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  • 1
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    Construction and analysis of a human-chimpanzee comparative clone map (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-01-05
    Description: The recently released human genome sequences provide us with reference data to conduct comparative genomic research on primates, which will be important to understand what genetic information makes us human. Here we present a first-generation human-chimpanzee comparative genome map and its initial analysis. The map was constructed through paired alignment of 77,461 chimpanzee bacterial artificial chromosome end sequences with publicly available human genome sequences. We detected candidate positions, including two clusters on human chromosome 21 that suggest large, nonrandom regions of difference between the two genomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujiyama, Asao -- Watanabe, Hidemi -- Toyoda, Atsushi -- Taylor, Todd D -- Itoh, Takehiko -- Tsai, Shih-Feng -- Park, Hong-Seog -- Yaspo, Marie-Laure -- Lehrach, Hans -- Chen, Zhu -- Fu, Gang -- Saitou, Naruya -- Osoegawa, Kazutoyo -- de Jong, Pieter J -- Suto, Yumiko -- Hattori, Masahira -- Sakaki, Yoshiyuki -- New York, N.Y. -- Science. 2002 Jan 4;295(5552):131-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉RIKEN Genomic Sciences Center, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. afujiyam@gsc.riken.go.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11778049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosomes, Artificial, Bacterial ; Chromosomes, Human, Pair 21/genetics ; Cloning, Molecular ; Contig Mapping ; Female ; Gene Library ; *Genome ; *Genome, Human ; Humans ; Male ; Pan troglodytes/*genetics ; *Physical Chromosome Mapping ; Sequence Alignment ; Sequence Analysis, DNA ; Sequence Tagged Sites ; X Chromosome/genetics ; Y Chromosome/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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  • 2
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    A human genome diversity cell line panel (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cann, Howard M -- de Toma, Claudia -- Cazes, Lucien -- Legrand, Marie-Fernande -- Morel, Valerie -- Piouffre, Laurence -- Bodmer, Julia -- Bodmer, Walter F -- Bonne-Tamir, Batsheva -- Cambon-Thomsen, Anne -- Chen, Zhu -- Chu, J -- Carcassi, Carlo -- Contu, Licinio -- Du, Ruofu -- Excoffier, Laurent -- Ferrara, G B -- Friedlaender, Jonathan S -- Groot, Helena -- Gurwitz, David -- Jenkins, Trefor -- Herrera, Rene J -- Huang, Xiaoyi -- Kidd, Judith -- Kidd, Kenneth K -- Langaney, Andre -- Lin, Alice A -- Mehdi, S Qasim -- Parham, Peter -- Piazza, Alberto -- Pistillo, Maria Pia -- Qian, Yaping -- Shu, Qunfang -- Xu, Jiujin -- Zhu, S -- Weber, James L -- Greely, Henry T -- Feldman, Marcus W -- Thomas, Gilles -- Dausset, Jean -- Cavalli-Sforza, L Luca -- New York, N.Y. -- Science. 2002 Apr 12;296(5566):261-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11954565" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Specimen Banks ; *Cell Line ; Continental Population Groups/genetics ; DNA/genetics ; Databases, Factual ; Female ; *Genetic Variation ; *Genome, Human ; Haplotypes ; Humans ; Informed Consent ; *Lymphocytes ; Male ; Polymorphism, Single Nucleotide
    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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  • 3
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    African origin of modern humans in East Asia: a tale of 12,000 Y chromosomes (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-05-12
    Description: To test the hypotheses of modern human origin in East Asia, we sampled 12,127 male individuals from 163 populations and typed for three Y chromosome biallelic markers (YAP, M89, and M130). All the individuals carried a mutation at one of the three sites. These three mutations (YAP+, M89T, and M130T) coalesce to another mutation (M168T), which originated in Africa about 35,000 to 89,000 years ago. Therefore, the data do not support even a minimal in situ hominid contribution in the origin of anatomically modern humans in East Asia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ke, Y -- Su, B -- Song, X -- Lu, D -- Chen, L -- Li, H -- Qi, C -- Marzuki, S -- Deka, R -- Underhill, P -- Xiao, C -- Shriver, M -- Lell, J -- Wallace, D -- Wells, R S -- Seielstad, M -- Oefner, P -- Zhu, D -- Jin, J -- Huang, W -- Chakraborty, R -- Chen, Z -- Jin, L -- New York, N.Y. -- Science. 2001 May 11;292(5519):1151-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, 220 Handan Road, Shanghai, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11349147" target="_blank"〉PubMed〈/a〉
    Keywords: Africa/ethnology ; Alleles ; Asia ; Female ; Gene Frequency/genetics ; Haplotypes/genetics ; Humans ; Male ; Mutation/genetics ; Pacific Islands ; *Phylogeny ; Polymorphism, Genetic/genetics ; Population Density ; Y Chromosome/*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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  • 4
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    The changing face of HIV in China (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-10-04
    Description: HIV has advanced from high-risk groups such as intravenous drug users to some in the general population, according to comprehensive new data from the south of China. What needs to be done to halt its spread?〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Lin -- Jia, Manhong -- Ma, Yanling -- Yang, Li -- Chen, Zhiwei -- Ho, David D -- Jiang, Yan -- Zhang, Linqi -- England -- Nature. 2008 Oct 2;455(7213):609-11. doi: 10.1038/455609a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yunnan Center for Disease Control and Prevention, Yunnan, People's Republic of China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18833270" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; China/epidemiology ; Ethnic Groups/statistics & numerical data ; Female ; HIV Infections/*epidemiology/prevention & control/transmission/virology ; HIV-1/genetics ; Humans ; Male ; Pregnancy ; Prevalence ; Prostitution/statistics & numerical data ; Sentinel Surveillance ; Sex Ratio ; Substance Abuse, Intravenous/epidemiology
    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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  • 5
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    E2f1-3 switch from activators in progenitor cells to repressors in differentiating cells (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-12-18
    Description: In the established model of mammalian cell cycle control, the retinoblastoma protein (Rb) functions to restrict cells from entering S phase by binding and sequestering E2f activators (E2f1, E2f2 and E2f3), which are invariably portrayed as the ultimate effectors of a transcriptional program that commit cells to enter and progress through S phase. Using a panel of tissue-specific cre-transgenic mice and conditional E2f alleles we examined the effects of E2f1, E2f2 and E2f3 triple deficiency in murine embryonic stem cells, embryos and small intestines. We show that in normal dividing progenitor cells E2f1-3 function as transcriptional activators, but contrary to the current view, are dispensable for cell division and instead are necessary for cell survival. In differentiating cells E2f1-3 function in a complex with Rb as repressors to silence E2f targets and facilitate exit from the cell cycle. The inactivation of Rb in differentiating cells resulted in a switch of E2f1-3 from repressors to activators, leading to the superactivation of E2f responsive targets and ectopic cell divisions. Loss of E2f1-3 completely suppressed these phenotypes caused by Rb deficiency. This work contextualizes the activator versus repressor functions of E2f1-3 in vivo, revealing distinct roles in dividing versus differentiating cells and in normal versus cancer-like cell cycles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806193/" 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/PMC2806193/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chong, Jean-Leon -- Wenzel, Pamela L -- Saenz-Robles, M Teresa -- Nair, Vivek -- Ferrey, Antoney -- Hagan, John P -- Gomez, Yorman M -- Sharma, Nidhi -- Chen, Hui-Zi -- Ouseph, Madhu -- Wang, Shu-Huei -- Trikha, Prashant -- Culp, Brian -- Mezache, Louise -- Winton, Douglas J -- Sansom, Owen J -- Chen, Danian -- Bremner, Rod -- Cantalupo, Paul G -- Robinson, Michael L -- Pipas, James M -- Leone, Gustavo -- 5 T32 CA106196-04/CA/NCI NIH HHS/ -- CA098956/CA/NCI NIH HHS/ -- P01CA097189/CA/NCI NIH HHS/ -- R01 CA098956/CA/NCI NIH HHS/ -- R01 CA098956-06A2/CA/NCI NIH HHS/ -- R01CA82259/CA/NCI NIH HHS/ -- R01CA85619/CA/NCI NIH HHS/ -- R01HD04470/HD/NICHD NIH HHS/ -- England -- Nature. 2009 Dec 17;462(7275):930-4. doi: 10.1038/nature08677.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Virology, Immunology and Medical Genetics, College of Medicine, The Ohio State University, Columbus, Ohio 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016602" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Apoptosis ; Cell Cycle/genetics/physiology ; *Cell Differentiation ; Cell Proliferation ; E2F Transcription Factors/deficiency/genetics/*metabolism ; E2F1 Transcription Factor/deficiency/genetics/metabolism ; E2F2 Transcription Factor/deficiency/genetics/metabolism ; E2F3 Transcription Factor/deficiency/genetics/metabolism ; Embryo, Mammalian/cytology/metabolism ; Embryonic Stem Cells/*cytology/*metabolism ; Female ; *Gene Expression Regulation ; Intestine, Small/cytology/metabolism ; Mice ; Mice, Transgenic ; Repressor Proteins/deficiency/genetics/*metabolism ; Retinoblastoma Protein/deficiency/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Paired-end mapping reveals extensive structural variation in the human genome (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-29
    Description: Structural variation of the genome involves kilobase- to megabase-sized deletions, duplications, insertions, inversions, and complex combinations of rearrangements. We introduce high-throughput and massive paired-end mapping (PEM), a large-scale genome-sequencing method to identify structural variants (SVs) approximately 3 kilobases (kb) or larger that combines the rescue and capture of paired ends of 3-kb fragments, massive 454 sequencing, and a computational approach to map DNA reads onto a reference genome. PEM was used to map SVs in an African and in a putatively European individual and identified shared and divergent SVs relative to the reference genome. Overall, we fine-mapped more than 1000 SVs and documented that the number of SVs among humans is much larger than initially hypothesized; many of the SVs potentially affect gene function. The breakpoint junction sequences of more than 200 SVs were determined with a novel pooling strategy and computational analysis. Our analysis provided insights into the mechanisms of SV formation in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674581/" 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/PMC2674581/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korbel, Jan O -- Urban, Alexander Eckehart -- Affourtit, Jason P -- Godwin, Brian -- Grubert, Fabian -- Simons, Jan Fredrik -- Kim, Philip M -- Palejev, Dean -- Carriero, Nicholas J -- Du, Lei -- Taillon, Bruce E -- Chen, Zhoutao -- Tanzer, Andrea -- Saunders, A C Eugenia -- Chi, Jianxiang -- Yang, Fengtang -- Carter, Nigel P -- Hurles, Matthew E -- Weissman, Sherman M -- Harkins, Timothy T -- Gerstein, Mark B -- Egholm, Michael -- Snyder, Michael -- 077008/Wellcome Trust/United Kingdom -- 077014/Wellcome Trust/United Kingdom -- RR19895/RR/NCRR NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):420-6. Epub 2007 Sep 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biophysics and Biochemistry Department, Yale University, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17901297" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Inversion ; Chromosome Mapping ; Computational Biology ; Female ; Gene Fusion ; *Genetic Variation ; *Genome, Human ; Humans ; Mutagenesis, Insertional ; *Mutation ; Oligonucleotide Array Sequence Analysis ; Recombination, Genetic ; Repetitive Sequences, Nucleic Acid ; Retroelements ; Sequence Analysis, DNA ; Sequence Deletion
    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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  • 7
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    Rare structural variants disrupt multiple genes in neurodevelopmental pathways in schizophrenia (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-29
    Description: Schizophrenia is a devastating neurodevelopmental disorder whose genetic influences remain elusive. We hypothesize that individually rare structural variants contribute to the illness. Microdeletions and microduplications 〉100 kilobases were identified by microarray comparative genomic hybridization of genomic DNA from 150 individuals with schizophrenia and 268 ancestry-matched controls. All variants were validated by high-resolution platforms. Novel deletions and duplications of genes were present in 5% of controls versus 15% of cases and 20% of young-onset cases, both highly significant differences. The association was independently replicated in patients with childhood-onset schizophrenia as compared with their parents. Mutations in cases disrupted genes disproportionately from signaling networks controlling neurodevelopment, including neuregulin and glutamate pathways. These results suggest that multiple, individually rare mutations altering genes in neurodevelopmental pathways contribute to schizophrenia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walsh, Tom -- McClellan, Jon M -- McCarthy, Shane E -- Addington, Anjene M -- Pierce, Sarah B -- Cooper, Greg M -- Nord, Alex S -- Kusenda, Mary -- Malhotra, Dheeraj -- Bhandari, Abhishek -- Stray, Sunday M -- Rippey, Caitlin F -- Roccanova, Patricia -- Makarov, Vlad -- Lakshmi, B -- Findling, Robert L -- Sikich, Linmarie -- Stromberg, Thomas -- Merriman, Barry -- Gogtay, Nitin -- Butler, Philip -- Eckstrand, Kristen -- Noory, Laila -- Gochman, Peter -- Long, Robert -- Chen, Zugen -- Davis, Sean -- Baker, Carl -- Eichler, Evan E -- Meltzer, Paul S -- Nelson, Stanley F -- Singleton, Andrew B -- Lee, Ming K -- Rapoport, Judith L -- King, Mary-Claire -- Sebat, Jonathan -- HD043569/HD/NICHD NIH HHS/ -- M01 RR000046/RR/NCRR NIH HHS/ -- MH061355/MH/NIMH NIH HHS/ -- MH061464/MH/NIMH NIH HHS/ -- MH061528/MH/NIMH NIH HHS/ -- NS052108/NS/NINDS NIH HHS/ -- R01 HD043569/HD/NICHD NIH HHS/ -- RR000046/RR/NCRR NIH HHS/ -- RR025014/RR/NCRR NIH HHS/ -- U01 MH061355/MH/NIMH NIH HHS/ -- U01 MH061464/MH/NIMH NIH HHS/ -- U01 MH061528/MH/NIMH NIH HHS/ -- U24 NS052108/NS/NINDS NIH HHS/ -- UL1 RR025014/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):539-43. doi: 10.1126/science.1155174. Epub 2008 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369103" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Age of Onset ; Amino Acid Sequence ; Brain/cytology/*growth & development/metabolism ; Case-Control Studies ; Child ; Excitatory Amino Acid Transporter 1/chemistry/genetics/physiology ; Female ; *Gene Deletion ; *Gene Duplication ; Genetic Predisposition to Disease ; Genome, Human ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Neurons/cytology/physiology ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Receptor, Epidermal Growth Factor/chemistry/genetics/physiology ; Receptor, ErbB-4 ; Schizophrenia/*genetics/physiopathology ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 8
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    Projection of an immunological self shadow within the thymus by the aire protein (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-10-12
    Description: Humans expressing a defective form of the transcription factor AIRE (autoimmune regulator) develop multiorgan autoimmune disease. We used aire- deficient mice to test the hypothesis that this transcription factor regulates autoimmunity by promoting the ectopic expression of peripheral tissue- restricted antigens in medullary epithelial cells of the thymus. This hypothesis proved correct. The mutant animals exhibited a defined profile of autoimmune diseases that depended on the absence of aire in stromal cells of the thymus. Aire-deficient thymic medullary epithelial cells showed a specific reduction in ectopic transcription of genes encoding peripheral antigens. These findings highlight the importance of thymically imposed "central" tolerance in controlling autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, Mark S -- Venanzi, Emily S -- Klein, Ludger -- Chen, Zhibin -- Berzins, Stuart P -- Turley, Shannon J -- von Boehmer, Harald -- Bronson, Roderick -- Dierich, Andree -- Benoist, Christophe -- Mathis, Diane -- 2 P30 DK36836-16/DK/NIDDK NIH HHS/ -- 2T32 DK07260-26/DK/NIDDK NIH HHS/ -- KO8-DK59958-01A1/DK/NIDDK NIH HHS/ -- R01 DK60027-01/DK/NIDDK NIH HHS/ -- T32CA70083-05/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Nov 15;298(5597):1395-401. Epub 2002 Oct 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Immunology and Immunogenetics, Joslin Diabetes Center; Department of Medicine, Brigham and Women's Hospital; Harvard Medical School, 1 Joslin Place, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12376594" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Autoantibodies/analysis/blood ; Autoantigens/biosynthesis/genetics ; Autoimmune Diseases/genetics/immunology/metabolism ; Autoimmunity ; Epithelial Cells/physiology ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Targeting ; Humans ; Lymphocytes/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Polyendocrinopathies, Autoimmune/genetics/immunology/metabolism ; Radiation Chimera ; Reverse Transcriptase Polymerase Chain Reaction ; *Self Tolerance ; Stromal Cells/immunology/metabolism ; T-Lymphocytes/*immunology ; Thymus Gland/cytology/*immunology/*metabolism ; Transcription Factors/genetics/*metabolism
    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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  • 9
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    Axons guided by insulin receptor in Drosophila visual system (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-19
    Description: Insulin receptors are abundant in the central nervous system, but their roles remain elusive. Here we show that the insulin receptor functions in axon guidance. The Drosophila insulin receptor (DInR) is required for photoreceptor-cell (R-cell) axons to find their way from the retina to the brain during development of the visual system. DInR functions as a guidance receptor for the adapter protein Dock/Nck. This function is independent of Chico, the Drosophila insulin receptor substrate (IRS) homolog.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, Jianbo -- Wu, Lingling -- Chen, Zun -- Kohanski, Ronald A -- Pick, Leslie -- New York, N.Y. -- Science. 2003 Apr 18;300(5618):502-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brookdale Department for Molecular, Cell, and Developmental Biology, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702880" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Axons/*physiology ; Binding Sites ; Blotting, Western ; Brain/cytology/growth & development ; Carrier Proteins/genetics/immunology/metabolism/*physiology ; Cell Differentiation ; Cell Size ; Drosophila/genetics/*growth & development/physiology ; Drosophila Proteins/genetics/metabolism ; Eye/cytology/growth & development ; Female ; Growth Cones/physiology ; Insulin Receptor Substrate Proteins ; *Intracellular Signaling Peptides and Proteins ; Male ; Mutation ; Nerve Tissue Proteins/chemistry/genetics/metabolism ; Photoreceptor Cells, Invertebrate/cytology/*physiology ; Precipitin Tests ; Protein-Tyrosine Kinases/genetics/immunology/metabolism/*physiology ; *Receptor Protein-Tyrosine Kinases ; Receptor, Insulin/genetics/immunology/metabolism/*physiology ; Retina/cytology/growth & development ; Signal Transduction ; Two-Hybrid System Techniques ; Visual Pathways ; src Homology Domains
    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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  • 10
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    KCNQ1 gain-of-function mutation in familial atrial fibrillation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-11
    Description: Atrial fibrillation (AF) is a common cardiac arrhythmia whose molecular etiology is poorly understood. We studied a family with hereditary persistent AF and identified the causative mutation (S140G) in the KCNQ1 (KvLQT1) gene on chromosome 11p15.5. The KCNQ1 gene encodes the pore-forming alpha subunit of the cardiac I(Ks) channel (KCNQ1/KCNE1), the KCNQ1/KCNE2 and the KCNQ1/KCNE3 potassium channels. Functional analysis of the S140G mutant revealed a gain-of-function effect on the KCNQ1/KCNE1 and the KCNQ1/KCNE2 currents, which contrasts with the dominant negative or loss-of-function effects of the KCNQ1 mutations previously identified in patients with long QT syndrome. Thus, the S140G mutation is likely to initiate and maintain AF by reducing action potential duration and effective refractory period in atrial myocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Yi-Han -- Xu, Shi-Jie -- Bendahhou, Said -- Wang, Xiao-Liang -- Wang, Ying -- Xu, Wen-Yuan -- Jin, Hong-Wei -- Sun, Hao -- Su, Xiao-Yan -- Zhuang, Qi-Nan -- Yang, Yi-Qing -- Li, Yue-Bin -- Liu, Yi -- Xu, Hong-Ju -- Li, Xiao-Fei -- Ma, Ning -- Mou, Chun-Ping -- Chen, Zhu -- Barhanin, Jacques -- Huang, Wei -- New York, N.Y. -- Science. 2003 Jan 10;299(5604):251-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Tongji Hospital, and Institute of Medical Genetics, Tongji University, 399 Xin Cun Road, Shanghai 200065, People's Republic of China. drchen@public7.sta.net.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12522251" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Adolescent ; Adult ; Aged ; Animals ; Atrial Fibrillation/*genetics/physiopathology ; COS Cells ; Child ; China ; Chromosomes, Human, Pair 11/genetics ; Electrocardiography ; Female ; Haplotypes ; Heart Atria/physiopathology ; Heart Ventricles/physiopathology ; Humans ; KCNQ Potassium Channels ; KCNQ1 Potassium Channel ; Lod Score ; Long QT Syndrome/genetics/physiopathology ; Male ; Microsatellite Repeats ; Middle Aged ; Mutation ; *Mutation, Missense ; Myocytes, Cardiac/*physiology ; Patch-Clamp Techniques ; Pedigree ; Potassium Channels/*genetics/physiology ; *Potassium Channels, Voltage-Gated
    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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