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Books on the topic 'Centromer'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

Choo, K. H. Andy. The centromere. Oxford: Oxford University Press, 1997.

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2

service), SpringerLink (Online, ed. Centromere: Structure and evolution. Berlin: Springer, 2009.

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3

Ugarkovic, Durdica, ed. Centromere. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00182-6.

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4

Jiang, Jiming, and James A. Birchler, eds. Plant Centromere Biology. Oxford, UK: Wiley-Blackwell, 2013. http://dx.doi.org/10.1002/9781118525715.

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5

Black, Ben E., ed. Centromeres and Kinetochores. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-58592-5.

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6

Palme, Gerhard. Wirtschaftregion "CENTROPE Europaregion Mitte": Eine Bestandsaufnahme. Wien: Österreichisches Institut für Wirtschaftsforschung, 2006.

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7

Teologi a desde la mujer en Centroame rica. San Jose , Costa Rica: SEBILA, 1989.

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8

Huber, Peter. Wandel der Sektorstruktur in der Wirtschaftsregion: "Centrope Europaregion Mitte". Wien: Österreichisches Institut für Wirtschaftsforschung, 2006.

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9

Cheng-Pei, Choh-Vivian. Organisation of centromeric domains in nuclei of murine dorsal root ganglion neurons in vitro. Ottawa: National Library of Canada, 1996.

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10

Aliaga, Carlos Alarcón. Catástrofe ecológica en la Sierra Central del Perú: Incidencia de la actividad minero-metalúrgica en el medio ambiente. Lima: IPEMIN, 1994.

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11

Carlos, Punta, ed. Ame rica precolombina: Si ntesis histo rica : antologi a y ana lisis de su arte pla stico : Norteame rica, Mesoame rica, Centroame rica, Surame rica. [Buenos Aires]: Nobuko, 2004.

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12

Ugarkovic, Durdica. Centromere. Springer, 2009.

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13

Jiang, Jiming, and James A. Birchler. Plant Centromere Biology. Wiley & Sons, Incorporated, John, 2013.

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14

Jiang, Jiming, and James A. Birchler. Plant Centromere Biology. Wiley & Sons, Incorporated, John, 2013.

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15

Plant Centromere Biology. John Wiley & Sons Inc, 2013.

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16

Jiang, Jiming, and James A. Birchler. Plant Centromere Biology. Wiley & Sons, Incorporated, John, 2013.

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17

Ugarkovic, Durdica. Centromere: Structure and Evolution. Springer, 2010.

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18

McKinlay Gardner, R. J., and David J. Amor. Centromere Fissions, Complementary Isochromosomes, Telomeric Fusions, Balancing Supernumerary Chromosomes, Neocentromeres, Jumping Translocations, and Chromothripsis. Edited by R. J. McKinlay Gardner and David J. Amor. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199329007.003.0012.

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This chapter reviews a number of very rare chromosomal rearrangements: centromere fissions, complementary isochromosomes, telomeric fusions, balancing supernumerary chromosomes, neocentromeres, jumping translocations, and chromothripsis. Centromere fission results when a metacentric or submetacentric chromosome splits at the centromere, giving rise to two stable telocentric products. The Robertsonian fission reverses the fusion that had originally generated it. Telomeric fusion leads to a 45-chromosome count. With the balanced complementary isochromosome carrier, two stable exactly metacentric products are generated. A balancing small supernumerary marker chromosome contains material deleted from the normal homolog. A supernumerary chromosome lacking a normal centromere can become stable and functional due to the generation of a neocentromere. In jumping translocations, a segment can move from one chromosome to two or more recipient chromosomes. Chromothripsis takes complex rearrangement to a yet more complex level. The reproductive risks associated with each are noted.

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19

Centroame rica: crisi y poli tica internacional. 3rd ed. (Mexico City): Siglo veintiuno editores, 1985.

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20

Gestion de empresas publicas mineras centromin Peru S.A. Lima: Junta del Acuerdo de Cartagena, 1989.

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21

Black, Ben E. Centromeres and Kinetochores: Discovering the Molecular Mechanisms Underlying Chromosome Inheritance. Springer, 2017.

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22

Black, Ben E. Centromeres and Kinetochores: Discovering the Molecular Mechanisms Underlying Chromosome Inheritance. Springer, 2018.

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23

Surtees, Jennifer A. P1 ParB: The structural and functional domains of the P1 plasmid centromere-binding protein. 2001.

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24

Moreno, Stanley Heckadon. Hacia una Centroame rica verde: Seis casos de conservacio n integrada. 2nd ed. 1993.

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25

Wevrick, Rachel. Organization and behaviour of Alpha satellite DNA at the centromeres of human chromosomes. 1992.

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26

Ltd, ICON Group. CENTROTEC HOCHLEISTUNGSKUNSTSTOFFE AG: International Competitive Benchmarks and Financial Gap Analysis (Financial Performance Series). 2nd ed. Icon Group International, Inc., 2000.

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27

Ltd, ICON Group. CENTROTEC HOCHLEISTUNGSKUNSTSTOFFE AG: Labor Productivity Benchmarks and International Gap Analysis (Labor Productivity Series). 2nd ed. Icon Group International, Inc., 2000.

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28

kurtis, luke, and Brian Centrone. I Voted for Biddy Schumacher: Mismatched Tales from the Mind of Brian Centrone. New Lit Salon Press, 2016.

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29

Instituto Centroamericano de Estudios Poli ticos., ed. Derechos humanos en Centroame rica, 1986: Situacio n en El Salvador, Guatemala y Nicaragua. Guatemala: INCEP, 1986.

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30

McKinlay Gardner, R. J., and David J. Amor. Inversions. Edited by R. J. McKinlay Gardner and David J. Amor. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199329007.003.0009.

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Inversions are intrachromosomal structural rearrangements. The most common is the simple (or single) inversion. If the inversion coexists with another rearrangement in the same chromosome, it is a complex inversion. In an inversion, a segment of chromosome is switched 180 degrees. If this segment includes the centromere, this is a pericentric inversion; if not, it is a paracentric inversion. In principle, and almost always in practice, it is only the pericentric inversion that conveys an important genetic risk to carriers of the inversion: Their children may inherit a “recombinant” chromosome that would inevitably be imbalanced. This chapter considers these two type of inversions and discusses the degree of genetic risk that may—or may not—be associated.

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31

Movement of centromeric domains: Tracking in live cells in resposne to induced changes in gene expression. Ottawa: National Library of Canada, 2002.

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32

Vadakkan, Kunjumon Ittira. Clustering of centromeric domains in cerebellar Purkinje and granule neurons is chromosome-specific and cell-type specific. 2004.

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33

McKinlay Gardner, R. J., and David J. Amor. Chromosome Instability Syndromes. Edited by R. J. McKinlay Gardner and David J. Amor. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199329007.003.0016.

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A defect of DNA repair is the factor underlying the chromosome instability syndromes, also known as chromosome breakage syndromes. The “instability” refers to the predisposition of the chromosomes to undergo rearrangement or to display other abnormal cytogenetic behavior. The classic chromosome instability syndromes are individually rare: Fanconi syndrome, ataxia-telangiectasia, and Bloom syndrome. Smaller-print conditions are yet more rare, including Roberts syndrome; the immunodeficiency, centromeric instability, facial anomalies (ICF) syndrome; and Nijmegen breakage syndrome. The role of cytogenetics in diagnosis is less central than formerly, but the interest in these conditions remains, and this chapter provides a full listing. Autosomal recessive inheritance is typical, albeit not universal.

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34

Organization of centromeric domains in interphase nuclei of hepatocytes from Xenopus laevis: Changes associated with novo activation of the vitellogenin gene family. Ottawa: National Library of Canada, 1994.

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35

Denton, Christopher P., and Pia Moinzadeh. Systemic sclerosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0121.

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The term 'scleroderma' describes a group of conditions in which the development of thickened, fibrotic skin is a cardinal feature. This includes localized forms of scleroderma (e.g. morphoea) and also systemic forms of the disease that are more correctly termed systemic sclerosis. Systemic sclerosis (SSc) is a multiorgan, autoimmune disease that has a high clinical burden and mortality, due to affecting the skin as well as internal organs. As with other related diseases there is a female predominance and marked clinical diversity. The pathogenesis of SSc is not fully elucidated; it includes endothelial cell injury fibroblast activation and autoimmunity that lead to skin and internal organ manifestations. The majority of cases exhibit characteristic serum autoantibodies. Some of these antibodies are scleroderma-specific reactivities including anti-centromere (ACA), anti-topoisomerase-1 (ATA or Scl 70) or anti-RNA polymerase III antibodies. These anti-nuclear antibody (ANA) patterns are generally mutually exclusive and serve as useful clinical markers of disease subgroups. Additional subsetting of scleroderma cases, based on the extent of skin sclerosis, permits classification into limited and diffuse subsets. Because of the heterogeneity of the disease patients may suffer from different organ manifestations, such as lung fibrosis, hypertensive renal crisis, severe cardiac disease, gastrointestinal involvement, and pulmonary arterial hypertension. Although outcomes have improved recently, systemic sclerosis still has the highest case-specific mortality of any of the autoimmune rheumatic diseases and requires careful and systematic investigation, management and follow-up. Treatment includes symptomatic strategies with attention to each involved organ system; it is still an area where therapeutic progress and better understanding of pathogenesis is increasingly anticipated.

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