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  • 1
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    Induction of self-tolerance in T cells but not B cells of transgenic mice expressing little self antigen (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: Self-tolerance to a transgene-encoded protein, hen egg lysozyme, was examined in the T and B cell repertoires of a series of lines of transgenic mice that expressed different serum concentrations of soluble lysozyme. T cells were tolerant in all lines in which lysozyme was expressed irrespective of the antigen concentration, whereas B cell tolerance did not occur when the serum lysozyme concentration was less than 1.5 nanograms per milliliter (0.1 nM). Induction of elevated transgene expression could restore B cell tolerance. These findings support the hypothesis that autoimmune disease may in some instances arise through a bypass of T cell tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adelstein, S -- Pritchard-Briscoe, H -- Anderson, T A -- Crosbie, J -- Gammon, G -- Loblay, R H -- Basten, A -- Goodnow, C C -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1223-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1900950" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Chickens ; Egg White ; Enzyme-Linked Immunosorbent Assay ; Female ; Fluorescein-5-isothiocyanate ; Fluoresceins ; Fluorescent Dyes ; *Immune Tolerance ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muramidase/blood/*genetics/immunology ; T-Lymphocytes/*immunology ; Thiocyanates
    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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    Linkage of early-onset familial breast cancer to chromosome 17q21 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-21
    Description: Human breast cancer is usually caused by genetic alterations of somatic cells of the breast, but occasionally, susceptibility to the disease is inherited. Mapping the genes responsible for inherited breast cancer may also allow the identification of early lesions that are critical for the development of breast cancer in the general population. Chromosome 17q21 appears to be the locale of a gene for inherited susceptibility to breast cancer in families with early-onset disease. Genetic analysis yields a lod score (logarithm of the likelihood ratio for linkage) of 5.98 for linkage of breast cancer susceptibility to D17S74 in early-onset families and negative lod scores in families with late-onset disease. Likelihood ratios in favor of linkage heterogeneity among families ranged between 2000:1 and greater than 10(6):1 on the basis of multipoint analysis of four loci in the region.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hall, J M -- Lee, M K -- Newman, B -- Morrow, J E -- Anderson, L A -- Huey, B -- King, M C -- CA27632/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1684-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Public Health, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270482" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/diagnosis/etiology/*genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 17 ; Female ; Humans ; Male ; Pedigree ; Polymorphism, Genetic ; Pregnancy ; Risk Factors
    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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    The evolution of sexes (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, A -- New York, N.Y. -- Science. 1992 Jul 17;257(5068):324-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1631551" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryonic and Fetal Development/genetics ; Female ; Gene Expression Regulation/genetics ; Humans ; Insulin-Like Growth Factor II/physiology ; Male ; Mice ; Paramecium ; Plants ; Reproduction/*genetics ; *Sex
    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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    The influence of CCL3L1 gene-containing segmental duplications on HIV-1/AIDS susceptibility (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-08
    Description: Segmental duplications in the human genome are selectively enriched for genes involved in immunity, although the phenotypic consequences for host defense are unknown. We show that there are significant interindividual and interpopulation differences in the copy number of a segmental duplication encompassing the gene encoding CCL3L1 (MIP-1alphaP), a potent human immunodeficiency virus-1 (HIV-1)-suppressive chemokine and ligand for the HIV coreceptor CCR5. Possession of a CCL3L1 copy number lower than the population average is associated with markedly enhanced HIV/acquired immunodeficiency syndrome (AIDS) susceptibility. This susceptibility is even greater in individuals who also possess disease-accelerating CCR5 genotypes. This relationship between CCL3L1 dose and altered HIV/AIDS susceptibility points to a central role for CCL3L1 in HIV/AIDS pathogenesis and indicates that differences in the dose of immune response genes may constitute a genetic basis for variable responses to infectious diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gonzalez, Enrique -- Kulkarni, Hemant -- Bolivar, Hector -- Mangano, Andrea -- Sanchez, Racquel -- Catano, Gabriel -- Nibbs, Robert J -- Freedman, Barry I -- Quinones, Marlon P -- Bamshad, Michael J -- Murthy, Krishna K -- Rovin, Brad H -- Bradley, William -- Clark, Robert A -- Anderson, Stephanie A -- O'connell, Robert J -- Agan, Brian K -- Ahuja, Seema S -- Bologna, Rosa -- Sen, Luisa -- Dolan, Matthew J -- Ahuja, Sunil K -- AI043279/AI/NIAID NIH HHS/ -- AI046326/AI/NIAID NIH HHS/ -- MH069270/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 4;307(5714):1434-40. Epub 2005 Jan 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Veterans Administration Research Center for AIDS and HIV-1 Infection, South Texas Veterans Health Care System, and Department of Medicine, University of Texas Health Science Center, San Antonio, TX 78229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15637236" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Animals ; Chemokines, CC/*genetics/metabolism ; Child ; Cohort Studies ; Continental Population Groups/genetics ; Disease Progression ; Ethnic Groups/genetics ; Female ; *Gene Dosage ; *Gene Duplication ; *Genetic Predisposition to Disease ; Genotype ; HIV Infections/epidemiology/*genetics/*immunology/virology ; *HIV-1/metabolism ; Humans ; Male ; Middle Aged ; Pan troglodytes/genetics ; Phenotype ; Public Health ; Receptors, CCR5/genetics/metabolism ; Selection, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    SEX DETERMINATION. A male-determining factor in the mosquito Aedes aegypti (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-05-23
    Description: Sex determination in the mosquito Aedes aegypti is governed by a dominant male-determining factor (M factor) located within a Y chromosome-like region called the M locus. Here, we show that an M-locus gene, Nix, functions as an M factor in A. aegypti. Nix exhibits persistent M linkage and early embryonic expression, two characteristics required of an M factor. Nix knockout with clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 resulted in largely feminized genetic males and the production of female isoforms of two key regulators of sexual differentiation: doublesex and fruitless. Ectopic expression of Nix resulted in genetic females with nearly complete male genitalia. Thus, Nix is both required and sufficient to initiate male development. This study provides a foundation for mosquito control strategies that convert female mosquitoes into harmless males.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hall, Andrew Brantley -- Basu, Sanjay -- Jiang, Xiaofang -- Qi, Yumin -- Timoshevskiy, Vladimir A -- Biedler, James K -- Sharakhova, Maria V -- Elahi, Rubayet -- Anderson, Michelle A E -- Chen, Xiao-Guang -- Sharakhov, Igor V -- Adelman, Zach N -- Tu, Zhijian -- AI113643/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2015 Jun 12;348(6240):1268-70. doi: 10.1126/science.aaa2850. Epub 2015 May 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Interdisciplinary PhD Program in Genetics, Bioinformatics, and Computational Biology, Virginia Polytechnic Institute and State University (Virginia Tech), Blacksburg, VA, USA. Department of Biochemistry, Virginia Tech, Blacksburg, VA, USA. Fralin Life Science Institute, Virginia Tech, Blacksburg, VA, USA. ; Fralin Life Science Institute, Virginia Tech, Blacksburg, VA, USA. Department of Entomology, Virginia Tech, Blacksburg, VA, USA. ; Department of Biochemistry, Virginia Tech, Blacksburg, VA, USA. Fralin Life Science Institute, Virginia Tech, Blacksburg, VA, USA. ; Department of Biochemistry, Virginia Tech, Blacksburg, VA, USA. ; School of Public Health and Tropical Medicine, Southern Medical University, Guangdong, People's Republic of China. ; Interdisciplinary PhD Program in Genetics, Bioinformatics, and Computational Biology, Virginia Polytechnic Institute and State University (Virginia Tech), Blacksburg, VA, USA. Fralin Life Science Institute, Virginia Tech, Blacksburg, VA, USA. Department of Entomology, Virginia Tech, Blacksburg, VA, USA. ; Interdisciplinary PhD Program in Genetics, Bioinformatics, and Computational Biology, Virginia Polytechnic Institute and State University (Virginia Tech), Blacksburg, VA, USA. Fralin Life Science Institute, Virginia Tech, Blacksburg, VA, USA. Department of Entomology, Virginia Tech, Blacksburg, VA, USA. jaketu@vt.edu zachadel@vt.edu. ; Interdisciplinary PhD Program in Genetics, Bioinformatics, and Computational Biology, Virginia Polytechnic Institute and State University (Virginia Tech), Blacksburg, VA, USA. Department of Biochemistry, Virginia Tech, Blacksburg, VA, USA. Fralin Life Science Institute, Virginia Tech, Blacksburg, VA, USA. jaketu@vt.edu zachadel@vt.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25999371" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/*genetics/*growth & development ; Animals ; Caspase 9 ; Clustered Regularly Interspaced Short Palindromic Repeats ; Female ; Gene Knockout Techniques ; *Genes, Insect ; *Genetic Loci ; Male ; Molecular Sequence Data ; Mosquito Control/methods ; Sex Determination Processes/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Astrocyte scar formation aids central nervous system axon regeneration (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-03-31
    Description: Transected axons fail to regrow in the mature central nervous system. Astrocytic scars are widely regarded as causal in this failure. Here, using three genetically targeted loss-of-function manipulations in adult mice, we show that preventing astrocyte scar formation, attenuating scar-forming astrocytes, or ablating chronic astrocytic scars all failed to result in spontaneous regrowth of transected corticospinal, sensory or serotonergic axons through severe spinal cord injury (SCI) lesions. By contrast, sustained local delivery via hydrogel depots of required axon-specific growth factors not present in SCI lesions, plus growth-activating priming injuries, stimulated robust, laminin-dependent sensory axon regrowth past scar-forming astrocytes and inhibitory molecules in SCI lesions. Preventing astrocytic scar formation significantly reduced this stimulated axon regrowth. RNA sequencing revealed that astrocytes and non-astrocyte cells in SCI lesions express multiple axon-growth-supporting molecules. Our findings show that contrary to the prevailing dogma, astrocyte scar formation aids rather than prevents central nervous system axon regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, Mark A -- Burda, Joshua E -- Ren, Yilong -- Ao, Yan -- O'Shea, Timothy M -- Kawaguchi, Riki -- Coppola, Giovanni -- Khakh, Baljit S -- Deming, Timothy J -- Sofroniew, Michael V -- MH099559A/MH/NIMH NIH HHS/ -- MH104069/MH/NIMH NIH HHS/ -- NS057624/NS/NINDS NIH HHS/ -- NS060677/NS/NINDS NIH HHS/ -- NS084030/NS/NINDS NIH HHS/ -- P30 NS062691/NS/NINDS NIH HHS/ -- England -- Nature. 2016 Apr 14;532(7598):195-200. doi: 10.1038/nature17623. Epub 2016 Mar 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095-1763, USA. ; Departments of Psychiatry and Neurology, David Geffen School of Medicine, University of California, Los Angeles, California 90095-1761, USA. ; Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095-1751, USA. ; Departments of Bioengineering, Chemistry and Biochemistry, University of California Los Angeles, Los Angeles, California 90095-1600, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27027288" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*pathology ; Axons/*physiology ; Central Nervous System/cytology/*pathology/*physiology ; Chondroitin Sulfate Proteoglycans/biosynthesis ; Cicatrix/*pathology/prevention & control ; Female ; Genomics ; Mice ; *Models, Biological ; *Nerve Regeneration ; Reproducibility of Results ; Spinal Cord Injuries/genetics/pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
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    DNA markers for nervous system diseases (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-09-21
    Description: Recombinant DNA technology has provided a vast new source of DNA markers displaying heritable sequence variation in humans. These markers can be used in family studies to identify the chromosomal location of defective genes causing nervous system disorders. The discovery of a DNA marker linked to Huntington's disease has opened new avenues of research into this disorder and may ultimately permit cloning and characterization of the defective gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gusella, J F -- Tanzi, R E -- Anderson, M A -- Hobbs, W -- Gibbons, K -- Raschtchian, R -- Gilliam, T C -- Wallace, M R -- Wexler, N S -- Conneally, P M -- NS16367/NS/NINDS NIH HHS/ -- NS20012/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1984 Sep 21;225(4668):1320-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089346" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Base Sequence ; Chromosome Mapping ; Cloning, Molecular ; DNA/*genetics ; DNA Restriction Enzymes ; *DNA, Recombinant ; Female ; *Genes ; *Genetic Linkage ; *Genetic Markers ; Genetic Vectors ; Humans ; Huntington Disease/*genetics ; Male ; Mutation ; Pedigree ; Phenotype ; Polymorphism, 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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