

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7

Zhou, Xiufen. Molecular genetic analysis of an unusual DNA modification and a phage defence system of streptomyces lividans 66. Norwich: University of East Anglia, 1993.

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8

A 'Toolkit' of Small Molecules for Polymer Assembly and Post-Synthetic Modification Using 'Click' and Photoactive Chemistries. [New York, N.Y.?]: [publisher not identified], 2011.

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9

1952-, Zouali Moncef, red. The epigenetics of autoimmune diseases. Chichester: Wiley-Blackwell, 2009.

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10

Lamond, Angus I. Pre-mRNA processing. New York: Springer-Verlag, 1995.

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11

Lamond, Angus I. Pre-mRNA processing. Austin: R.G. Landes Co., 1995.

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12

Modifications Of Nuclear Dna And Its Regulatory Proteins. Academic Press, 2011.

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13

Blumenthal, Robert M., i XiaoDong Cheng. Modifications of Nuclear DNA and Its Regulatory Proteins. Elsevier Science & Technology Books, 2011.

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14

Ravanello, Monica P. G. Post-translational modifications of vaccinia virus proteins: Molecular analysis of the myristylated L1R gene product. 1994.

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15

Rubenstein, Irwin, Ronald L. Phillips i Charles E. Green. Molecular Genetic Modification of Eucaryotes. Elsevier Science & Technology Books, 2013.

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16

(Contributor), P. Anderson, H. K. Beyer (Contributor), P. Gallezot (Contributor), R. Harjula (Contributor), H. G. Karge (Contributor), U. Rymsa (Contributor), G. Schulz-Ekloff (Contributor) i in., red. Post-Synthesis Modification I (Molecular Sieves). Springer, 2002.

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17

Taniguchi, Naoyuki, i Shozo Tuboi. The Post-Translational Modification of Proteins: Roles in Molecular and Cellular Biology. Japan Scientific Societies Press, 1992.

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18

1929-, Tsuboi Shōzō, Taniguchi Naoyuki 1942- i Katunuma Nobuhiko 1926-, red. The Post-translational modification of proteins: Roles in molecular and cellular biology. Tokyo: Japan Scientific Societies Press, 1992.

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19

The Post-translational modification of proteins: Roles in molecular and cellular biology. CRC Press, 1992.

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20

Launay, Jean-Pierre, i Michel Verdaguer. The excited electron: photophysical properties. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198814597.003.0004.

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After a review of fundamental notions such as absorption, emission and the properties of excited states, the chapter introduces excited-state electron transfer. Several examples are given, using molecules to realize photodiodes, light emitting diodes, photovoltaic cells, and even harnessing photochemical energy for water photolysis. The specificities of ultrafast electron transfer are outlined. Energy transfer is then defined, starting from its theoretical description, and showing its involvement in photonic wires or molecular assemblies realizing an antenna effect for light harvesting. Photomagnetic effects; that is, the modification of magnetic properties after a photonic excitation, are then studied. The examples are taken from systems presenting a spin cross-over, with the LIESST effect, and from systems presenting metal–metal charge transfer, in particular in Prussian Blue analogues and their molecular version.

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21

Kannicht, Christoph. Posttranslational Modification of Proteins: Tools for Functional Proteomics (Methods in Molecular Biology). Humana Press, 2002.

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22

Kannicht, Christoph. Posttranslational Modification of Proteins: Tools for Functional Proteomics (Methods in Molecular Biology). Wyd. 2. Humana Press, 2008.

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23

Singh, Sandeep, i Dhiraj Kumar, red. Protocols used in Molecular Biology. BENTHAM SCIENCE PUBLISHERS, 2020. http://dx.doi.org/10.2174/97898114393151200101.

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Protocols used in Molecular Biology is a compilation of several examples of molecular biology protocols. Each example is presented with a concise introduction, materials and chemicals required, a step-by-step procedure and troubleshooting tips. Information about the application of the protocol is also provided. The techniques included in this book are essential to research in the fields of proteomics, genomics, cell culture, epigenetic modification and structural biology. The protocols can also be used by clinical researchers (neuroscientists and oncologists, for example) for medical applications (diagnostics, therapeutics and multidisciplinary projects).

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24

Adkins, Daniel E., Kelli M. Rasmussen i Anna R. Docherty. Social Epigenetics of Human Behavior. Redaktor Rosemary L. Hopcroft. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780190299323.013.40.

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It is well established that extreme social adversity can lead to negative health outcomes decades after the resolution of the precipitating environmental insult. Although the underlying mechanisms through which such adversity gets “under the skin” to become biologically embedded have long been considered a black box, recent research has indicated an important mediating role for epigenetic mechanisms—molecular modifications that regulate gene activity without changing the DNA sequence. With technical and scientific developments now enabling genome-wide epigenetic studies in humans, behavioral researchers have an unprecedented opportunity to empirically map the ways in which social dynamics become epigenetically embedded, influencing downstream gene expression, health, and behavior. This chapter examines the current state of social epigenetics research and discusses the opportunities and challenges facing this emerging field.

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25

Hodgkiss, Andrew. Introduction to biological and molecular psychiatry. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0002.

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An introduction to biological and molecular psychiatry is offered, intended for oncology and palliative medicine clinicians. A recent historical perspective is used, beginning with a summary of monoaminergic and cholinergic neurotransmission as understood in the 1980s. One endocrine theory of depression, based on HPA axis dysfunction, is described. Recognition of the limits of these models has led to a deeper molecular psychiatry ‘beyond the synapse’ and to an appreciation of the importance of amino acid neurotransmission. Selective expression of proteins, and their covalent and allosteric modification, is now seen as central to neuroplasticity. The NMDA receptor and excitotoxicity are introduced. The chapter closes with an overview of the amygdala and of hippocampal neurogenesis.

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26

Yu, Shirley P., i David J. Hunter. Prospects for disease modification. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0035.

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The tremendous individual and societal burden underpin a strong rationale for the development of disease-modifying agents for osteoarthritis. Current approaches to managing the disease remain largely palliative and focused on alleviating symptoms, specifically pain and functional limitation. The chapter considers the multitude of tissues that potentially can be targeted in this heterogeneous disease of osteoarthritis and the agents that can modify these tissues. It first focuses on molecules targeting inflammatory pathways and then breaks that down by particular tissue targeted: specifically and in particular synovium, cartilage, and bone. There is widespread demonstration of the ability to modify osteoarthritis in preclinical models; however, this has not been translated to the human disease to the satisfaction of regulatory bodies at this point in time. There are a number of products currently in testing that demonstrate great promise although there remain considerable challenges to the demonstration of disease modification.

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27

Gott, Jonatha M. RNA Interference, Editing, and Modification: Methods and Protocols (Methods in Molecular Biology). Humana Press, 2004.

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28

Wetzel, Ronald, i Rakesh Mishra. Structural Biology. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0012.

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The 3,144–amino acid huntingtin protein (HTT) folds in water into a structure consisting of compact, organized domains interspersed with intrinsically disordered protein (IDP) elements. The IDPs function as sites of post-translational modifications and proteolysis as well as in targeting, binding, and aggregation. Although the dominant structural motif of HTT is the α‎-helix–rich HEAT repeat, the expanded polyglutamine (polyQ) toxicity responsible for Huntington’s disease is most likely played out within intrinsically disordered HTT exon 1–like fragments consisting of the 16– to 17–amino acid N-terminal HTTNT segment, the polyQ segment, and a proline-rich segment. The physical behavior of HTT exon 1 fragments is dominated by interactive, polyQ repeat length–dependent structural transitions responsible for membrane and protein–protein interactions and the formation of tetramers, higher oligomers, amyloid fibrils, and inclusions. Understanding the basis of this solution behavior may be the key to disease mechanisms and molecular therapeutic strategies.

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29

Chess, Andrew, i Schahram Akbarian. The Human Brain and its Epigenomes. Redaktorzy Dennis S. Charney, Eric J. Nestler, Pamela Sklar i Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0003.

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Conventional psychopharmacology elicits an insufficient therapeutic response in more than one half of patients diagnosed with schizophrenia, bipolar disorder, depression, anxiety, or related disorders. This underscores the need to further explore the neurobiology and molecular pathology of mental disorders in order to develop novel treatment strategies of higher efficacy. One promising avenue of research is epigenetics.Deeper understanding of genome organization and function in normal and diseased human brain will require comprehensive charting of neuronal and glial epigenomes. This includes DNA cytosine and adenine methylation, hundred(s) of residue-specific post-translational histone modifications and histone variants, transcription factor occupancies, and chromosomal conformations and loopings. Epigenome mappings provide an important avenue to assign function to many risk-associated DNA variants and mutations that do not affect protein-coding sequences. Powerful novel single cell technologies offer the opportunity to understand genome function in context of the vastly complex cellular heterogeneity and neuroanatomical diversity of the human brain.

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30

Grosjean, Henri. DNA and RNA Modification Enzymes: Structure, Mechanism, Function and Evolution. Taylor & Francis Group, 2009.

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31

Grosjean, Henri. DNA and RNA Modification Enzymes: Structure, Mechanism, Function and Evolution. Taylor & Francis Group, 2009.

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32

Ducruix, Arnaud, i Richard Giegé, red. Crystallization of Nucleic Acids and Proteins. Oxford University Press, 1999. http://dx.doi.org/10.1093/oso/9780199636792.001.0001.

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Crystallography is the major method of determining structures of biological macromolecules yet crystallization techniques are still regarded as difficult to perform. This new edition of Crystallization of Nucleic Acids and Proteins: A Practical Approach continues in the vein of the first edition by providing a detailed and rational guide to producing crystals of proteins and nucleic acids of sufficient quantity and quality for diffraction studies. It has been thoroughly updated to include all the major new techniques such as the uses of molecular biology in structural biology (maximizing expression systems, sequence modifications to enable crystallization, and the introduction of anomalous scatterers); diagnostic analysis of prenucleation and nucleation by spectroscopic methods; and the two- dimensional electron crystallography of soluble proteins on planar lipid films. As well as an introduction to crystallogenesis, the other topics covered are: Handling macromolecular solutions, experimental design, seeding, proceeding from solutions to crystals Crystallization in gels Crystallization of nucleic acid complexes and membrane proteins Soaking techniques Preliminary characterization of crystals in order to tell whether they are suitable for diffraction studies. As with all Practical Approach books the protocols have been written by experienced researchers and are tried an tested methods. The underlying theory is brought together with the laboratory protocols to provide researchers with the conceptual and methodological tools necessary to exploit these powerful techniques. Crystallization of Nucleic Acids and Proteins: A Practical Approach 2e will be an invaluable manual of practical crystallization methods to researchers in molecular biology, crystallography, protein engineering, and biological chemistry.

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33

(Editor), Susanne Brakmann, i Kai Johnsson (Editor), red. Directed Molecular Evolution of Proteins: Or How to Improve Enzymes for Biocatalysis. Wiley-VCH, 2002.

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34

Gott, Jonatha M. Rna Interference, Editing, And Modification: Methods And Protocols (Methods in Molecular Biology (Clifton, N.J.);, V. 265.). Humana Pr, 2004.

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35

Marino, Ana. Dynamic modification of graphite surfaces with surfactants for electrochemical detection of biological molecules. 1994.

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36

Brakmann, Susanne, i Kai Johnsson. Directed Molecular Evolution of Proteins: Or How to Improve Enzymes for Biocatalysis. Wiley & Sons, Incorporated, John, 2020.

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37

Frigione, Mariaenrica. Miscibility studies and chemical modification of functionalised low molecular weight polyethylene for use as toughening agents in epoxy resins. 1997.

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38

O’Callaghan, Chris A. Renal function. Redaktor Rutger Ploeg. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0126.

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The kidneys play a central role in homeostasis by maintaining extracellular fluid composition and volume. They do this by continuous filtration of plasma in the renal glomeruli and then subsequent modification of the filtered fluid as it passes along the nephron. The filtration process excludes large molecules, but most small molecules and ions are freely filtered. The filtrate that is produced in the glomeruli has a similar composition to plasma with respect to small molecules and ions. Most of the water and solutes are reabsorbed along the tubules and this process requires high levels of metabolic activity. In addition, a range of compounds and ions are secreted into the tubules along the nephron. Renal function is central to homeostasis and an appreciation of normal renal physiology is essential to understand the role of the kidney in a wide variety of disease processes.

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39

Jicha, Gregory A., i Frederick A. Schmitt. Alzheimer’s Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0017.

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Advances in the current management and treatment of Alzheimer’s disease have grown directly from our increased understanding of the neurobiology underlying this disease. Currently available pharmacologic and nonpharmacologic treatment strategies remain focused on symptomatic management of disease rather than disease modification. Despite a wealth of evidence supporting the clinical benefits of existing therapies in the management of symptomatic progression, there is limited evidence that these available therapies modify disease progression over the course of dementia progression. More recent research discoveries in the areas of genetics, molecular and cell biology, and environmental risk factors have become the focal point for an explosive growth in experimental disease-modifying strategies designed to prevent, slow, or potentially halt the progression of Alzheimer’s disease.

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40

Rajeev, S. G. The Navier–Stokes Equations. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198805021.003.0003.

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When different layers of a fluid move at different velocities, there is some friction which results in loss of energy and momentum to molecular degrees of freedom. This dissipation is measured by a property of the fluid called viscosity. The Navier–Stokes (NS) equations are the modification of Euler’s equations that include this effect. In the incompressible limit, the NS equations have a residual scale invariance. The flow depends only on a dimensionless ratio (the Reynolds number). In the limit of small Reynolds number, the NS equations become linear, equivalent to the diffusion equation. Ideal flow is the limit of infinite Reynolds number. In general, the larger the Reynolds number, the more nonlinear (complicated, turbulent) the flow.

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41

Lachmann, Robin H., i Timothy M. Cox. Disorders of Fructose Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0003.

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Hereditary fructose intolerance is an autosomal recessive disease which is manifest at weaning but formal diagnosis is often delayed until late childhood or adult life. Fructose, sucrose and sorbitol present in offending foods and drinks induce hypoglycaemia, hypophosphatemia, acidosis, hyperuricemia and hypermagnesemia. If unrecognized, the disease causes failure to thrive, a reno-tubular syndrome with nephrocalcinosis, jaundice, and ultimately liver injury. Parenteral administration of fructose or its congeners can be fatal. Molecular analysis of the aldolase B gene has revolutionized diagnosis. Treatment by a strict dietary exclusion (supplemented by water-soluble vitamins) is successful and, if instituted in a timely manner, is compatible with a normal life span. Early diagnosis and dietary modification are critical for well-being and normal development in affected children.

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42

Dodds, Chris, Chandra M. Kumar i Frédérique Servin. Pathophysiological changes of ageing and their relevance to anaesthesia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198735571.003.0002.

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The molecular basis of ageing is reviewed. This includes the concept of a summation of DNA damage over a lifetime causing genome instability. Epigenetic alterations, telomeric shortening, and the possibility of their modification are discussed. Oxidative and mitochondrial DNA damage and the resulting dysfunction leading to senescence are briefly described. Systemic problems and resultant behavioural adaptation may mask the decline in functional reserve and cause some of the difficulties in identifying its presence in ill elderly patients. Specific organ system changes are then described in some detail. These include the major concerns with the cardiovascular, respiratory, renal, hepatic, neurologic, endocrine, and musculoskeletal systems. The effect of ageing on the special senses of vision and hearing are covered, with emphasis on issues of informed consent.

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43

Divan, Aysha, i Janice A. Royds. 4. Proteins. Oxford University Press, 2016. http://dx.doi.org/10.1093/actrade/9780198723882.003.0004.

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Biological functions require protein and the protein makeup of a cell determines its behaviour and identity. Proteins, therefore, are the most abundant molecules in the body except for water. The approximately 20,000 protein coding genes in the human genome can, by alternative splicing, multiple translation starts, and post-translational modifications, produce over 1,000,000 different proteins, collectively called ‘the proteome’. It is the size of the proteome and not the genome that defines the complexity of an organism. ‘Proteins’ describes the composition and structure of proteins and how they are studied. What information is required in order to understand how proteins work and what happens when this function is impaired in disease?

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44

Crous-Bou, Marta, Immaculata de Vivo i Pagona Lagiou. Endometrial Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0018.

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Lifestyle factors contribute appreciably to endometrial cancer risk, with obesity accounting for over one-third of incident cases in high-income societies. Unlike cervical cancer, which is a model of viral carcinogenesis, endometrial cancer is considered a model of hormonal carcinogenesis, as use of unopposed estrogens postmenopausally and obesity are the best-established risk factors. Endometrial cancer is also the only known malignancy for which cigarette smoking has been shown to confer protection. Risk reduction conferred by current smoking, past oral contraceptive use, childbearing, and physical activity is believed to be mediated by hormones. This may also apply to the increase in risk associated with obesity, which increases peripheral production of estrogens, and with diabetes mellitus. Hence, it should be possible to prevent a substantial fraction of endometrial cancers through lifestyle modification. Pathological classification of endometrial cancer is currently evolving and studies are revealing different molecular subtypes within the same histological groups.

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45

Burton, Derek, i Margaret Burton. Transport: blood and circulation. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198785552.003.0005.

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The blood system transports nutrients, oxygen, carbon dioxide and nitrogenous wastes; other functions include defence. Fish have a closed, single circulation in which blood is pumped by a contractile heart via a ventral aorta to the gills, then via the dorsal aorta to vessels supplying the tissues and organs, with a venous return to the heart. Large venous sinuses occur in elasmobranchs. Air-breathing fish have modifications of the circulation. Complex networks of narrow blood vessels can occur as red patches, retia, maximizing transfer of nutrients, oxygen or heat. Most fish have nucleated red blood cells (erythrocytes) with haemoglobin. The types of white blood cells (leucocytes) are similar to those of other vertebrates but there are thrombocytes rather than platelets. Nutrient transport is in the plasma, the fluid component of the blood, which may also carry antifreeze agents and molecules (e.g. urea in elasmobranchs) which counteract deleterious osmotic effects

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46

Zouali, Moncef. Epigenetics of Autoimmune Diseases. Wiley & Sons, Incorporated, John, 2009.

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47

The Enzymes, Third Edition (The Enzymes). Wyd. 3. Academic Press, 2001.

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48

Sigman, David S., i Ross Dalbey. Co- and Posttranslational Proteolysis of Proteins. Elsevier Science & Technology Books, 2001.

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49

Nakamura, Tomohiro, i Stuart A. Lipton. Neurodegenerative Diseases as Protein Misfolding Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0002.

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Neurodegenerative diseases (NDDs) often represent disorders of protein folding. Rather than large aggregates, recent evidence suggests that soluble oligomers of misfolded proteins are the most neurotoxic species. Emerging evidence points to small, soluble oligomers of misfolded proteins as the cause of synaptic dysfunction and loss, the major pathological correlate to disease progression in many NDDs including Alzheimer’s disease. The protein quality control machinery of the cell, which includes molecular chaperones as found in the endoplasmic reticulum (ER), the ubiquitin-proteasome system (UPS), and various forms of autophagy, can counterbalance the accumulation of misfolded proteins to some extent. Their ability to eliminate the neurotoxic effects of misfolded proteins, however, declines with age. A plausible explanation for the age-dependent deterioration of the quality control machinery involves compromise of these systems by excessive generation of reactive oxygen species (ROS), such as superoxide anion (O2-), and reactive nitrogen species (RNS), such as nitric oxide (NO). The resulting redox stress contributes to the accumulation of misfolded proteins. Here, we focus on aberrantly increased generation of NO-related species since this process appears to accelerate the manifestation of key neuropathological features, including protein misfolding. We review the chemical mechanisms of posttranslational modification by RNS such as protein S-nitrosylation of critical cysteine thiol groups and nitration of tyrosine residues, showing how they contribute to the pathogenesis of NDDs.

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50

Miu, Andrei C., Judith R. Homberg i Klaus-Peter Lesch, red. Genes, brain, and emotions. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198793014.001.0001.

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With the advent of methods from behavioral genetics, molecular biology, and cognitive neuroscience, affective science has recently started to approach genetic influences on emotion, and the underlying intermediate neural mechanisms through which genes and experience shape emotion. The aim of this volume is to offer a comprehensive account of current research in the genetics of emotion, written by leading researchers, with extensive sections focused on methods, intermediate phenotypes, and clinical and translational work. Major methodological approaches are reviewed in the first section, including the two traditional “workhorses” in the field, twin studies and gene–environment interaction studies, and the more recently developed epigenetic modification assays, genome-wide association studies, and optogenetic methods. Parts 2 and 3 focus on a variety of psychological (e.g. fear conditioning, emotional action control, emotion regulation, emotional memory, decision-making) and biological (e.g. neural activity assessed using functional neuroimaging, electroencephalography, and psychophysiological methods; telomere length) mechanisms, respectively, that may be viewed as intermediate phenotypes in the pathways between genes and emotional experience. Part 4 concentrates on the genetics of emotional dysregulation in neuropsychiatric disorders (e.g. post-traumatic stress disorder, eating disorders, obsessive–compulsive disorder, Tourette’s syndrome), including factors contributing to the risk and persistence of these disorders (e.g. child maltreatment, personality, emotional resilience, impulsivity). In addition, two chapters in Part 4 review genetic influences on the response to psychotherapy (i.e. therapygenetics) and pharmacological interventions (i.e. pharmacogenetics) in anxiety and affective disorders.

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