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  • Articles  (20)
  • Amino Acid Sequence  (20)
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  • Articles  (20)
  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-04-01
    Description: Mechanosensory transduction underlies a wide range of senses, including proprioception, touch, balance, and hearing. The pivotal element of these senses is a mechanically gated ion channel that transduces sound, pressure, or movement into changes in excitability of specialized sensory cells. Despite the prevalence of mechanosensory systems, little is known about the molecular nature of the transduction channels. To identify such a channel, we analyzed Drosophila melanogaster mechanoreceptive mutants for defects in mechanosensory physiology. Loss-of-function mutations in the no mechanoreceptor potential C (nompC) gene virtually abolished mechanosensory signaling. nompC encodes a new ion channel that is essential for mechanosensory transduction. As expected for a transduction channel, D. melanogaster NOMPC and a Caenorhabditis elegans homolog were selectively expressed in mechanosensory organs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walker, R G -- Willingham, A T -- Zuker, C S -- 5T32GM08107/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2229-34.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Howard Hughes Medical Institute, University of California, San Diego,CA 92093-0649, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10744543" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Adaptation, Physiological ; Amino Acid Sequence ; Animals ; Caenorhabditis elegans/genetics/physiology ; Chromosome Mapping ; Cloning, Molecular ; Dendrites/physiology ; *Drosophila Proteins ; Drosophila melanogaster/genetics/*physiology ; Gene Expression Profiling ; Genes, Insect ; Hair Cells, Auditory/physiology ; Insect Proteins/chemistry/genetics/physiology ; Ion Channels/chemistry/*genetics/*physiology ; Mechanoreceptors/*physiology ; Molecular Sequence Data ; Mutation ; Neurons, Afferent/*physiology ; Patch-Clamp Techniques ; Physical Stimulation ; Proprioception ; Sensation/physiology ; Sense Organs/physiology ; Signal Transduction ; Touch ; Transient Receptor Potential Channels
    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
    Publication Date: 2008-10-10
    Description: Plasmodium knowlesi is an intracellular malaria parasite whose natural vertebrate host is Macaca fascicularis (the 'kra' monkey); however, it is now increasingly recognized as a significant cause of human malaria, particularly in southeast Asia. Plasmodium knowlesi was the first malaria parasite species in which antigenic variation was demonstrated, and it has a close phylogenetic relationship to Plasmodium vivax, the second most important species of human malaria parasite (reviewed in ref. 4). Despite their relatedness, there are important phenotypic differences between them, such as host blood cell preference, absence of a dormant liver stage or 'hypnozoite' in P. knowlesi, and length of the asexual cycle (reviewed in ref. 4). Here we present an analysis of the P. knowlesi (H strain, Pk1(A+) clone) nuclear genome sequence. This is the first monkey malaria parasite genome to be described, and it provides an opportunity for comparison with the recently completed P. vivax genome and other sequenced Plasmodium genomes. In contrast to other Plasmodium genomes, putative variant antigen families are dispersed throughout the genome and are associated with intrachromosomal telomere repeats. One of these families, the KIRs, contains sequences that collectively match over one-half of the host CD99 extracellular domain, which may represent an unusual form of molecular mimicry.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656934/" 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/PMC2656934/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pain, A -- Bohme, U -- Berry, A E -- Mungall, K -- Finn, R D -- Jackson, A P -- Mourier, T -- Mistry, J -- Pasini, E M -- Aslett, M A -- Balasubrammaniam, S -- Borgwardt, K -- Brooks, K -- Carret, C -- Carver, T J -- Cherevach, I -- Chillingworth, T -- Clark, T G -- Galinski, M R -- Hall, N -- Harper, D -- Harris, D -- Hauser, H -- Ivens, A -- Janssen, C S -- Keane, T -- Larke, N -- Lapp, S -- Marti, M -- Moule, S -- Meyer, I M -- Ormond, D -- Peters, N -- Sanders, M -- Sanders, S -- Sargeant, T J -- Simmonds, M -- Smith, F -- Squares, R -- Thurston, S -- Tivey, A R -- Walker, D -- White, B -- Zuiderwijk, E -- Churcher, C -- Quail, M A -- Cowman, A F -- Turner, C M R -- Rajandream, M A -- Kocken, C H M -- Thomas, A W -- Newbold, C I -- Barrell, B G -- Berriman, M -- 085775/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2008 Oct 9;455(7214):799-803. doi: 10.1038/nature07306.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Genome Campus, Hinxton, Cambridgeshire CB10 1SA, UK. ap2@sanger.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18843368" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD/chemistry/genetics ; Chromosomes/genetics ; Conserved Sequence ; Genes, Protozoan/genetics ; Genome, Protozoan/*genetics ; *Genomics ; Humans ; Macaca mulatta/*parasitology ; Malaria/*parasitology ; Molecular Sequence Data ; Plasmodium knowlesi/classification/*genetics/physiology ; Protein Structure, Tertiary ; Protozoan Proteins/chemistry/genetics ; Sequence Analysis, DNA ; Telomere/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2008-01-05
    Description: We used authentication tests developed for ancient DNA to evaluate claims by Asara et al. (Reports, 13 April 2007, p. 280) of collagen peptide sequences recovered from mastodon and Tyrannosaurus rex fossils. Although the mastodon samples pass these tests, absence of amino acid composition data, lack of evidence for peptide deamidation, and association of alpha1(I) collagen sequences with amphibians rather than birds suggest that T. rex does not.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2694913/" 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/PMC2694913/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buckley, Mike -- Walker, Angela -- Ho, Simon Y W -- Yang, Yue -- Smith, Colin -- Ashton, Peter -- Oates, Jane Thomas -- Cappellini, Enrico -- Koon, Hannah -- Penkman, Kirsty -- Elsworth, Ben -- Ashford, Dave -- Solazzo, Caroline -- Andrews, Phillip -- Strahler, John -- Shapiro, Beth -- Ostrom, Peggy -- Gandhi, Hasand -- Miller, Webb -- Raney, Brian -- Zylber, Maria Ines -- Gilbert, M Thomas P -- Prigodich, Richard V -- Ryan, Michael -- Rijsdijk, Kenneth F -- Janoo, Anwar -- Collins, Matthew J -- 076905/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Jan 4;319(5859):33; author reply 33. doi: 10.1126/science.1147046.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BioArch, Departments of Biology, Archaeology, Chemistry and Technology Facility, University of York, Post Office Box 373, York YO10 5YW, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18174420" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bone and Bones/*chemistry ; Collagen/*chemistry ; *Dinosaurs ; *Elephants ; *Fossils ; Mass Spectrometry ; Phylogeny
    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
    Publication Date: 2011-07-19
    Description: Passive transfer of broadly neutralizing HIV antibodies can prevent infection, which suggests that vaccines that elicit such antibodies would be protective. Thus far, however, few broadly neutralizing HIV antibodies that occur naturally have been characterized. To determine whether these antibodies are part of a larger group of related molecules, we cloned 576 new HIV antibodies from four unrelated individuals. All four individuals produced expanded clones of potent broadly neutralizing CD4-binding-site antibodies that mimic binding to CD4. Despite extensive hypermutation, the new antibodies shared a consensus sequence of 68 immunoglobulin H (IgH) chain amino acids and arise independently from two related IgH genes. Comparison of the crystal structure of one of the antibodies to the broadly neutralizing antibody VRC01 revealed conservation of the contacts to the HIV spike.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3351836/" 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/PMC3351836/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheid, Johannes F -- Mouquet, Hugo -- Ueberheide, Beatrix -- Diskin, Ron -- Klein, Florian -- Oliveira, Thiago Y K -- Pietzsch, John -- Fenyo, David -- Abadir, Alexander -- Velinzon, Klara -- Hurley, Arlene -- Myung, Sunnie -- Boulad, Farid -- Poignard, Pascal -- Burton, Dennis R -- Pereyra, Florencia -- Ho, David D -- Walker, Bruce D -- Seaman, Michael S -- Bjorkman, Pamela J -- Chait, Brian T -- Nussenzweig, Michel C -- P01 AI081677/AI/NIAID NIH HHS/ -- P30 AI060354/AI/NIAID NIH HHS/ -- R01 AI033292/AI/NIAID NIH HHS/ -- RR00862/RR/NCRR NIH HHS/ -- RR022220/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 16;333(6049):1633-7. doi: 10.1126/science.1207227. Epub 2011 Jul 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764753" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antibodies, Neutralizing/*chemistry/*immunology/metabolism ; Antibody Affinity ; Antibody Specificity ; Antigens, CD4/immunology/*metabolism ; Binding Sites ; Binding Sites, Antibody ; Cloning, Molecular ; Consensus Sequence ; Crystallography, X-Ray ; Genes, Immunoglobulin Heavy Chain ; HIV Antibodies/*chemistry/*immunology/metabolism ; HIV Envelope Protein gp120/chemistry/*immunology/metabolism ; HIV Infections/immunology ; Humans ; Immunoglobulin Fab Fragments/chemistry ; Immunoglobulin Heavy Chains/chemistry ; Immunoglobulin Light Chains/chemistry ; Molecular Mimicry ; Molecular Sequence Data ; Mutation ; Protein Conformation
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  • 5
    Publication Date: 2013-04-06
    Description: A variant upstream of human leukocyte antigen C (HLA-C) shows the most significant genome-wide effect on HIV control in European Americans and is also associated with the level of HLA-C expression. We characterized the differential cell surface expression levels of all common HLA-C allotypes and tested directly for effects of HLA-C expression on outcomes of HIV infection in 5243 individuals. Increasing HLA-C expression was associated with protection against multiple outcomes independently of individual HLA allelic effects in both African and European Americans, regardless of their distinct HLA-C frequencies and linkage relationships with HLA-B and HLA-A. Higher HLA-C expression was correlated with increased likelihood of cytotoxic T lymphocyte responses and frequency of viral escape mutation. In contrast, high HLA-C expression had a deleterious effect in Crohn's disease, suggesting a broader influence of HLA expression levels in human disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3784322/" 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/PMC3784322/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Apps, Richard -- Qi, Ying -- Carlson, Jonathan M -- Chen, Haoyan -- Gao, Xiaojiang -- Thomas, Rasmi -- Yuki, Yuko -- Del Prete, Greg Q -- Goulder, Philip -- Brumme, Zabrina L -- Brumme, Chanson J -- John, Mina -- Mallal, Simon -- Nelson, George -- Bosch, Ronald -- Heckerman, David -- Stein, Judy L -- Soderberg, Kelly A -- Moody, M Anthony -- Denny, Thomas N -- Zeng, Xue -- Fang, Jingyuan -- Moffett, Ashley -- Lifson, Jeffrey D -- Goedert, James J -- Buchbinder, Susan -- Kirk, Gregory D -- Fellay, Jacques -- McLaren, Paul -- Deeks, Steven G -- Pereyra, Florencia -- Walker, Bruce -- Michael, Nelson L -- Weintrob, Amy -- Wolinsky, Steven -- Liao, Wilson -- Carrington, Mary -- 5-M01-RR-00722/RR/NCRR NIH HHS/ -- HHSN261200800001E/CA/NCI NIH HHS/ -- HHSN261200800001E/PHS HHS/ -- K08 AR057763/AR/NIAMS NIH HHS/ -- K08AR057763/AR/NIAMS NIH HHS/ -- K24 AI069994/AI/NIAID NIH HHS/ -- K24AI069994/AI/NIAID NIH HHS/ -- N02-CP-55504/CP/NCI NIH HHS/ -- P30 AI027763/AI/NIAID NIH HHS/ -- P30 AI027767/AI/NIAID NIH HHS/ -- P30 AI027767-24/AI/NIAID NIH HHS/ -- P30 MH62246/MH/NIMH NIH HHS/ -- PG/09/077/27964/British Heart Foundation/United Kingdom -- R01 AI046995/AI/NIAID NIH HHS/ -- R01 AI060460/AI/NIAID NIH HHS/ -- R01 AI087145/AI/NIAID NIH HHS/ -- R01 AR065174/AR/NIAMS NIH HHS/ -- R01-AI046995/AI/NIAID NIH HHS/ -- R01-AI060460/AI/NIAID NIH HHS/ -- R01-DA-04334/DA/NIDA NIH HHS/ -- R01-DA-12568/DA/NIDA NIH HHS/ -- R01-DA04334/DA/NIDA NIH HHS/ -- R01-DA12568/DA/NIDA NIH HHS/ -- R24 AI067039/AI/NIAID NIH HHS/ -- U01-AI-067854/AI/NIAID NIH HHS/ -- U01-AI-35039/AI/NIAID NIH HHS/ -- U01-AI-35040/AI/NIAID NIH HHS/ -- U01-AI-35041/AI/NIAID NIH HHS/ -- U01-AI-35042/AI/NIAID NIH HHS/ -- U01-AI-35043/AI/NIAID NIH HHS/ -- U01-AI-37613/AI/NIAID NIH HHS/ -- U01-AI-37984/AI/NIAID NIH HHS/ -- UL1 RR024131/RR/NCRR NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2013 Apr 5;340(6128):87-91. doi: 10.1126/science.1232685.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer and Inflammation Program, Laboratory of Experimental Immunology, Science Applications International Corporation-Frederick, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23559252" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/genetics ; Alleles ; Amino Acid Sequence ; Anti-Retroviral Agents/therapeutic use ; Crohn Disease/genetics/immunology ; *Gene Expression Regulation ; HIV/genetics/*immunology ; HIV Infections/drug therapy/*genetics/*immunology ; HLA-C Antigens/*genetics ; Humans ; Immunodominant Epitopes/genetics ; Molecular Sequence Data ; Mutation ; Peptide Fragments/immunology ; Polymorphism, Single Nucleotide ; T-Lymphocytes, Cytotoxic/*immunology ; Viral Load/genetics
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  • 6
    Publication Date: 2013-01-05
    Description: The ubiquitin system regulates virtually all aspects of cellular function. We report a method to target the myriad enzymes that govern ubiquitination of protein substrates. We used massively diverse combinatorial libraries of ubiquitin variants to develop inhibitors of four deubiquitinases (DUBs) and analyzed the DUB-inhibitor complexes with crystallography. We extended the selection strategy to the ubiquitin conjugating (E2) and ubiquitin ligase (E3) enzymes and found that ubiquitin variants can also enhance enzyme activity. Last, we showed that ubiquitin variants can bind selectively to ubiquitin-binding domains. Ubiquitin variants exhibit selective function in cells and thus enable orthogonal modulation of specific enzymatic steps in the ubiquitin system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815447/" 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/PMC3815447/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ernst, Andreas -- Avvakumov, George -- Tong, Jiefei -- Fan, Yihui -- Zhao, Yanling -- Alberts, Philipp -- Persaud, Avinash -- Walker, John R -- Neculai, Ana-Mirela -- Neculai, Dante -- Vorobyov, Andrew -- Garg, Pankaj -- Beatty, Linda -- Chan, Pak-Kei -- Juang, Yu-Chi -- Landry, Marie-Claude -- Yeh, Christina -- Zeqiraj, Elton -- Karamboulas, Konstantina -- Allali-Hassani, Abdellah -- Vedadi, Masoud -- Tyers, Mike -- Moffat, Jason -- Sicheri, Frank -- Pelletier, Laurence -- Durocher, Daniel -- Raught, Brian -- Rotin, Daniela -- Yang, Jianhua -- Moran, Michael F -- Dhe-Paganon, Sirano -- Sidhu, Sachdev S -- 092076/Wellcome Trust/United Kingdom -- 092381/Wellcome Trust/United Kingdom -- 1R01NS072420-01/Canadian Institutes of Health Research/Canada -- MOP-102536/Canadian Institutes of Health Research/Canada -- MOP-111149/Canadian Institutes of Health Research/Canada -- MOP-13494/Canadian Institutes of Health Research/Canada -- MOP-57795/Canadian Institutes of Health Research/Canada -- R01 NS072420/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 1;339(6119):590-5. doi: 10.1126/science.1230161. Epub 2013 Jan 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Terrence Donnelly Center for Cellular and Biomolecular Research, University of Toronto, 160 College Street, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23287719" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Combinatorial Chemistry Techniques ; Conserved Sequence ; Drug Design ; Endopeptidases/chemistry/*metabolism ; HEK293 Cells ; Humans ; Molecular Sequence Data ; Protease Inhibitors/chemistry/*isolation & purification/pharmacology ; Protein Conformation ; Protein Structure, Secondary ; Small Molecule Libraries ; Ubiquitin/chemistry/genetics/*metabolism ; Ubiquitin Thiolesterase/chemistry/*metabolism ; Ubiquitin-Conjugating Enzymes/chemistry/metabolism ; Ubiquitin-Protein Ligases/chemistry/metabolism ; Ubiquitination/*drug effects
    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
    Publication Date: 1997-12-31
    Description: Virus-specific CD4+ T helper lymphocytes are critical to the maintenance of effective immunity in a number of chronic viral infections, but are characteristically undetectable in chronic human immunodeficiency virus-type 1 (HIV-1) infection. In individuals who control viremia in the absence of antiviral therapy, polyclonal, persistent, and vigorous HIV-1-specific CD4+ T cell proliferative responses were present, resulting in the elaboration of interferon-gamma and antiviral beta chemokines. In persons with chronic infection, HIV-1-specific proliferative responses to p24 were inversely related to viral load. Strong HIV-1-specific proliferative responses were also detected following treatment of acutely infected persons with potent antiviral therapy. The HIV-1-specific helper cells are likely to be important in immunotherapeutic interventions and vaccine development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenberg, E S -- Billingsley, J M -- Caliendo, A M -- Boswell, S L -- Sax, P E -- Kalams, S A -- Walker, B D -- F32-AI09738/AI/NIAID NIH HHS/ -- R01-A136550/PHS HHS/ -- R01-AI28568/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Nov 21;278(5342):1447-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Partners AIDS Research Center and Infectious Disease Unit, Massachusetts General Hospital, and Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9367954" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Anti-HIV Agents/therapeutic use ; Chemokines/biosynthesis ; Cohort Studies ; Cytotoxicity, Immunologic ; Disease Progression ; Drug Therapy, Combination ; HIV Core Protein p24/immunology ; HIV Envelope Protein gp160/immunology ; HIV Infections/drug therapy/*immunology/*virology ; HIV-1/*immunology/physiology ; Humans ; Immunologic Memory ; Interferon-gamma/biosynthesis ; Lymphocyte Activation ; Molecular Sequence Data ; Peptide Fragments/immunology ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Helper-Inducer/*immunology ; Viral Load ; Viremia/*immunology/virology ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 1997-08-15
    Description: Members of the recently recognized SRC-1 family of transcriptional coactivators interact with steroid hormone receptors to enhance ligand-dependent transcription. AIB1, a member of the SRC-1 family, was cloned during a search on the long arm of chromosome 20 for genes whose expression and copy number were elevated in human breast cancers. AIB1 amplification and overexpression were observed in four of five estrogen receptor-positive breast and ovarian cancer cell lines. Subsequent evaluation of 105 unselected specimens of primary breast cancer found AIB1 amplification in approximately 10 percent and high expression in 64 percent of the primary tumors analyzed. AIB1 protein interacted with estrogen receptors in a ligand-dependent fashion, and transfection of AIB1 resulted in enhancement of estrogen-dependent transcription. These observations identify AIB1 as a nuclear receptor coactivator whose altered expression may contribute to development of steroid-dependent cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anzick, S L -- Kononen, J -- Walker, R L -- Azorsa, D O -- Tanner, M M -- Guan, X Y -- Sauter, G -- Kallioniemi, O P -- Trent, J M -- Meltzer, P S -- New York, N.Y. -- Science. 1997 Aug 15;277(5328):965-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cancer Genetics, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9252329" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Breast/metabolism ; Breast Neoplasms/*genetics/metabolism ; Chromosomes, Human, Pair 20 ; Cloning, Molecular ; Estradiol/metabolism/pharmacology ; Female ; *Gene Amplification ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Histone Acetyltransferases ; Humans ; In Situ Hybridization, Fluorescence ; Ligands ; Molecular Sequence Data ; Neoplasms, Hormone-Dependent/*genetics/metabolism ; Nuclear Receptor Coactivator 1 ; Nuclear Receptor Coactivator 2 ; Ovarian Neoplasms/*genetics/metabolism ; Receptors, Estrogen/genetics/*metabolism ; Transcription Factors/genetics ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2004-04-17
    Description: Mitochondrial dysfunction is a hallmark of beta-amyloid (Abeta)-induced neuronal toxicity in Alzheimer's disease (AD). Here, we demonstrate that Abeta-binding alcohol dehydrogenase (ABAD) is a direct molecular link from Abeta to mitochondrial toxicity. Abeta interacts with ABAD in the mitochondria of AD patients and transgenic mice. The crystal structure of Abeta-bound ABAD shows substantial deformation of the active site that prevents nicotinamide adenine dinucleotide (NAD) binding. An ABAD peptide specifically inhibits ABAD-Abeta interaction and suppresses Abeta-induced apoptosis and free-radical generation in neurons. Transgenic mice overexpressing ABAD in an Abeta-rich environment manifest exaggerated neuronal oxidative stress and impaired memory. These data suggest that the ABAD-Abeta interaction may be a therapeutic target in AD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lustbader, Joyce W -- Cirilli, Maurizio -- Lin, Chang -- Xu, Hong Wei -- Takuma, Kazuhiro -- Wang, Ning -- Caspersen, Casper -- Chen, Xi -- Pollak, Susan -- Chaney, Michael -- Trinchese, Fabrizio -- Liu, Shumin -- Gunn-Moore, Frank -- Lue, Lih-Fen -- Walker, Douglas G -- Kuppusamy, Periannan -- Zewier, Zay L -- Arancio, Ottavio -- Stern, David -- Yan, Shirley ShiDu -- Wu, Hao -- 1K07AG00959/AG/NIA NIH HHS/ -- AG16736/AG/NIA NIH HHS/ -- AG17490/AG/NIA NIH HHS/ -- NS42855/NS/NINDS NIH HHS/ -- P50AG08702/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2004 Apr 16;304(5669):448-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Reproductive Sciences and Department of Obstetrics and Gynecology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15087549" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Hydroxyacyl CoA Dehydrogenases/chemistry/*metabolism ; Aged ; Aged, 80 and over ; Alzheimer Disease/*metabolism ; Amino Acid Sequence ; Amyloid beta-Peptides/chemistry/genetics/*metabolism ; Animals ; Binding Sites ; Brain/*metabolism ; Brain Chemistry ; Carrier Proteins/chemistry/*metabolism ; Cells, Cultured ; Cerebral Cortex/chemistry/metabolism ; Crystallization ; DNA Fragmentation ; Hippocampus/physiology ; Humans ; Learning ; Memory ; Mice ; Mice, Transgenic ; Microscopy, Confocal ; Microscopy, Immunoelectron ; Mitochondria/chemistry/*metabolism ; Models, Molecular ; Molecular Sequence Data ; Mutation ; NAD/metabolism ; Neurons/metabolism ; Protein Binding ; Protein Conformation ; Reactive Oxygen Species/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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  • 10
    Publication Date: 2003-10-25
    Description: Spontaneous resolution of hepatitis C virus (HCV) infection in humans usually affords long-term immunity to persistent viremia and associated liver diseases. Here, we report that memory CD4+ Tcells are essential for this protection. Antibody-mediated depletion of CD4+ Tcells before reinfection of two immune chimpanzees resulted in persistent, low-level viremia despite functional intra-hepatic memory CD8+ Tcell responses. Incomplete control of HCV replication by memory CD8+ Tcells in the absence of adequate CD4+ Tcell help was associated with emergence of viral escape mutations in class I major histocompatibility complex-restricted epitopes and failure to resolve HCV infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grakoui, Arash -- Shoukry, Naglaa H -- Woollard, David J -- Han, Jin-Hwan -- Hanson, Holly L -- Ghrayeb, John -- Murthy, Krishna K -- Rice, Charles M -- Walker, Christopher M -- A14736/PHS HHS/ -- AI40034/AI/NIAID NIH HHS/ -- AI48231/AI/NIAID NIH HHS/ -- CA57973/CA/NCI NIH HHS/ -- CA85883/CA/NCI NIH HHS/ -- N01 HB27091/HB/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 24;302(5645):659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Hepatitis C, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576438" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Antigen Presentation ; Antigens, Viral/chemistry/genetics/immunology ; CD4-Positive T-Lymphocytes/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Epitopes ; Evolution, Molecular ; Hepacivirus/genetics/*immunology/*physiology ; Hepatitis C/*immunology/virology ; *Immunologic Memory ; Liver/immunology ; Major Histocompatibility Complex ; Molecular Sequence Data ; Mutation ; Pan troglodytes ; T-Lymphocyte Subsets/immunology ; Time Factors ; Viral Core Proteins/chemistry/genetics/immunology ; Viral Nonstructural Proteins/chemistry/genetics/immunology ; Viremia ; Virus Replication
    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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