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  • Humans  (160)
  • Chemistry
  • Life and Medical Sciences
  • 2000-2004  (160)
  • 1980-1984
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  • 2003  (160)
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  • 2000-2004  (160)
  • 1980-1984
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  • 1
    Publication Date: 2003-11-01
    Description: Because of its requirement for signaling by multiple cytokines, Janus kinase 3 (JAK3) is an excellent target for clinical immunosuppression. We report the development of a specific, orally active inhibitor of JAK3, CP-690,550, that significantly prolonged survival in a murine model of heart transplantation and in cynomolgus monkeys receiving kidney transplants. CP-690,550 treatment was not associated with hypertension, hyperlipidemia, or lymphoproliferative disease. On the basis of these preclinical results, we believe JAK3 blockade by CP-690,550 has potential for therapeutically desirable immunosuppression in human organ transplantation and in other clinical settings.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Changelian, Paul S -- Flanagan, Mark E -- Ball, Douglas J -- Kent, Craig R -- Magnuson, Kelly S -- Martin, William H -- Rizzuti, Bonnie J -- Sawyer, Perry S -- Perry, Bret D -- Brissette, William H -- McCurdy, Sandra P -- Kudlacz, Elizabeth M -- Conklyn, Maryrose J -- Elliott, Eileen A -- Koslov, Erika R -- Fisher, Michael B -- Strelevitz, Timothy J -- Yoon, Kwansik -- Whipple, David A -- Sun, Jianmin -- Munchhof, Michael J -- Doty, John L -- Casavant, Jeffrey M -- Blumenkopf, Todd A -- Hines, Michael -- Brown, Matthew F -- Lillie, Brett M -- Subramanyam, Chakrapani -- Shang-Poa, Chang -- Milici, Anthony J -- Beckius, Gretchen E -- Moyer, James D -- Su, Chunyan -- Woodworth, Thasia G -- Gaweco, Anderson S -- Beals, Chan R -- Littman, Bruce H -- Fisher, Douglas A -- Smith, James F -- Zagouras, Panayiotis -- Magna, Holly A -- Saltarelli, Mary J -- Johnson, Kimberly S -- Nelms, Linda F -- Des Etages, Shelley G -- Hayes, Lisa S -- Kawabata, Thomas T -- Finco-Kent, Deborah -- Baker, Deanna L -- Larson, Michael -- Si, Ming-Sing -- Paniagua, Ricardo -- Higgins, John -- Holm, Bari -- Reitz, Bruce -- Zhou, Yong-Jie -- Morris, Randall E -- O'Shea, John J -- Borie, Dominic C -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):875-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Group, Department of Antibacterials and Immunology, Pfizer Global Researchand Development, Groton, CT 06340, USA. paul_s_changelian@groton.pfizer.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593182" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enzyme Inhibitors/administration & dosage/pharmacology/therapeutic use/toxicity ; Gene Expression Regulation/drug effects ; Graft Rejection/*prevention & control ; Graft Survival/drug effects ; *Heart Transplantation ; Humans ; Immunosuppressive Agents/administration & dosage/*pharmacology/therapeutic ; use/toxicity ; Interleukin-2/immunology ; Janus Kinase 3 ; *Kidney Transplantation ; Lymphocyte Activation/drug effects ; Lymphocyte Count ; Lymphocyte Culture Test, Mixed ; Lymphocyte Subsets/drug effects ; Macaca fascicularis ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Myocardium/metabolism ; Piperidines ; Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Pyrimidines/administration & dosage/*pharmacology/therapeutic use/toxicity ; Pyrroles/administration & dosage/*pharmacology/therapeutic use/toxicity ; Transplantation, Heterotopic ; Transplantation, Homologous ; Tumor Cells, Cultured
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    Electronic ISSN: 1095-9203
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  • 2
    Publication Date: 2003-04-12
    Description: DNA sequence and annotation of the entire human chromosome 7, encompassing nearly 158 million nucleotides of DNA and 1917 gene structures, are presented. To generate a higher order description, additional structural features such as imprinted genes, fragile sites, and segmental duplications were integrated at the level of the DNA sequence with medical genetic data, including 440 chromosome rearrangement breakpoints associated with disease. This approach enabled the discovery of candidate genes for developmental diseases including autism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882961/" 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/PMC2882961/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scherer, Stephen W -- Cheung, Joseph -- MacDonald, Jeffrey R -- Osborne, Lucy R -- Nakabayashi, Kazuhiko -- Herbrick, Jo-Anne -- Carson, Andrew R -- Parker-Katiraee, Layla -- Skaug, Jennifer -- Khaja, Razi -- Zhang, Junjun -- Hudek, Alexander K -- Li, Martin -- Haddad, May -- Duggan, Gavin E -- Fernandez, Bridget A -- Kanematsu, Emiko -- Gentles, Simone -- Christopoulos, Constantine C -- Choufani, Sanaa -- Kwasnicka, Dorota -- Zheng, Xiangqun H -- Lai, Zhongwu -- Nusskern, Deborah -- Zhang, Qing -- Gu, Zhiping -- Lu, Fu -- Zeesman, Susan -- Nowaczyk, Malgorzata J -- Teshima, Ikuko -- Chitayat, David -- Shuman, Cheryl -- Weksberg, Rosanna -- Zackai, Elaine H -- Grebe, Theresa A -- Cox, Sarah R -- Kirkpatrick, Susan J -- Rahman, Nazneen -- Friedman, Jan M -- Heng, Henry H Q -- Pelicci, Pier Giuseppe -- Lo-Coco, Francesco -- Belloni, Elena -- Shaffer, Lisa G -- Pober, Barbara -- Morton, Cynthia C -- Gusella, James F -- Bruns, Gail A P -- Korf, Bruce R -- Quade, Bradley J -- Ligon, Azra H -- Ferguson, Heather -- Higgins, Anne W -- Leach, Natalia T -- Herrick, Steven R -- Lemyre, Emmanuelle -- Farra, Chantal G -- Kim, Hyung-Goo -- Summers, Anne M -- Gripp, Karen W -- Roberts, Wendy -- Szatmari, Peter -- Winsor, Elizabeth J T -- Grzeschik, Karl-Heinz -- Teebi, Ahmed -- Minassian, Berge A -- Kere, Juha -- Armengol, Lluis -- Pujana, Miguel Angel -- Estivill, Xavier -- Wilson, Michael D -- Koop, Ben F -- Tosi, Sabrina -- Moore, Gudrun E -- Boright, Andrew P -- Zlotorynski, Eitan -- Kerem, Batsheva -- Kroisel, Peter M -- Petek, Erwin -- Oscier, David G -- Mould, Sarah J -- Dohner, Hartmut -- Dohner, Konstanze -- Rommens, Johanna M -- Vincent, John B -- Venter, J Craig -- Li, Peter W -- Mural, Richard J -- Adams, Mark D -- Tsui, Lap-Chee -- 38103/Canadian Institutes of Health Research/Canada -- P01 GM061354/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 May 2;300(5620):767-72. Epub 2003 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Genomic Biology, The Hospital for Sick Children, Toronto, Ontario, Canada, M5G 1X8. steve@genet.sickkids.on.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690205" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/genetics ; Chromosome Aberrations ; Chromosome Fragile Sites ; Chromosome Fragility ; Chromosome Mapping ; Chromosomes, Human, Pair 7/*genetics ; Computational Biology ; Congenital Abnormalities/genetics ; CpG Islands ; DNA, Complementary ; Databases, Genetic ; Euchromatin/genetics ; Expressed Sequence Tags ; Gene Duplication ; Genes, Overlapping ; Genetic Diseases, Inborn/genetics ; Genomic Imprinting ; Humans ; In Situ Hybridization, Fluorescence ; Limb Deformities, Congenital/genetics ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasms/genetics ; Pseudogenes ; RNA/genetics ; Retroelements ; *Sequence Analysis, DNA ; Williams Syndrome/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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  • 3
    Publication Date: 2003-05-06
    Description: We sequenced the 29,751-base genome of the severe acute respiratory syndrome (SARS)-associated coronavirus known as the Tor2 isolate. The genome sequence reveals that this coronavirus is only moderately related to other known coronaviruses, including two human coronaviruses, HCoV-OC43 and HCoV-229E. Phylogenetic analysis of the predicted viral proteins indicates that the virus does not closely resemble any of the three previously known groups of coronaviruses. The genome sequence will aid in the diagnosis of SARS virus infection in humans and potential animal hosts (using polymerase chain reaction and immunological tests), in the development of antivirals (including neutralizing antibodies), and in the identification of putative epitopes for vaccine development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marra, Marco A -- Jones, Steven J M -- Astell, Caroline R -- Holt, Robert A -- Brooks-Wilson, Angela -- Butterfield, Yaron S N -- Khattra, Jaswinder -- Asano, Jennifer K -- Barber, Sarah A -- Chan, Susanna Y -- Cloutier, Alison -- Coughlin, Shaun M -- Freeman, Doug -- Girn, Noreen -- Griffith, Obi L -- Leach, Stephen R -- Mayo, Michael -- McDonald, Helen -- Montgomery, Stephen B -- Pandoh, Pawan K -- Petrescu, Anca S -- Robertson, A Gordon -- Schein, Jacqueline E -- Siddiqui, Asim -- Smailus, Duane E -- Stott, Jeff M -- Yang, George S -- Plummer, Francis -- Andonov, Anton -- Artsob, Harvey -- Bastien, Nathalie -- Bernard, Kathy -- Booth, Timothy F -- Bowness, Donnie -- Czub, Martin -- Drebot, Michael -- Fernando, Lisa -- Flick, Ramon -- Garbutt, Michael -- Gray, Michael -- Grolla, Allen -- Jones, Steven -- Feldmann, Heinz -- Meyers, Adrienne -- Kabani, Amin -- Li, Yan -- Normand, Susan -- Stroher, Ute -- Tipples, Graham A -- Tyler, Shaun -- Vogrig, Robert -- Ward, Diane -- Watson, Brynn -- Brunham, Robert C -- Krajden, Mel -- Petric, Martin -- Skowronski, Danuta M -- Upton, Chris -- Roper, Rachel L -- New York, N.Y. -- Science. 2003 May 30;300(5624):1399-404. Epub 2003 May 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉British Columbia Cancer Agency (BCCA) Genome Sciences Centre, 600 West 10th Avenue, Vancouver, British Columbia V5Z 4E6, Canada. mmarra@bccgsc.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730501" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; 5' Untranslated Regions ; Animals ; Base Sequence ; Conserved Sequence ; Coronavirus/classification/genetics ; DNA, Complementary ; Frameshifting, Ribosomal ; *Genome, Viral ; Humans ; Membrane Glycoproteins/chemistry/genetics ; Nucleocapsid Proteins/chemistry/genetics ; Open Reading Frames ; Phylogeny ; RNA Replicase/chemistry/genetics ; RNA, Viral/*genetics/isolation & purification ; Regulatory Sequences, Nucleic Acid ; SARS Virus/classification/*genetics/isolation & purification ; Sequence Analysis, DNA ; Severe Acute Respiratory Syndrome/virology ; Spike Glycoprotein, Coronavirus ; Viral Envelope Proteins/chemistry/genetics ; Viral Matrix Proteins/chemistry/genetics ; Viral Proteins/chemistry/*genetics
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  • 4
    Publication Date: 2003-05-06
    Description: In March 2003, a novel coronavirus (SARS-CoV) was discovered in association with cases of severe acute respiratory syndrome (SARS). The sequence of the complete genome of SARS-CoV was determined, and the initial characterization of the viral genome is presented in this report. The genome of SARS-CoV is 29,727 nucleotides in length and has 11 open reading frames, and its genome organization is similar to that of other coronaviruses. Phylogenetic analyses and sequence comparisons showed that SARS-CoV is not closely related to any of the previously characterized coronaviruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rota, Paul A -- Oberste, M Steven -- Monroe, Stephan S -- Nix, W Allan -- Campagnoli, Ray -- Icenogle, Joseph P -- Penaranda, Silvia -- Bankamp, Bettina -- Maher, Kaija -- Chen, Min-Hsin -- Tong, Suxiong -- Tamin, Azaibi -- Lowe, Luis -- Frace, Michael -- DeRisi, Joseph L -- Chen, Qi -- Wang, David -- Erdman, Dean D -- Peret, Teresa C T -- Burns, Cara -- Ksiazek, Thomas G -- Rollin, Pierre E -- Sanchez, Anthony -- Liffick, Stephanie -- Holloway, Brian -- Limor, Josef -- McCaustland, Karen -- Olsen-Rasmussen, Melissa -- Fouchier, Ron -- Gunther, Stephan -- Osterhaus, Albert D M E -- Drosten, Christian -- Pallansch, Mark A -- Anderson, Larry J -- Bellini, William J -- New York, N.Y. -- Science. 2003 May 30;300(5624):1394-9. Epub 2003 May 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA. prota@cdc.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730500" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Conserved Sequence ; Coronavirus/classification/genetics ; DNA, Complementary ; Endopeptidases/chemistry/genetics ; *Genome, Viral ; Humans ; Membrane Glycoproteins/chemistry/genetics ; Molecular Sequence Data ; Nucleocapsid Proteins/chemistry/genetics ; Open Reading Frames ; Phylogeny ; Polyproteins/chemistry/genetics ; RNA Replicase/chemistry/genetics ; RNA, Messenger/genetics/metabolism ; RNA, Viral/*genetics ; Regulatory Sequences, Nucleic Acid ; SARS Virus/chemistry/classification/*genetics/isolation & purification ; Sequence Analysis, DNA ; Severe Acute Respiratory Syndrome/virology ; Spike Glycoprotein, Coronavirus ; Transcription, Genetic ; Viral Envelope Proteins/chemistry/genetics ; Viral Matrix Proteins/chemistry/genetics ; Viral Proteins/chemistry/*genetics
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  • 5
    Publication Date: 2003-06-28
    Description: A new collaborative model of research is needed to increase resources, to prioritize the R (ii) to increase the pace, reduce the overlap, and more systematically explore the elements of and delivery systems for vaccines; (iii) to use common standards for the prompt comparative testing of vaccine candidates; (iv) to expand resources for manufacturing vaccine candidates to speed their use in human trials; and (v) to increase the capacity for international clinical trials and to focus this effort toward quickly measuring the effectiveness of vaccine protection as prototype vaccine candidates are identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klausner, Richard D -- Fauci, Anthony S -- Corey, Lawrence -- Nabel, Gary J -- Gayle, Helene -- Berkley, Seth -- Haynes, Barton F -- Baltimore, David -- Collins, Chris -- Douglas, R Gordon -- Esparza, Jose -- Francis, Donald P -- Ganguly, N K -- Gerberding, Julie Louise -- Johnston, Margaret I -- Kazatchkine, Michel D -- McMichael, Andrew J -- Makgoba, Malegapuru W -- Pantaleo, Giuseppe -- Piot, Peter -- Shao, Yiming -- Tramont, Edmund -- Varmus, Harold -- Wasserheit, Judith N -- New York, N.Y. -- Science. 2003 Jun 27;300(5628):2036-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bill and Melinda Gates Foundation, Seattle, WA 98102, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12829768" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines/administration & dosage/economics/immunology ; Academies and Institutes/economics/organization & administration ; Biotechnology/economics ; Clinical Trials as Topic/standards ; Drug Design ; Drug Evaluation, Preclinical/standards ; Drug Industry/economics ; Financial Support ; *Global Health ; HIV Infections/*prevention & control ; HIV-1/*immunology ; Humans ; Intellectual Property ; International Cooperation ; Multicenter Studies as Topic ; Private Sector ; *Public Policy ; Public Sector ; Research Support as Topic ; Vaccination
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  • 6
    Publication Date: 2003-12-13
    Description: Even though human and chimpanzee gene sequences are nearly 99% identical, sequence comparisons can nevertheless be highly informative in identifying biologically important changes that have occurred since our ancestral lineages diverged. We analyzed alignments of 7645 chimpanzee gene sequences to their human and mouse orthologs. These three-species sequence alignments allowed us to identify genes undergoing natural selection along the human and chimp lineage by fitting models that include parameters specifying rates of synonymous and nonsynonymous nucleotide substitution. This evolutionary approach revealed an informative set of genes with significantly different patterns of substitution on the human lineage compared with the chimpanzee and mouse lineages. Partitions of genes into inferred biological classes identified accelerated evolution in several functional classes, including olfaction and nuclear transport. In addition to suggesting adaptive physiological differences between chimps and humans, human-accelerated genes are significantly more likely to underlie major known Mendelian disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, Andrew G -- Glanowski, Stephen -- Nielsen, Rasmus -- Thomas, Paul D -- Kejariwal, Anish -- Todd, Melissa A -- Tanenbaum, David M -- Civello, Daniel -- Lu, Fu -- Murphy, Brian -- Ferriera, Steve -- Wang, Gary -- Zheng, Xianqgun -- White, Thomas J -- Sninsky, John J -- Adams, Mark D -- Cargill, Michele -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1960-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671302" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus/genetics ; Amino Acids/metabolism ; Animals ; Biological Evolution ; Computational Biology ; *Evolution, Molecular ; Female ; Genes ; Genetic Diseases, Inborn/genetics ; *Genome ; *Genome, Human ; Humans ; Likelihood Functions ; Male ; Mice/genetics ; Models, Genetic ; Models, Statistical ; Mutation ; Pan troglodytes/*genetics ; Phylogeny ; Proteins/chemistry/genetics ; Pseudogenes ; Receptors, Odorant/genetics ; *Selection, Genetic ; Sequence Alignment ; Sequence Homology, Nucleic Acid ; Signal Transduction/genetics ; Smell/genetics ; Species Specificity
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  • 7
    Publication Date: 2003-09-27
    Description: Tumor necrosis factor (TNF) is a key regulator of inflammatory responses and has been implicated in many pathological conditions. We used structure-based design to engineer variant TNF proteins that rapidly form heterotrimers with native TNF to give complexes that neither bind to nor stimulate signaling through TNF receptors. Thus, TNF is inactivated by sequestration. Dominant-negative TNFs represent a possible approach to anti-inflammatory biotherapeutics, and experiments in animal models show that the strategy can attenuate TNF-mediated pathology. Similar rational design could be used to engineer inhibitors of additional TNF superfamily cytokines as well as other multimeric ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steed, Paul M -- Tansey, Malu G -- Zalevsky, Jonathan -- Zhukovsky, Eugene A -- Desjarlais, John R -- Szymkowski, David E -- Abbott, Christina -- Carmichael, David -- Chan, Cheryl -- Cherry, Lisa -- Cheung, Peter -- Chirino, Arthur J -- Chung, Hyo H -- Doberstein, Stephen K -- Eivazi, Araz -- Filikov, Anton V -- Gao, Sarah X -- Hubert, Rene S -- Hwang, Marian -- Hyun, Linus -- Kashi, Sandhya -- Kim, Alice -- Kim, Esther -- Kung, James -- Martinez, Sabrina P -- Muchhal, Umesh S -- Nguyen, Duc-Hanh T -- O'Brien, Christopher -- O'Keefe, Donald -- Singer, Karen -- Vafa, Omid -- Vielmetter, Jost -- Yoder, Sean C -- Dahiyat, Bassil I -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1895-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Xencor, 111 West Lemon Avenue, Monrovia, CA 91016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512626" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Antigens, CD/metabolism ; Apoptosis ; Arthritis, Experimental/drug therapy ; Biopolymers ; Caspases/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Computer Simulation ; Disease Progression ; Enzyme-Linked Immunosorbent Assay ; Female ; Galactosamine/pharmacology ; HeLa Cells ; Humans ; Liver/drug effects ; NF-kappa B/metabolism ; Point Mutation ; *Protein Engineering ; Rats ; Receptors, Tumor Necrosis Factor/metabolism ; Receptors, Tumor Necrosis Factor, Type I ; Receptors, Tumor Necrosis Factor, Type II ; *Signal Transduction ; Transcription Factor RelA ; Transcription, Genetic ; Tumor Necrosis Factor-alpha/*antagonists & ; inhibitors/genetics/metabolism/*pharmacology
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  • 8
    Publication Date: 2003-07-05
    Description: Raf kinases have been linked to endothelial cell survival. Here, we show that basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) differentially activate Raf, resulting in protection from distinct pathways of apoptosis in human endothelial cells and chick embryo vasculature. bFGF activated Raf-1 via p21-activated protein kinase-1 (PAK-1) phosphorylation of serines 338 and 339, resulting in Raf-1 mitochondrial translocation and endothelial cell protection from the intrinsic pathway of apoptosis, independent of the mitogen-activated protein kinase kinase-1 (MEK1). In contrast, VEGF activated Raf-1 via Src kinase, leading to phosphorylation of tyrosines 340 and 341 and MEK1-dependent protection from extrinsic-mediated apoptosis. These findings implicate Raf-1 as a pivotal regulator of endothelial cell survival during angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alavi, Alireza -- Hood, John D -- Frausto, Ricardo -- Stupack, Dwayne G -- Cheresh, David A -- CA45726/CA/NCI NIH HHS/ -- CA50286/CA/NCI NIH HHS/ -- CA75924/CA/NCI NIH HHS/ -- P01 CA78045/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):94-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Survival ; Cells, Cultured ; Chick Embryo ; Endothelial Growth Factors/pharmacology ; Endothelium, Vascular/*cytology/drug effects ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Fibroblast Growth Factor 2/pharmacology ; Flavonoids/pharmacology ; Humans ; Intercellular Signaling Peptides and Proteins/pharmacology ; Lymphokines/pharmacology ; MAP Kinase Kinase 1 ; Mitochondria/metabolism ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Neovascularization, Pathologic ; *Neovascularization, Physiologic/drug effects ; Phosphorylation ; Point Mutation ; Protein Transport ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins B-raf ; Proto-Oncogene Proteins c-raf/chemistry/genetics/*metabolism ; Signal Transduction ; Umbilical Veins ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; p21-Activated Kinases ; src-Family Kinases/antagonists & inhibitors/metabolism
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  • 9
    Publication Date: 2003-03-29
    Description: The complete genome sequence of Enterococcus faecalis V583, a vancomycin-resistant clinical isolate, revealed that more than a quarter of the genome consists of probable mobile or foreign DNA. One of the predicted mobile elements is a previously unknown vanB vancomycin-resistance conjugative transposon. Three plasmids were identified, including two pheromone-sensing conjugative plasmids, one encoding a previously undescribed pheromone inhibitor. The apparent propensity for the incorporation of mobile elements probably contributed to the rapid acquisition and dissemination of drug resistance in the enterococci.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paulsen, I T -- Banerjei, L -- Myers, G S A -- Nelson, K E -- Seshadri, R -- Read, T D -- Fouts, D E -- Eisen, J A -- Gill, S R -- Heidelberg, J F -- Tettelin, H -- Dodson, R J -- Umayam, L -- Brinkac, L -- Beanan, M -- Daugherty, S -- DeBoy, R T -- Durkin, S -- Kolonay, J -- Madupu, R -- Nelson, W -- Vamathevan, J -- Tran, B -- Upton, J -- Hansen, T -- Shetty, J -- Khouri, H -- Utterback, T -- Radune, D -- Ketchum, K A -- Dougherty, B A -- Fraser, C M -- AI40963-02/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2003 Mar 28;299(5615):2071-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Research, 9712 Medical Center Drive, Rockville, MD 20850, USA. ipaulsen@tigr.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12663927" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/genetics ; Bacterial Adhesion ; Bacterial Proteins/genetics ; *Biological Evolution ; Carrier Proteins/genetics/metabolism ; Chromosomes, Bacterial/genetics ; Conjugation, Genetic ; Conserved Sequence ; DNA Transposable Elements ; Digestive System/microbiology ; Drug Resistance, Multiple, Bacterial ; Enterococcus faecalis/drug effects/*genetics/pathogenicity/physiology ; Gene Transfer, Horizontal ; *Genome, Bacterial ; Gram-Positive Bacterial Infections/microbiology ; Humans ; *Interspersed Repetitive Sequences ; Lysogeny ; Open Reading Frames ; Oxidative Stress ; Plasmids ; *Sequence Analysis, DNA ; Synteny ; Vancomycin Resistance/*genetics ; Virulence/genetics ; Virulence Factors/genetics
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  • 10
    Publication Date: 2003-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bass, Gary D -- Blumenthal, Paul D -- Corfman, Phil -- Darney, Philip D -- Gonsalves, Gregg -- Levin, Arthur A -- Trussell, James -- Shields, Wayne C -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1313.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610277" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/prevention & control ; *Advisory Committees ; Federal Government ; Humans ; *Politics ; *Public Health ; *Science ; United States
    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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