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In eukaryotic cells, sister DNA molecules remain physically connected from their production at S phase until their separation during anaphase. This cohesion is essential for the separation of sister chromatids to opposite poles of the cell at mitosis. It also permits chromosome segregation to take place long after duplication has been completed. Recent work has identified a multisubunit complex called cohesin that is essential for connecting sisters. Proteolytic cleavage of one of cohesin's subunits may trigger sister separation at the onset of anaphase. 相似文献
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Lazarides E 《Science (New York, N.Y.)》1986,234(4782):1448
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Scherer SW Cheung J MacDonald JR Osborne LR Nakabayashi K Herbrick JA Carson AR Parker-Katiraee L Skaug J Khaja R Zhang J Hudek AK Li M Haddad M Duggan GE Fernandez BA Kanematsu E Gentles S Christopoulos CC Choufani S Kwasnicka D Zheng XH Lai Z Nusskern D Zhang Q Gu Z Lu F Zeesman S Nowaczyk MJ Teshima I Chitayat D Shuman C Weksberg R Zackai EH Grebe TA Cox SR Kirkpatrick SJ Rahman N Friedman JM Heng HH Pelicci PG Lo-Coco F Belloni E Shaffer LG Pober B Morton CC Gusella JF Bruns GA Korf BR 《Science (New York, N.Y.)》2003,300(5620):767-772
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Interferon: clinical application of molecular biology 总被引:1,自引:0,他引:1
M Harris 《Science (New York, N.Y.)》1970,170(962):1068-1070
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Origins of molecular biology 总被引:1,自引:0,他引:1
E L Hess 《Science (New York, N.Y.)》1970,168(932):664-669
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Walsh J 《Science (New York, N.Y.)》1968,159(3816):718-721
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Pathogenesis of dengue: challenges to molecular biology 总被引:89,自引:0,他引:89
S B Halstead 《Science (New York, N.Y.)》1988,239(4839):476-481
Dengue viruses occur as four antigenically related but distinct serotypes transmitted to humans by Aedes aegypti mosquitoes. These viruses generally cause a benign syndrome, dengue fever, in the American and African tropics, and a severe syndrome, dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS), in Southeast Asian children. This severe syndrome, which recently has also been identified in children infected with the virus in Puerto Rico, is characterized by increased vascular permeability and abnormal hemostasis. It occurs in infants less than 1 year of age born to dengue-immune mothers and in children 1 year and older who are immune to one serotype of dengue virus and are experiencing infection with a second serotype. Dengue viruses replicate in cells of mononuclear phagocyte lineage, and subneutralizing concentrations of dengue antibody enhance dengue virus infection in these cells. This antibody-dependent enhancement of infection regulates dengue disease in human beings, although disease severity may also be controlled genetically, possibly by permitting and restricting the growth of virus in monocytes. Monoclonal antibodies show heterogeneous distribution of antigenic epitopes on dengue viruses. These epitopes serve to regulate disease: when antibodies to shared antigens partially neutralize heterotypic virus, infection and disease are dampened; enhancing antibodies alone result in heightened disease response. Further knowledge of the structure of dengue genomes should permit rapid advances in understanding the pathogenetic mechanisms of dengue. 相似文献
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Pennisi E 《Science (New York, N.Y.)》2005,308(5727):1401-1402
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Walt DR 《Science (New York, N.Y.)》2000,287(5452):451-452
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Luna E 《Science (New York, N.Y.)》1989,244(4909):1201-1202
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That was the molecular biology that was 总被引:2,自引:0,他引:2
G S Stent 《Science (New York, N.Y.)》1968,160(826):390-395
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J T Edsall 《Science (New York, N.Y.)》1970,170(955):349-351
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Kolata GB 《Science (New York, N.Y.)》1976,192(4240):645-647
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D Botstein 《Science (New York, N.Y.)》1986,232(4747):142-143