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  • Humans  (10)
  • Life and Medical Sciences
  • Polymer and Materials Science
  • American Association for the Advancement of Science (AAAS)  (10)
  • 2010-2014  (6)
  • 1995-1999  (4)
  • 1970-1974
Collection
Keywords
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Years
Year
  • 1
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    Unknown
    Report casts doubt Korean experiment (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, M -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):617, 619.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9988653" target="_blank"〉PubMed〈/a〉
    Keywords: Bioethics ; Cell Division ; *Cloning, Organism/legislation & jurisprudence ; Embryo Research ; *Embryo, Mammalian/cytology ; Ethical Review ; Government Regulation ; Humans ; Korea ; Nuclear Transfer Techniques ; Public Policy
    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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    Human cloning. Korean report sparks anger and inquiry (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, M -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):16-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917255" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Bioethics ; *Cloning, Organism ; Embryo Research ; Female ; Government Regulation ; Humans ; Korea ; Nuclear Transfer Techniques ; Research
    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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    Control of TRAIL-induced apoptosis by a family of signaling and decoy receptors (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: TRAIL (also called Apo2L) belongs to the tumor necrosis factor family, activates rapid apoptosis in tumor cells, and binds to the death-signaling receptor DR4. Two additional TRAIL receptors were identified. The receptor designated death receptor 5 (DR5) contained a cytoplasmic death domain and induced apoptosis much like DR4. The receptor designated decoy receptor 1 (DcR1) displayed properties of a glycophospholipid-anchored cell surface protein. DcR1 acted as a decoy receptor that inhibited TRAIL signaling. Thus, a cell surface mechanism exists for the regulation of cellular responsiveness to pro-apoptotic stimuli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheridan, J P -- Marsters, S A -- Pitti, R M -- Gurney, A -- Skubatch, M -- Baldwin, D -- Ramakrishnan, L -- Gray, C L -- Baker, K -- Wood, W I -- Goddard, A D -- Godowski, P -- Ashkenazi, A -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, South San Francisco, CA 94080-4918, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242611" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Apoptosis ; Apoptosis Regulatory Proteins ; Cell Membrane/metabolism ; Cells, Cultured ; GPI-Linked Proteins ; Glycosylphosphatidylinositols/metabolism ; HeLa Cells ; Humans ; Ligands ; Membrane Glycoproteins/*metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha/*metabolism
    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 major genetic determinants of HIV-1 control affect HLA class I peptide presentation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-06
    Description: Infectious and inflammatory diseases have repeatedly shown strong genetic associations within the major histocompatibility complex (MHC); however, the basis for these associations remains elusive. To define host genetic effects on the outcome of a chronic viral infection, we performed genome-wide association analysis in a multiethnic cohort of HIV-1 controllers and progressors, and we analyzed the effects of individual amino acids within the classical human leukocyte antigen (HLA) proteins. We identified 〉300 genome-wide significant single-nucleotide polymorphisms (SNPs) within the MHC and none elsewhere. Specific amino acids in the HLA-B peptide binding groove, as well as an independent HLA-C effect, explain the SNP associations and reconcile both protective and risk HLA alleles. These results implicate the nature of the HLA-viral peptide interaction as the major factor modulating durable control of HIV infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235490/" 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/PMC3235490/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉International HIV Controllers Study -- Pereyra, Florencia -- Jia, Xiaoming -- McLaren, Paul J -- Telenti, Amalio -- de Bakker, Paul I W -- Walker, Bruce D -- Ripke, Stephan -- Brumme, Chanson J -- Pulit, Sara L -- Carrington, Mary -- Kadie, Carl M -- Carlson, Jonathan M -- Heckerman, David -- Graham, Robert R -- Plenge, Robert M -- Deeks, Steven G -- Gianniny, Lauren -- Crawford, Gabriel -- Sullivan, Jordan -- Gonzalez, Elena -- Davies, Leela -- Camargo, Amy -- Moore, Jamie M -- Beattie, Nicole -- Gupta, Supriya -- Crenshaw, Andrew -- Burtt, Noel P -- Guiducci, Candace -- Gupta, Namrata -- Gao, Xiaojiang -- Qi, Ying -- Yuki, Yuko -- Piechocka-Trocha, Alicja -- Cutrell, Emily -- Rosenberg, Rachel -- Moss, Kristin L -- Lemay, Paul -- O'Leary, Jessica -- Schaefer, Todd -- Verma, Pranshu -- Toth, Ildiko -- Block, Brian -- Baker, Brett -- Rothchild, Alissa -- Lian, Jeffrey -- Proudfoot, Jacqueline -- Alvino, Donna Marie L -- Vine, Seanna -- Addo, Marylyn M -- Allen, Todd M -- Altfeld, Marcus -- Henn, Matthew R -- Le Gall, Sylvie -- Streeck, Hendrik -- Haas, David W -- Kuritzkes, Daniel R -- Robbins, Gregory K -- Shafer, Robert W -- Gulick, Roy M -- Shikuma, Cecilia M -- Haubrich, Richard -- Riddler, Sharon -- Sax, Paul E -- Daar, Eric S -- Ribaudo, Heather J -- Agan, Brian -- Agarwal, Shanu -- Ahern, Richard L -- Allen, Brady L -- Altidor, Sherly -- Altschuler, Eric L -- Ambardar, Sujata -- Anastos, Kathryn -- Anderson, Ben -- Anderson, Val -- Andrady, Ushan -- Antoniskis, Diana -- Bangsberg, David -- Barbaro, Daniel -- Barrie, William -- Bartczak, J -- Barton, Simon -- Basden, Patricia -- Basgoz, Nesli -- Bazner, Suzane -- Bellos, Nicholaos C -- Benson, Anne M -- Berger, Judith -- Bernard, Nicole F -- Bernard, Annette M -- Birch, Christopher -- Bodner, Stanley J -- Bolan, Robert K -- Boudreaux, Emilie T -- Bradley, Meg -- Braun, James F -- Brndjar, Jon E -- Brown, Stephen J -- Brown, Katherine -- Brown, Sheldon T -- Burack, Jedidiah -- Bush, Larry M -- Cafaro, Virginia -- Campbell, Omobolaji -- Campbell, John -- Carlson, Robert H -- Carmichael, J Kevin -- Casey, Kathleen K -- Cavacuiti, Chris -- Celestin, Gregory -- Chambers, Steven T -- Chez, Nancy -- Chirch, Lisa M -- Cimoch, Paul J -- Cohen, Daniel -- Cohn, Lillian E -- Conway, Brian -- Cooper, David A -- Cornelson, Brian -- Cox, David T -- Cristofano, Michael V -- Cuchural, George Jr -- Czartoski, Julie L -- Dahman, Joseph M -- Daly, Jennifer S -- Davis, Benjamin T -- Davis, Kristine -- Davod, Sheila M -- DeJesus, Edwin -- Dietz, Craig A -- Dunham, Eleanor -- Dunn, Michael E -- Ellerin, Todd B -- Eron, Joseph J -- Fangman, John J W -- Farel, Claire E -- Ferlazzo, Helen -- Fidler, Sarah -- Fleenor-Ford, Anita -- Frankel, Renee -- Freedberg, Kenneth A -- French, Neel K -- Fuchs, Jonathan D -- Fuller, Jon D -- Gaberman, Jonna -- Gallant, Joel E -- Gandhi, Rajesh T -- Garcia, Efrain -- Garmon, Donald -- Gathe, Joseph C Jr -- Gaultier, Cyril R -- Gebre, Wondwoosen -- Gilman, Frank D -- Gilson, Ian -- Goepfert, Paul A -- Gottlieb, Michael S -- Goulston, Claudia -- Groger, Richard K -- Gurley, T Douglas -- Haber, Stuart -- Hardwicke, Robin -- Hardy, W David -- Harrigan, P Richard -- Hawkins, Trevor N -- Heath, Sonya -- Hecht, Frederick M -- Henry, W Keith -- Hladek, Melissa -- Hoffman, Robert P -- Horton, James M -- Hsu, Ricky K -- Huhn, Gregory D -- Hunt, Peter -- Hupert, Mark J -- Illeman, Mark L -- Jaeger, Hans -- Jellinger, Robert M -- John, Mina -- Johnson, Jennifer A -- Johnson, Kristin L -- Johnson, Heather -- Johnson, Kay -- Joly, Jennifer -- Jordan, Wilbert C -- Kauffman, Carol A -- Khanlou, Homayoon -- Killian, Robert K -- Kim, Arthur Y -- Kim, David D -- Kinder, Clifford A -- Kirchner, Jeffrey T -- Kogelman, Laura -- Kojic, Erna Milunka -- Korthuis, P Todd -- Kurisu, Wayne -- Kwon, Douglas S -- LaMar, Melissa -- Lampiris, Harry -- Lanzafame, Massimiliano -- Lederman, Michael M -- Lee, David M -- Lee, Jean M L -- Lee, Marah J -- Lee, Edward T Y -- Lemoine, Janice -- Levy, Jay A -- Llibre, Josep M -- Liguori, Michael A -- Little, Susan J -- Liu, Anne Y -- Lopez, Alvaro J -- Loutfy, Mono R -- Loy, Dawn -- Mohammed, Debbie Y -- Man, Alan -- Mansour, Michael K -- Marconi, Vincent C -- Markowitz, Martin -- Marques, Rui -- Martin, Jeffrey N -- Martin, Harold L Jr -- Mayer, Kenneth Hugh -- McElrath, M Juliana -- McGhee, Theresa A -- McGovern, Barbara H -- McGowan, Katherine -- McIntyre, Dawn -- Mcleod, Gavin X -- Menezes, Prema -- Mesa, Greg -- Metroka, Craig E -- Meyer-Olson, Dirk -- Miller, Andy O -- Montgomery, Kate -- Mounzer, Karam C -- Nagami, Ellen H -- Nagin, Iris -- Nahass, Ronald G -- Nelson, Margret O -- Nielsen, Craig -- Norene, David L -- O'Connor, David H -- Ojikutu, Bisola O -- Okulicz, Jason -- Oladehin, Olakunle O -- Oldfield, Edward C 3rd -- Olender, Susan A -- Ostrowski, Mario -- Owen, William F Jr -- Pae, Eunice -- Parsonnet, Jeffrey -- Pavlatos, Andrew M -- Perlmutter, Aaron M -- Pierce, Michael N -- Pincus, Jonathan M -- Pisani, Leandro -- Price, Lawrence Jay -- Proia, Laurie -- Prokesch, Richard C -- Pujet, Heather Calderon -- Ramgopal, Moti -- Rathod, Almas -- Rausch, Michael -- Ravishankar, J -- Rhame, Frank S -- Richards, Constance Shamuyarira -- Richman, Douglas D -- Rodes, Berta -- Rodriguez, Milagros -- Rose, Richard C 3rd -- Rosenberg, Eric S -- Rosenthal, Daniel -- Ross, Polly E -- Rubin, David S -- Rumbaugh, Elease -- Saenz, Luis -- Salvaggio, Michelle R -- Sanchez, William C -- Sanjana, Veeraf M -- Santiago, Steven -- Schmidt, Wolfgang -- Schuitemaker, Hanneke -- Sestak, Philip M -- Shalit, Peter -- Shay, William -- Shirvani, Vivian N -- Silebi, Vanessa I -- Sizemore, James M Jr -- Skolnik, Paul R -- Sokol-Anderson, Marcia -- Sosman, James M -- Stabile, Paul -- Stapleton, Jack T -- Starrett, Sheree -- Stein, Francine -- Stellbrink, Hans-Jurgen -- Sterman, F Lisa -- Stone, Valerie E -- Stone, David R -- Tambussi, Giuseppe -- Taplitz, Randy A -- Tedaldi, Ellen M -- Theisen, William -- Torres, Richard -- Tosiello, Lorraine -- Tremblay, Cecile -- Tribble, Marc A -- Trinh, Phuong D -- Tsao, Alice -- Ueda, Peggy -- Vaccaro, Anthony -- Valadas, Emilia -- Vanig, Thanes J -- Vecino, Isabel -- Vega, Vilma M -- Veikley, Wenoah -- Wade, Barbara H -- Walworth, Charles -- Wanidworanun, Chingchai -- Ward, Douglas J -- Warner, Daniel A -- Weber, Robert D -- Webster, Duncan -- Weis, Steve -- Wheeler, David A -- White, David J -- Wilkins, Ed -- Winston, Alan -- Wlodaver, Clifford G -- van't Wout, Angelique -- Wright, David P -- Yang, Otto O -- Yurdin, David L -- Zabukovic, Brandon W -- Zachary, Kimon C -- Zeeman, Beth -- Zhao, Meng -- AI030914/AI/NIAID NIH HHS/ -- AI068636/AI/NIAID NIH HHS/ -- AI069415/AI/NIAID NIH HHS/ -- AI069419/AI/NIAID NIH HHS/ -- AI069423/AI/NIAID NIH HHS/ -- AI069424/AI/NIAID NIH HHS/ -- AI069428/AI/NIAID NIH HHS/ -- AI069432/AI/NIAID NIH HHS/ -- AI069434/AI/NIAID NIH HHS/ -- AI069450/AI/NIAID NIH HHS/ -- AI069452/AI/NIAID NIH HHS/ -- AI069465/AI/NIAID NIH HHS/ -- AI069471/AI/NIAID NIH HHS/ -- AI069472/AI/NIAID NIH HHS/ -- AI069474/AI/NIAID NIH HHS/ -- AI069477/AI/NIAID NIH HHS/ -- AI069484/AI/NIAID NIH HHS/ -- AI069495/AI/NIAID NIH HHS/ -- AI069501/AI/NIAID NIH HHS/ -- AI069502/AI/NIAID NIH HHS/ -- AI069511/AI/NIAID NIH HHS/ -- AI069513/AI/NIAID NIH HHS/ -- AI069532/AI/NIAID NIH HHS/ -- AI069556/AI/NIAID NIH HHS/ -- AI077505/AI/NIAID NIH HHS/ -- AI087145/AI/NIAID NIH HHS/ -- AI25859/AI/NIAID NIH HHS/ -- AI27661/AI/NIAID NIH HHS/ -- AI28568/AI/NIAID NIH HHS/ -- AI30914/AI/NIAID NIH HHS/ -- AI34835/AI/NIAID NIH HHS/ -- AI34853/AI/NIAID NIH HHS/ -- AI38844/AI/NIAID NIH HHS/ -- AI46370/AI/NIAID NIH HHS/ -- AI68634/AI/NIAID NIH HHS/ -- AI69467/AI/NIAID NIH HHS/ -- AL32782/PHS HHS/ -- HHSN261200800001E/PHS HHS/ -- K23 DA019809/DA/NIDA NIH HHS/ -- K24 AI051966/AI/NIAID NIH HHS/ -- K24 AI064086/AI/NIAID NIH HHS/ -- K24 AI064086-05/AI/NIAID NIH HHS/ -- K24 AI069994/AI/NIAID NIH HHS/ -- K24 AI069994-04/AI/NIAID NIH HHS/ -- K24 AI069994-05/AI/NIAID NIH HHS/ -- K24AI069994/AI/NIAID NIH HHS/ -- KL2 RR024977/RR/NCRR NIH HHS/ -- MH071205/MH/NIMH NIH HHS/ -- MH085520/MH/NIMH NIH HHS/ -- P-30 AI27763/AI/NIAID NIH HHS/ -- P-30-AI060354/AI/NIAID NIH HHS/ -- P30 AI027763/AI/NIAID NIH HHS/ -- P30 AI027763-19/AI/NIAID NIH HHS/ -- P30 AI027763-20/AI/NIAID NIH HHS/ -- P30 AI050410/AI/NIAID NIH HHS/ -- P30 AI060354/AI/NIAID NIH HHS/ -- P30 AI060354-08/AI/NIAID NIH HHS/ -- P30 AI060354-09/AI/NIAID NIH HHS/ -- R01 AI028568/AI/NIAID NIH HHS/ -- R01 AI028568-18/AI/NIAID NIH HHS/ -- R01 AI028568-19/AI/NIAID NIH HHS/ -- R01 AI028568-20/AI/NIAID NIH HHS/ -- R01 AI030914/AI/NIAID NIH HHS/ -- R01 AI030914-16/AI/NIAID NIH HHS/ -- R01 AI030914-17/AI/NIAID NIH HHS/ -- R01 AI077505/AI/NIAID NIH HHS/ -- R01 AI077505-04/AI/NIAID NIH HHS/ -- R01 AI077505-05/AI/NIAID NIH HHS/ -- R01 AI087145/AI/NIAID NIH HHS/ -- R01 AI087145-01/AI/NIAID NIH HHS/ -- R01 AI087145-02/AI/NIAID NIH HHS/ -- R01 MH054907/MH/NIMH NIH HHS/ -- R01 MH071205/MH/NIMH NIH HHS/ -- R01 MH071205-04/MH/NIMH NIH HHS/ -- R01 MH071205-05/MH/NIMH NIH HHS/ -- R24 AI067039/AI/NIAID NIH HHS/ -- R24 AI067039-06/AI/NIAID NIH HHS/ -- R24 AI067039-07/AI/NIAID NIH HHS/ -- R37 AI028568/AI/NIAID NIH HHS/ -- R37 AI028568-15/AI/NIAID NIH HHS/ -- RR024975/RR/NCRR NIH HHS/ -- T32 AI007061/AI/NIAID NIH HHS/ -- TL1 RR024978/RR/NCRR NIH HHS/ -- U01 AI027661-18/AI/NIAID NIH HHS/ -- U01 AI027661-19/AI/NIAID NIH HHS/ -- U01 AI032782-13/AI/NIAID NIH HHS/ -- U01 AI034835-07/AI/NIAID NIH HHS/ -- U01 AI034835-07S3/AI/NIAID NIH HHS/ -- U01 AI034853/AI/NIAID NIH HHS/ -- U01 AI034853-11/AI/NIAID NIH HHS/ -- U01 AI034853-12/AI/NIAID NIH HHS/ -- U01 AI038844-04/AI/NIAID NIH HHS/ -- U01 AI038844-04S1/AI/NIAID NIH HHS/ -- U01 AI038844-04S2/AI/NIAID NIH HHS/ -- U01 AI038844-04S3/AI/NIAID NIH HHS/ -- U01 AI046370-04/AI/NIAID NIH HHS/ -- U01 AI046370-05/AI/NIAID NIH HHS/ -- U01 AI069419/AI/NIAID NIH HHS/ -- U01 AI069419-05/AI/NIAID NIH HHS/ -- U01 AI069419-06/AI/NIAID NIH HHS/ -- U01 AI069423/AI/NIAID NIH HHS/ -- U01 AI069423-05/AI/NIAID NIH HHS/ -- U01 AI069423-06/AI/NIAID NIH HHS/ -- U01 AI069424/AI/NIAID NIH HHS/ -- U01 AI069424-05/AI/NIAID NIH HHS/ -- U01 AI069424-06/AI/NIAID NIH HHS/ -- U01 AI069428/AI/NIAID NIH HHS/ -- U01 AI069428-05/AI/NIAID NIH HHS/ -- U01 AI069428-06/AI/NIAID NIH HHS/ -- U01 AI069432/AI/NIAID NIH HHS/ -- U01 AI069432-05/AI/NIAID NIH HHS/ -- U01 AI069432-06/AI/NIAID NIH HHS/ -- U01 AI069434/AI/NIAID NIH HHS/ -- U01 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HHS/ -- U01 AI069484-06/AI/NIAID NIH HHS/ -- U01 AI069495/AI/NIAID NIH HHS/ -- U01 AI069495-05/AI/NIAID NIH HHS/ -- U01 AI069495-06/AI/NIAID NIH HHS/ -- U01 AI069501/AI/NIAID NIH HHS/ -- U01 AI069501-05/AI/NIAID NIH HHS/ -- U01 AI069501-06/AI/NIAID NIH HHS/ -- U01 AI069502/AI/NIAID NIH HHS/ -- U01 AI069502-05/AI/NIAID NIH HHS/ -- U01 AI069502-06/AI/NIAID NIH HHS/ -- U01 AI069511/AI/NIAID NIH HHS/ -- U01 AI069511-05/AI/NIAID NIH HHS/ -- U01 AI069511-06/AI/NIAID NIH HHS/ -- U01 AI069513-05/AI/NIAID NIH HHS/ -- U01 AI069513-06/AI/NIAID NIH HHS/ -- U01 AI069532/AI/NIAID NIH HHS/ -- U01 AI069532-05/AI/NIAID NIH HHS/ -- U01 AI069532-06/AI/NIAID NIH HHS/ -- U01 AI069556-05/AI/NIAID NIH HHS/ -- U01 AI069556-06/AI/NIAID NIH HHS/ -- U01 MH085520/MH/NIMH NIH HHS/ -- U01 MH085520-01/MH/NIMH NIH HHS/ -- UL1 RR024131/RR/NCRR NIH HHS/ -- UL1 RR024131-06/RR/NCRR NIH HHS/ -- UL1 RR024131-07/RR/NCRR NIH HHS/ -- UL1 RR024975/RR/NCRR NIH HHS/ -- UL1 RR024975-04/RR/NCRR NIH HHS/ -- UL1 RR024975-05/RR/NCRR NIH HHS/ -- UM1 AI068634/AI/NIAID NIH HHS/ -- UM1 AI068634-06/AI/NIAID NIH HHS/ -- UM1 AI068634-07/AI/NIAID NIH HHS/ -- UM1 AI068636-06/AI/NIAID NIH HHS/ -- UM1 AI068636-07/AI/NIAID NIH HHS/ -- UM1 AI069477/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 10;330(6010):1551-7. doi: 10.1126/science.1195271. Epub 2010 Nov 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology (MIT) and Harvard, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21051598" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/genetics ; Alleles ; Amino Acids/physiology ; *Antigen Presentation ; CD8-Positive T-Lymphocytes/immunology ; Cohort Studies ; Disease Progression ; European Continental Ancestry Group/genetics ; *Genes, MHC Class I ; Genome-Wide Association Study ; HIV Antigens/immunology ; HIV Infections/ethnology/*genetics/*immunology/virology ; HIV Long-Term Survivors ; *HIV-1/immunology ; HLA-A Antigens/chemistry/genetics/immunology/metabolism ; HLA-B Antigens/chemistry/*genetics/immunology/metabolism ; HLA-C Antigens/chemistry/genetics/immunology/metabolism ; Haplotypes ; Hispanic Americans/genetics ; Humans ; Immunity, Innate ; Logistic Models ; Models, Molecular ; Polymorphism, Single Nucleotide ; Protein Conformation ; Viral Load
    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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  • 5
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    Rapid pneumococcal evolution in response to clinical interventions (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-29
    Description: Epidemiological studies of the naturally transformable bacterial pathogen Streptococcus pneumoniae have previously been confounded by high rates of recombination. Sequencing 240 isolates of the PMEN1 (Spain(23F)-1) multidrug-resistant lineage enabled base substitutions to be distinguished from polymorphisms arising through horizontal sequence transfer. More than 700 recombinations were detected, with genes encoding major antigens frequently affected. Among these were 10 capsule-switching events, one of which accompanied a population shift as vaccine-escape serotype 19A isolates emerged in the USA after the introduction of the conjugate polysaccharide vaccine. The evolution of resistance to fluoroquinolones, rifampicin, and macrolides was observed to occur on multiple occasions. This study details how genomic plasticity within lineages of recombinogenic bacteria can permit adaptation to clinical interventions over remarkably short time scales.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648787/" 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/PMC3648787/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Croucher, Nicholas J -- Harris, Simon R -- Fraser, Christophe -- Quail, Michael A -- Burton, John -- van der Linden, Mark -- McGee, Lesley -- von Gottberg, Anne -- Song, Jae Hoon -- Ko, Kwan Soo -- Pichon, Bruno -- Baker, Stephen -- Parry, Christopher M -- Lambertsen, Lotte M -- Shahinas, Dea -- Pillai, Dylan R -- Mitchell, Timothy J -- Dougan, Gordon -- Tomasz, Alexander -- Klugman, Keith P -- Parkhill, Julian -- Hanage, William P -- Bentley, Stephen D -- 076962/Wellcome Trust/United Kingdom -- 076964/Wellcome Trust/United Kingdom -- G0800596/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):430-4. doi: 10.1126/science.1198545.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21273480" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Anti-Bacterial Agents/pharmacology ; Antigenic Variation ; DNA Transposable Elements ; Drug Resistance, Multiple, Bacterial ; *Evolution, Molecular ; Genome, Bacterial ; Humans ; Molecular Epidemiology ; Phylogeny ; Phylogeography ; Pneumococcal Infections/drug therapy/*microbiology ; Pneumococcal Vaccines/immunology ; Polymorphism, Single Nucleotide ; Prophages/genetics ; *Recombination, Genetic ; Selection, Genetic ; Serotyping ; Streptococcus Phages/genetics ; Streptococcus pneumoniae/classification/drug effects/*genetics/immunology
    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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  • 6
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    A Burkholderia pseudomallei toxin inhibits helicase activity of translation factor eIF4A (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-15
    Description: The structure of BPSL1549, a protein of unknown function from Burkholderia pseudomallei, reveals a similarity to Escherichia coli cytotoxic necrotizing factor 1. We found that BPSL1549 acted as a potent cytotoxin against eukaryotic cells and was lethal when administered to mice. Expression levels of bpsl1549 correlate with conditions expected to promote or suppress pathogenicity. BPSL1549 promotes deamidation of glutamine-339 of the translation initiation factor eIF4A, abolishing its helicase activity and inhibiting translation. We propose to name BPSL1549 Burkholderia lethal factor 1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3364511/" 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/PMC3364511/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cruz-Migoni, Abimael -- Hautbergue, Guillaume M -- Artymiuk, Peter J -- Baker, Patrick J -- Bokori-Brown, Monika -- Chang, Chung-Te -- Dickman, Mark J -- Essex-Lopresti, Angela -- Harding, Sarah V -- Mahadi, Nor Muhammad -- Marshall, Laura E -- Mobbs, George W -- Mohamed, Rahmah -- Nathan, Sheila -- Ngugi, Sarah A -- Ong, Catherine -- Ooi, Wen Fong -- Partridge, Lynda J -- Phillips, Helen L -- Raih, M Firdaus -- Ruzheinikov, Sergei -- Sarkar-Tyson, Mitali -- Sedelnikova, Svetlana E -- Smither, Sophie J -- Tan, Patrick -- Titball, Richard W -- Wilson, Stuart A -- Rice, David W -- 085162/Wellcome Trust/United Kingdom -- BB/D011795/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/D524975/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E025293/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- WT085162AIA/Wellcome Trust/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):821-4. doi: 10.1126/science.1211915.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Biotechnology, Krebs Institute, University of Sheffield, Sheffield S10 2TN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22076380" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Bacterial Proteins/*chemistry/genetics/metabolism/*toxicity ; Bacterial Toxins/*chemistry/genetics/metabolism/*toxicity ; Burkholderia pseudomallei/*chemistry/*pathogenicity ; Catalytic Domain ; Cell Line ; Crystallography, X-Ray ; Cytotoxins/chemistry/genetics/metabolism/toxicity ; Escherichia coli Proteins/chemistry ; Eukaryotic Initiation Factor-4A/*antagonists & inhibitors/metabolism ; Glutamine/metabolism ; Humans ; Mice ; Mice, Inbred BALB C ; Models, Molecular ; Mutant Proteins/toxicity ; Peptide Chain Initiation, Translational/drug effects ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary
    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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    Trans-endocytosis of CD80 and CD86: a molecular basis for the cell-extrinsic function of CTLA-4 (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-09
    Description: Cytotoxic T lymphocyte antigen 4 (CTLA-4) is an essential negative regulator of T cell immune responses whose mechanism of action is the subject of debate. CTLA-4 shares two ligands (CD80 and CD86) with a stimulatory receptor, CD28. Here, we show that CTLA-4 can capture its ligands from opposing cells by a process of trans-endocytosis. After removal, these costimulatory ligands are degraded inside CTLA-4-expressing cells, resulting in impaired costimulation via CD28. Acquisition of CD86 from antigen-presenting cells is stimulated by T cell receptor engagement and observed in vitro and in vivo. These data reveal a mechanism of immune regulation in which CTLA-4 acts as an effector molecule to inhibit CD28 costimulation by the cell-extrinsic depletion of ligands, accounting for many of the known features of the CD28-CTLA-4 system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3198051/" 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/PMC3198051/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qureshi, Omar S -- Zheng, Yong -- Nakamura, Kyoko -- Attridge, Kesley -- Manzotti, Claire -- Schmidt, Emily M -- Baker, Jennifer -- Jeffery, Louisa E -- Kaur, Satdip -- Briggs, Zoe -- Hou, Tie Z -- Futter, Clare E -- Anderson, Graham -- Walker, Lucy S K -- Sansom, David M -- 17851/Arthritis Research UK/United Kingdom -- BB/D011000/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/H013598/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0400931/Medical Research Council/United Kingdom -- G0401620/Medical Research Council/United Kingdom -- G0802382/Medical Research Council/United Kingdom -- G1000213/Medical Research Council/United Kingdom -- G9818340/Medical Research Council/United Kingdom -- Arthritis Research UK/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Apr 29;332(6029):600-3. doi: 10.1126/science.1202947. Epub 2011 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Centre for Immune Regulation, School of Immunity and Infection, Institute of Biomedical Research, University of Birmingham Medical School, Birmingham B15 2TT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21474713" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*immunology/metabolism ; Antigens, CD28/*immunology ; Antigens, CD80/*immunology/metabolism ; Antigens, CD86/*immunology/metabolism ; CHO Cells ; CTLA-4 Antigen ; Cricetinae ; Cricetulus ; Dendritic Cells/immunology ; *Endocytosis ; Humans ; Jurkat Cells ; Ligands ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Models, Biological ; Ovalbumin/immunology ; Receptors, Antigen, T-Cell/immunology ; Recombinant Fusion Proteins/metabolism ; T-Lymphocyte Subsets/*immunology/metabolism ; T-Lymphocytes, Regulatory/immunology/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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  • 8
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    Thumbs, tools, and early humans (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-04-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ohman, J C -- Slanina, M -- Baker, G -- Mensforth, R P -- New York, N.Y. -- Science. 1995 Apr 28;268(5210):587-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7725113" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomechanical Phenomena ; Hominidae/*anatomy & histology ; Humans ; Metacarpophalangeal Joint/anatomy & histology ; Metacarpus ; Motor Skills ; Thumb/*anatomy & histology
    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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    A plant-like kinase in Plasmodium falciparum regulates parasite egress from erythrocytes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-15
    Description: Clinical malaria is associated with the proliferation of Plasmodium parasites in human erythrocytes. The coordinated processes of parasite egress from and invasion into erythrocytes are rapid and tightly regulated. We have found that the plant-like calcium-dependent protein kinase PfCDPK5, which is expressed in invasive merozoite forms of Plasmodium falciparum, was critical for egress. Parasites deficient in PfCDPK5 arrested as mature schizonts with intact membranes, despite normal maturation of egress proteases and invasion ligands. Merozoites physically released from stalled schizonts were capable of invading new erythrocytes, separating the pathways of egress and invasion. The arrest was downstream of cyclic guanosine monophosphate-dependent protein kinase (PfPKG) function and independent of protease processing. Thus, PfCDPK5 plays an essential role during the blood stage of malaria replication.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109083/" 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/PMC3109083/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dvorin, Jeffrey D -- Martyn, Derek C -- Patel, Saurabh D -- Grimley, Joshua S -- Collins, Christine R -- Hopp, Christine S -- Bright, A Taylor -- Westenberger, Scott -- Winzeler, Elizabeth -- Blackman, Michael J -- Baker, David A -- Wandless, Thomas J -- Duraisingh, Manoj T -- 086550/Wellcome Trust/United Kingdom -- G1000779/Medical Research Council/United Kingdom -- GM073046/GM/NIGMS NIH HHS/ -- K08 AI087874/AI/NIAID NIH HHS/ -- K12-HD000850/HD/NICHD NIH HHS/ -- MC_U117532063/Medical Research Council/United Kingdom -- R01 AI057919/AI/NIAID NIH HHS/ -- R01 AI057919-05/AI/NIAID NIH HHS/ -- R01 GM073046/GM/NIGMS NIH HHS/ -- R01AI057919/AI/NIAID NIH HHS/ -- U117532063/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 May 14;328(5980):910-2. doi: 10.1126/science.1188191.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466936" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium-Binding Proteins/chemistry/genetics/*metabolism ; Cyclic GMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Enzyme Inhibitors/pharmacology ; Erythrocytes/*parasitology ; Host-Parasite Interactions ; Humans ; Ligands ; Merozoites/enzymology/physiology ; Models, Biological ; Morpholines/metabolism ; Plasmodium falciparum/cytology/enzymology/growth & development/*physiology ; Protein Kinases/chemistry/genetics/*metabolism ; Protozoan Proteins/chemistry/genetics/*metabolism ; Pyridines/pharmacology ; Pyrroles/pharmacology ; Recombinant Fusion Proteins/chemistry/metabolism ; Schizonts/cytology/enzymology/physiology
    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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    Rational HIV immunogen design to target specific germline B cell receptors (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-03-30
    Description: Vaccine development to induce broadly neutralizing antibodies (bNAbs) against HIV-1 is a global health priority. Potent VRC01-class bNAbs against the CD4 binding site of HIV gp120 have been isolated from HIV-1-infected individuals; however, such bNAbs have not been induced by vaccination. Wild-type gp120 proteins lack detectable affinity for predicted germline precursors of VRC01-class bNAbs, making them poor immunogens to prime a VRC01-class response. We employed computation-guided, in vitro screening to engineer a germline-targeting gp120 outer domain immunogen that binds to multiple VRC01-class bNAbs and germline precursors, and elucidated germline binding crystallographically. When multimerized on nanoparticles, this immunogen (eOD-GT6) activates germline and mature VRC01-class B cells. Thus, eOD-GT6 nanoparticles have promise as a vaccine prime. In principle, germline-targeting strategies could be applied to other epitopes and pathogens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3689846/" 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/PMC3689846/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jardine, Joseph -- Julien, Jean-Philippe -- Menis, Sergey -- Ota, Takayuki -- Kalyuzhniy, Oleksandr -- McGuire, Andrew -- Sok, Devin -- Huang, Po-Ssu -- MacPherson, Skye -- Jones, Meaghan -- Nieusma, Travis -- Mathison, John -- Baker, David -- Ward, Andrew B -- Burton, Dennis R -- Stamatatos, Leonidas -- Nemazee, David -- Wilson, Ian A -- Schief, William R -- 5T32AI007606-10/AI/NIAID NIH HHS/ -- AI081625/AI/NIAID NIH HHS/ -- AI33292/AI/NIAID NIH HHS/ -- AI84817/AI/NIAID NIH HHS/ -- P01 AI094419/AI/NIAID NIH HHS/ -- P30 AI027767-24/AI/NIAID NIH HHS/ -- P41RR001209/RR/NCRR NIH HHS/ -- R01 AI033292/AI/NIAID NIH HHS/ -- R01 AI073148/AI/NIAID NIH HHS/ -- R01 AI081625/AI/NIAID NIH HHS/ -- R01 AI084817/AI/NIAID NIH HHS/ -- R37 AI033292/AI/NIAID NIH HHS/ -- T32 CA080416/CA/NCI NIH HHS/ -- T32CA080416/CA/NCI NIH HHS/ -- UM1 AI100663/AI/NIAID NIH HHS/ -- Y1-CO-1020/CO/NCI NIH HHS/ -- Y1-GM-1104/GM/NIGMS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2013 May 10;340(6133):711-6. doi: 10.1126/science.1234150. Epub 2013 Mar 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23539181" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/chemistry/genetics/*immunology ; Amino Acid Sequence ; Animals ; Antibodies, Neutralizing/immunology ; Antigens, CD4/immunology ; B-Lymphocytes/immunology ; Crystallography, X-Ray ; DNA Mutational Analysis ; Germ Cells/*immunology ; HIV Envelope Protein gp120/chemistry/genetics/*immunology ; HIV Infections/*prevention & control ; HIV-1/*immunology ; Humans ; Macaca ; Mice ; Models, Animal ; Molecular Sequence Data ; Nanoparticles ; Protein Engineering ; Protein Structure, Tertiary ; Receptors, Antigen, B-Cell/*immunology
    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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