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Books on the topic 'Function of genes'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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1

Genes and cardiovascular function. New York: Springer, 2011.

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2

Ostadal, Bohuslav, Makoto Nagano, and Naranjan S. Dhalla, eds. Genes and Cardiovascular Function. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-7207-1.

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3

NATO Advanced Research Workshop on Major Histocompatibility Complex--Genes/Molecules/Function (1987 Bar Harbor, Me.). H-2 antigens: Genes, molecules, function. New York: Plenum Press, 1987.

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4

Cortical deficits in schizophrenia: From genes to function. New York: Springer, 2008.

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5

Tsang, Michael Wai Kok. Characterisation of structure and function of mouse dishevelled genes. Dublin: University College Dublin, 1996.

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6

name, No. Tumor suppressor genes ; v. 2: Regulation, function, and medicinal applications. Totowa, NJ: Humana Press, 2003.

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7

Shearman, Claire Amy. Structure, function and regulation of modulation genes of Rhizobium leguminosarum. Norwich: University ofEast Anglia, 1986.

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8

Day, Trevor. Genetics: Investigating the function of genes and the science of heredity. New York: Rosen Central, 2012.

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9

International, Seminar/Workshop on the Molecular Structure Function and Assembly of ATP Synthases (1987 Honolulu Hawaii). Molecular structure, function, and assembly of the ATP synthases. New York: Plenum Press, 1989.

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10

International Meeting on Cholinesterases (3rd 1990 La Grande Motte, France). Cholinesterases: Structure, function, mechanism, genetics, and cell biology. Washington, DC: American Chemical Society, 1991.

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11

Pseudogenes: Functions and protocols. New York: Humana Press, 2014.

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12

Wiwanitkit, Viroj. Genes and nutrition. Hauppauge, NY: Nova Science, 2009.

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13

Tudományegyetem, Eötvös Loránd, ed. Function and genres: Studies on the linguistic features of discourse types. Frankfurt am Main: P. Lang, 2008.

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14

Roepke, Jonathon. Localization and functional characterization of iridoid biosynthetic genes in Catharanthus roseus. St. Catharines, Ont: Brock University, Centre for Biotechnology, 2008.

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15

The calcitonin gene-related peptide family: Form, function, and future perspectives. Heidelberg: Springer, 2010.

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16

Dominguez, Nicolás E., and Sofia M. Pereyra. Telomeres: Biological functions, sequencing and aging. Hauppauge] New York: Nova Biomedical, Nova Science Publishers, Inc., 2012.

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17

Human Genome Organisation. European Meeting. Genome analysis: From sequence to function : 1st European meeting 1990, Human Genome Organisation (HUGO). Edited by Collins J, Driesel Albert J, and Human Genome Organisation. Heidelberg: Hüthig, 1991.

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18

RNA therapeutics: Function, design, and delivery. New York: Humana Press, 2010.

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19

Third person references: Forms and functions in two spoken genres of Spanish. Amsterdam: John Benjamins Publishing Company, 2016.

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20

Alonso, Jose M., and Anna N. Stepanova. Plant functional genomics: Methods and protocols. New York: Humana Press, 2015.

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21

Nagano, Makoto, Naranjan S. Dhalla, and Bohuslav Ostadal. Genes and Cardiovascular Function. Springer, 2011.

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22

Genes, Brain Function, and Behavior. Elsevier, 2019. http://dx.doi.org/10.1016/c2016-0-03711-7.

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23

David, C. H-2 Antigens: Genes, Molecules, Function. Springer, 2014.

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24

Retrovirus Genes in Lymphocyte Function and Growth. Springer, 2012.

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25

Michael, Browning, and McMichael Andrew J, eds. HLA and MHC: Genes, molecules and function. Oxford: BIOS Scientific, 1996.

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26

O'Donnell, Patricio. Cortical Deficits in Schizophrenia: From Genes to Function. Springer, 2014.

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27

Morimyo, M. Function of Specific Genes to Enhance Tolerance to Oxygen. Routledge, 1989.

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28

A, Nicolini Claudio, North Atlantic Treaty Organization. Scientific Affairs Division., and NATO Advanced Study Institute on Genome Structure and Function (1996 : Marciana Marina, Italy), eds. Genome structure and function: From chromosomes characterization to genes technology. Dordrecht: Kluwer, 1997.

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29

Nicolini, C. Genome Structure and Function: From Chromosomes Characterization to Genes Technology. Springer, 2012.

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30

Nicolini, C. Genome Structure and Function: from Chromosomes Characterization to Genes Technology. Springer, 1997.

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31

Androgenresponsive Genes In Prostate Cancer Regulation Function And Clinical Applications. Springer-Verlag New York Inc., 2013.

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32

Browning, Michael, and Andrew McMichael. HLA and MHC: Genes, Molecules and Function (Human Molecular Genetics Series). Academic Pr, 1999.

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33

Wang, Zhou. Androgen-Responsive Genes in Prostate Cancer: Regulation, Function and Clinical Applications. Springer, 2013.

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34

Zuccato, Chiara, and Elena Cattaneo. Normal Function of Huntingtin. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0011.

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Huntingtin (HTT) is the 3,144–amino acid protein product of the Huntington’s disease gene (HTT), which can be traced back through 800 million years of evolution. It carries a trinucleotide CAG repeat that encodes polyglutamine (polyQ) at an evolutionarily conserved NH2-terminal position in exon 1. This chapter discusses the discoveries that have mapped the evolutionary history of HTT and the CAG repeat and the critical role of the protein in development as well as its activities in the adult brain. During embryogenesis, HTT is critical for gastrulation, neurulation, and neurogenesis. In the adult brain, HTT acts as an antiapoptotic protein and promotes transcription of neuronal genes and vesicle transport. Subversion or exacerbation of HTT brain function by an abnormally expanded polyQ repeat contributes to neuronal vulnerability in HD and suggests that loss of normal HTT function may be implicated in the disease.
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35

Slack, Jonathan. 4. Genes as markers. Oxford University Press, 2014. http://dx.doi.org/10.1093/actrade/9780199676507.003.0004.

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‘Genes as markers’ shows that most genetic variation does not affect gene function or activity, but it is still of enormous interest. Notably it enables the identification of individual people, useful in forensics in the form of DNA fingerprinting, the establishment of paternity, and other information about family relationships. It also provides some evidence about the migration of human populations in historic and prehistoric times. Genetic variation has also enabled biologists to examine the thorny issue of human racial differences and establish the degree to which there is any biological basis for perceived race.
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36

Marzuki, Sangkot. Molecular Structure, Function, and Assembly of the Atp Synthesis: International Seminar. Springer, 1990.

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37

El-Deiry, Wafik S. Tumor Suppressor Genes: Volume 2: Regulation, Function, and Medicinal Applications (Methods in Molecular Biology). Humana Press, 2003.

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38

Bailey, Matthew A. An overview of tubular function. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0020.

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This chapter provides an overview of transport processes, describing both the membrane proteins that effect transepithelial solute flux and the systems that allow integrated regulation of electrolyte transport. The emphasis is on the physiological mechanisms but links to human diseases are made in order to illuminate fundamental principles of control. The key transport proteins and encoding genes are listed. First, the major transport pathways and regulatory features for each nephron segment are described. The focus here is on the transepithelial flux of sodium, potassium, and water. In the second part, other important aspects of renal homeostasis, including urine concentration and acid–base balance, are summarized.
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39

(Editor), Jean Massoulie, Eric Barnard (Editor), Arnaud Chatonnet (Editor), Francis Bacou (Editor), Bhupendra P. Doctor (Editor), and Daniel M. Quinn (Editor), eds. Cholinesterases: Structure, Function, Mechanism, Genetics, and Cell Biology (Conference Proceedings Series). An American Chemical Society Publication, 1998.

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40

Immediate early genes and inducible transcription factors in mapping of the central nervous system function and dysfunction. Elsevier, 2002. http://dx.doi.org/10.1016/s0924-8196(02)x8010-5.

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41

L, Kaczmarek, and Robertson Harold A, eds. Immediate early genes and inducible transcription factors in mapping of the central nervous system function and dysfunction. Amsterdam: Elsevier, 2002.

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42

Larry and Horti Fairberg Cardiac Workshop. Cardiac Engineering: From Genes and Cells to Structure and Function (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2004.

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43

Monteggia, Lisa M., and Wei Xu. Methods for In Vivo Gene Manipulation. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0004.

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Recent advances in mouse genetics have opened many new avenues of research in which to explore gene function in the brain, and contributions to the pathophysiology and treatment of psychiatric disorders. The use of the mouse to explore gene function has contributed a better understanding of the role of specific genes in the nervous system including their influence on neural circuits and complex behavior.This chapter explores current approaches to manipulate gene function in a mouse. Genetically modified mice allow for the investigation of a particular gene in vivo. The approaches discussed highlight recent advances to specifically overexpress or disrupt a specific gene of interest in the brain. We also highlight viral-mediated gene transfer approaches to allow for spatial and temporal control of gene function.
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44

Cardiac Engineering: From Genes And Cells To Structure And Function (Annals of the New York Academy of Sciences, V. 1015). New York Academy of Sciences, 2004.

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45

Burghes, Arthur H. M., and Vicki L. McGovern. Spinal Muscular Atrophy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0034.

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Spinal muscular atrophies affect the lower motor neuron. The most common SMA maps to 5q is an autosomal recessive disorder. SMA is caused by loss or mutation of the SMN1 gene and retention of the SMN2 gene, and these genes lie in a complex area of the genome. Mild missense alleles of SMN1 work to complement SMN2 to give function and therapeutics that restore SMN levels are in clinical testing. Modifiers that lie outside the SMN gene locus and influence severity clearly exist, but what they are remains unknown as do the critical genes affected by SMN deficiency.
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46

Capone, George T. Down Syndrome. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0056.

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People with Down syndrome (trisomy 21) are distinguished by having an extra copy of chromosome 21. Chromosome 21 contains an estimated 562 genes, including 161 known to code for functional proteins, and at least 396 considered novel. Gene dosage imbalance is the primary mechanism, which results in the molecular, cellular, histological, and anatomical features characteristic of the condition. Throughout brain development, major neurobiological events go awry, resulting in a differently organized brain and characteristic developmental delays noted during infancy and the preschool years. The consequences of gene dosage imbalance continue to have repercussions on neurobiological function throughout childhood and adult life.
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47

(Editor), L. Kaczmarek, and H. A. Robertson (Editor), eds. Immediate Early Genes and Inducible Transcription Factors in Mapping of the Central Nervous System Function and Dysfunction (Handbook of Chemical Neuroanatomy). Elsevier Science, 2002.

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48

Tülümen, Erol, and Martin Borggrefe. Monogenic and oligogenic cardiovascular diseases: genetics of arrhythmias—short QT syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0150.

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Short QT syndrome (SQTS) is a very rare, sporadic or autosomal dominant inherited channelopathy characterized by abnormally short QT intervals on the electrocardiogram and increased propensity to atrial and ventricular tachyarrhythmias and/or sudden cardiac death. Since its recognition as a distinct clinical entity in 2000, significant progress has been made in defining the clinical, molecular, and genetic basis of SQTS. To date, several causative gain-of-function mutations in potassium channel genes and loss-of-function mutations in calcium channel genes have been identified. The physiological consequence of these mutations is an accelerated repolarization, thus abbreviated action potentials and shortened QT interval with an increased inhomogeneity and dispersion of repolarization. Regarding other rare monogenetic arrhythmias, a genetic basis of atrial fibrillation was considered very unlikely until very recently. However, in the last decade the heritability of atrial fibrillation in the general population has been well described in several epidemiological studies. So far, more than 30 genes have been implicated in atrial fibrillation through candidate gene approach studies, and 14 loci were found to be associated with atrial fibrillation through genome-wide association studies. This genetic heterogeneity and the low prevalence of mutations in any single gene restrict the clinical utility of genetic screening in atrial fibrillation.
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49

Said, Neveen, and Dan Theodorescu. Molecular biology of bladder cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0071.

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Bladder cancer is the most common malignancy involving the urinary system, caused primarily by tobacco use and exposure to industrial chemicals with an estimated 73,510 patients affected and 14,880 deaths in 2012. This chapter will summarize what is known about the most common molecular derangements in human bladder cancer. It will focus on the function and biological/clinical relevance of these genes in models of urothelial cancer and in patients with this disease. It is not meant as a comprehensive review of all the functions of the aforementioned genes in normal physiology or other cancer types. Furthermore, the selection of what genes/pathways are described is by necessity empirical and so we apologize to any author whose work was not described or quoted.
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50

Postma, Alex V., David Sedmera, Frantisek Vostarek, Vincent M. Christoffels, and Connie R. Bezzina. Developmental aspects of cardiac arrhythmias. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0027.

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The rhythmic and synchronized contraction of atria and ventricles is essential for efficient pumping of blood throughout the body. This process relies on the proper generation and conduction of the cardiac electrical impulse. Electrophysiological properties differ in various regions of the heart, revealing intrinsic heterogeneities rooted, at least in part, in regional differences in expression of ion channel and gap junction subunit genes. A causal relation between transcription factors and such regionalized gene expression has been established. Abnormal cardiac electrical function and arrhythmias in the postnatal heart may stem from a developmental changes in gene regulation. Genome-wide association studies have provided strong evidence that common genetic variation at developmental gene loci modulates electrocardiographic indices of conduction and repolarization and susceptibility to arrhythmia. Functional aspects are illustrated by description of selected prenatally occurring arrhythmias and their possible mechanisms. We also discuss recent findings and provide background insight into these complex mechanisms.
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