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  • Female  (3)
  • *Neurogenesis  (2)
  • American Association for the Advancement of Science (AAAS)  (4)
  • 2010-2014  (4)
  • 1990-1994
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  • 1
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    Erosion of lizard diversity by climate change and altered thermal niches (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-15
    Description: It is predicted that climate change will cause species extinctions and distributional shifts in coming decades, but data to validate these predictions are relatively scarce. Here, we compare recent and historical surveys for 48 Mexican lizard species at 200 sites. Since 1975, 12% of local populations have gone extinct. We verified physiological models of extinction risk with observed local extinctions and extended projections worldwide. Since 1975, we estimate that 4% of local populations have gone extinct worldwide, but by 2080 local extinctions are projected to reach 39% worldwide, and species extinctions may reach 20%. Global extinction projections were validated with local extinctions observed from 1975 to 2009 for regional biotas on four other continents, suggesting that lizards have already crossed a threshold for extinctions caused by climate change.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinervo, Barry -- Mendez-de-la-Cruz, Fausto -- Miles, Donald B -- Heulin, Benoit -- Bastiaans, Elizabeth -- Villagran-Santa Cruz, Maricela -- Lara-Resendiz, Rafael -- Martinez-Mendez, Norberto -- Calderon-Espinosa, Martha Lucia -- Meza-Lazaro, Rubi Nelsi -- Gadsden, Hector -- Avila, Luciano Javier -- Morando, Mariana -- De la Riva, Ignacio J -- Victoriano Sepulveda, Pedro -- Rocha, Carlos Frederico Duarte -- Ibarguengoytia, Nora -- Aguilar Puntriano, Cesar -- Massot, Manuel -- Lepetz, Virginie -- Oksanen, Tuula A -- Chapple, David G -- Bauer, Aaron M -- Branch, William R -- Clobert, Jean -- Sites, Jack W Jr -- New York, N.Y. -- Science. 2010 May 14;328(5980):894-9. doi: 10.1126/science.1184695.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of California, Santa Cruz, CA 95064, USA. lizardrps@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466932" target="_blank"〉PubMed〈/a〉
    Keywords: Acclimatization ; Animals ; *Biodiversity ; Biological Evolution ; Body Temperature ; *Climate Change ; *Ecosystem ; *Extinction, Biological ; Female ; Forecasting ; Geography ; Global Warming ; *Lizards/genetics/physiology ; Male ; Mexico ; Models, Biological ; Phylogeny ; Population Dynamics ; Reproduction ; Seasons ; Selection, Genetic ; Temperature
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Mutational inactivation of STAG2 causes aneuploidy in human cancer (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-20
    Description: Most cancer cells are characterized by aneuploidy, an abnormal number of chromosomes. We have identified a clue to the mechanistic origins of aneuploidy through integrative genomic analyses of human tumors. A diverse range of tumor types were found to harbor deletions or inactivating mutations of STAG2, a gene encoding a subunit of the cohesin complex, which regulates the separation of sister chromatids during cell division. Because STAG2 is on the X chromosome, its inactivation requires only a single mutational event. Studying a near-diploid human cell line with a stable karyotype, we found that targeted inactivation of STAG2 led to chromatid cohesion defects and aneuploidy, whereas in two aneuploid human glioblastoma cell lines, targeted correction of the endogenous mutant alleles of STAG2 led to enhanced chromosomal stability. Thus, genetic disruption of cohesin is a cause of aneuploidy in human cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3374335/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3374335/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solomon, David A -- Kim, Taeyeon -- Diaz-Martinez, Laura A -- Fair, Joshlean -- Elkahloun, Abdel G -- Harris, Brent T -- Toretsky, Jeffrey A -- Rosenberg, Steven A -- Shukla, Neerav -- Ladanyi, Marc -- Samuels, Yardena -- James, C David -- Yu, Hongtao -- Kim, Jung-Sik -- Waldman, Todd -- CA097257/CA/NCI NIH HHS/ -- R01 CA133662/CA/NCI NIH HHS/ -- R01 CA138212/CA/NCI NIH HHS/ -- R01 CA169345/CA/NCI NIH HHS/ -- R01CA115699/CA/NCI NIH HHS/ -- R21CA143282/CA/NCI NIH HHS/ -- Z01 HG200337-01/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Aug 19;333(6045):1039-43. doi: 10.1126/science.1203619.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, DC 20057, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21852505" target="_blank"〉PubMed〈/a〉
    Keywords: *Aneuploidy ; Antigens, Nuclear/*genetics/*physiology ; Cell Cycle ; Cell Line ; Cell Line, Tumor ; Chromatids/physiology ; *Chromosomal Instability ; Chromosomes, Human, X/genetics ; Female ; Gene Deletion ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Gene Targeting ; Glioblastoma/*genetics ; Humans ; Karyotyping ; Male ; Melanoma/genetics ; Mutation ; Neoplasms/*genetics ; Polymorphism, Single Nucleotide ; Sarcoma, Ewing/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Fate-restricted neural progenitors in the mammalian cerebral cortex (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-11
    Description: During development of the mammalian cerebral cortex, radial glial cells (RGCs) generate layer-specific subtypes of excitatory neurons in a defined temporal sequence, in which lower-layer neurons are formed before upper-layer neurons. It has been proposed that neuronal subtype fate is determined by birthdate through progressive restriction of the neurogenic potential of a common RGC progenitor. Here, we demonstrate that the murine cerebral cortex contains RGC sublineages with distinct fate potentials. Using in vivo genetic fate mapping and in vitro clonal analysis, we identified an RGC lineage that is intrinsically specified to generate only upper-layer neurons, independently of niche and birthdate. Because upper cortical layers were expanded during primate evolution, amplification of this RGC pool may have facilitated human brain evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4287277/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4287277/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Franco, Santos J -- Gil-Sanz, Cristina -- Martinez-Garay, Isabel -- Espinosa, Ana -- Harkins-Perry, Sarah R -- Ramos, Cynthia -- Muller, Ulrich -- MH078833/MH/NIMH NIH HHS/ -- NS046456/NS/NINDS NIH HHS/ -- NS060355/NS/NINDS NIH HHS/ -- R01 NS046456/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 10;337(6095):746-9. doi: 10.1126/science.1223616.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dorris Neuroscience Center and Department of Cell Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22879516" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Cerebral Cortex/*cytology/embryology ; Homeodomain Proteins/genetics ; Mice ; Neural Stem Cells/*cytology/physiology ; *Neurogenesis ; Neuroglia/*cytology ; Neurons/*cytology/physiology ; Recombination, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Hippocampal neurogenesis regulates forgetting during adulthood and infancy (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-05-09
    Description: Throughout life, new neurons are continuously added to the dentate gyrus. As this continuous addition remodels hippocampal circuits, computational models predict that neurogenesis leads to degradation or forgetting of established memories. Consistent with this, increasing neurogenesis after the formation of a memory was sufficient to induce forgetting in adult mice. By contrast, during infancy, when hippocampal neurogenesis levels are high and freshly generated memories tend to be rapidly forgotten (infantile amnesia), decreasing neurogenesis after memory formation mitigated forgetting. In precocial species, including guinea pigs and degus, most granule cells are generated prenatally. Consistent with reduced levels of postnatal hippocampal neurogenesis, infant guinea pigs and degus did not exhibit forgetting. However, increasing neurogenesis after memory formation induced infantile amnesia in these species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akers, Katherine G -- Martinez-Canabal, Alonso -- Restivo, Leonardo -- Yiu, Adelaide P -- De Cristofaro, Antonietta -- Hsiang, Hwa-Lin Liz -- Wheeler, Anne L -- Guskjolen, Axel -- Niibori, Yosuke -- Shoji, Hirotaka -- Ohira, Koji -- Richards, Blake A -- Miyakawa, Tsuyoshi -- Josselyn, Sheena A -- Frankland, Paul W -- MOP74650/Canadian Institutes of Health Research/Canada -- MOP86762/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2014 May 9;344(6184):598-602. doi: 10.1126/science.1248903.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24812394" target="_blank"〉PubMed〈/a〉
    Keywords: Amnesia/*pathology/*physiopathology ; Animals ; Dentate Gyrus/cytology ; Female ; Guinea Pigs ; Hippocampus/*cytology ; Male ; *Memory ; Mice ; Mice, Inbred C57BL ; *Neurogenesis ; Neurons/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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