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  • American Association for the Advancement of Science (AAAS)  (38)
  • 2000-2004  (38)
  • 1955-1959
  • 2003  (38)
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  • American Association for the Advancement of Science (AAAS)  (38)
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  • 2000-2004  (38)
  • 1955-1959
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  • 1
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    Mothers' transitions from welfare to work and the well-being of preschoolers and adolescents (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-08
    Description: Results from a longitudinal study of 2402 low-income families during the recent unprecedented era of welfare reform suggest that mothers' transitions off welfare and into employment are not associated with negative outcomes for preschoolers (ages 2 to 4 years) or young adolescents (ages 10 to 14 years). Indeed, no significant associations with mothers' welfare and employment transitions were found for preschoolers, and the dominant pattern was also of few statistically significant associations for adolescents. The associations that did occur provided slight evidence that mothers' entry into the labor force was related to improvements in adolescents' mental health, whereas exits from employment were linked with teenagers' increased behavior problems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chase-Lansdale, P Lindsay -- Moffitt, Robert A -- Lohman, Brenda J -- Cherlin, Andrew J -- Coley, Rebekah Levine -- Pittman, Laura D -- Roff, Jennifer -- Votruba-Drzal, Elizabeth -- New York, N.Y. -- Science. 2003 Mar 7;299(5612):1548-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Northwestern University, Evanston, IL 60208, USA. lcl@northwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12624259" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; *Adolescent Behavior ; Child ; *Child Behavior ; Child Behavior Disorders/epidemiology ; Child, Preschool ; Cognition ; *Employment ; Female ; Humans ; Income ; Infant ; Interviews as Topic ; Least-Squares Analysis ; Longitudinal Studies ; *Mental Health ; Mother-Child Relations ; *Mothers ; Parenting ; *Public Assistance ; Social Welfare ; United States/epidemiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Abnormal coronary function in mice deficient in alpha1H T-type Ca2+ channels (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: Calcium ion (Ca2+) influx through voltage-gated Ca2+ channels is important for the regulation of vascular tone. Activation of L-type Ca2+ channels initiates muscle contraction; however, the role of T-type Ca2+ channels (T-channels) is not clear. We show that mice deficient in the alpha1H T-type Ca2+ channel (alpha(1)3.2-null) have constitutively constricted coronary arterioles and focal myocardial fibrosis. Coronary arteries isolated from alpha(1)3.2-null arteries showed normal contractile responses, but reduced relaxation in response to acetylcholine and nitroprusside. Furthermore, acute blockade of T-channels with Ni2+ prevented relaxation of wild-type coronary arteries. Thus, Ca2+ influx through alpha1H T-type Ca2+ channels is essential for normal relaxation of coronary arteries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Chien-Chang -- Lamping, Kathryn G -- Nuno, Daniel W -- Barresi, Rita -- Prouty, Sally J -- Lavoie, Julie L -- Cribbs, Leanne L -- England, Sarah K -- Sigmund, Curt D -- Weiss, Robert M -- Williamson, Roger A -- Hill, Joseph A -- Campbell, Kevin P -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1416-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631046" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/pharmacology ; Animals ; Arteries/drug effects/*physiology ; Calcium/*metabolism ; Calcium Channels, T-Type/genetics/*physiology ; Coronary Vessels/drug effects/pathology/*physiology ; Echocardiography ; Electrocardiography ; Endothelium, Vascular/drug effects/physiology ; Female ; Fibrosis ; Ganglia, Spinal/cytology ; Gene Targeting ; Heart/physiology ; Heart Rate ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular/physiology ; Myocardium/pathology ; Neurons/metabolism ; Nickel/pharmacology ; Nitric Oxide/physiology ; Nitric Oxide Donors/pharmacology ; Nitroprusside/pharmacology ; Patch-Clamp Techniques ; Vasoconstriction/drug effects ; *Vasodilation/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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  • 3
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    Critical roles for Rac1 and Rac2 GTPases in B cell development and signaling (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: The Rac1 guanosine triphosphatase (GTPase) has been implicated in multiple cellular functions, including actin dynamics, proliferation, apoptosis, adhesion, and migration resulting from signaling by multiple receptors, including the B cell antigen receptor (BCR). We used conditional gene targeting to generate mice with specific Rac1 deficiency in the B cell lineage. In the absence of both Rac1 and the highly related Rac2, B cell development was almost completely blocked. Both GTPases were required to transduce BCR signals leading to proliferation, survival and up-regulation of BAFF-R, a receptor for BAFF, a key survival molecule required for B cell development and maintenance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walmsley, Marita J -- Ooi, Steen K T -- Reynolds, Lucinda F -- Smith, Susan Harless -- Ruf, Sandra -- Mathiot, Anne -- Vanes, Lesley -- Williams, David A -- Cancro, Michael P -- Tybulewicz, Victor L J -- R01 AI042990/AI/NIAID NIH HHS/ -- R01 AI054488/AI/NIAID NIH HHS/ -- R01 DK62757/DK/NIDDK NIH HHS/ -- T32 CA009140/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):459-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immune Cell Biology, National Institute for Medical Research, The Ridgeway, Mill Hill, London, NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564011" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Cell Activating Factor ; B-Cell Activation Factor Receptor ; B-Lymphocyte Subsets/physiology ; B-Lymphocytes/*physiology ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cell Survival ; Female ; Gene Targeting ; Lymphocyte Activation ; Male ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, B-Cell/*metabolism ; Receptors, Tumor Necrosis Factor/genetics/metabolism ; Recombination, Genetic ; *Signal Transduction ; Spleen/cytology ; Tumor Necrosis Factor-alpha/metabolism ; Up-Regulation ; rac GTP-Binding Proteins/*physiology ; rac1 GTP-Binding Protein/*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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  • 4
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    A mule cloned from fetal cells by nuclear transfer (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woods, Gordon L -- White, Kenneth L -- Vanderwall, Dirk K -- Li, Guang-Peng -- Aston, Kenneth I -- Bunch, Thomas D -- Meerdo, Lora N -- Pate, Barry J -- New York, N.Y. -- Science. 2003 Aug 22;301(5636):1063. Epub 2003 May 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Northwest Equine Reproduction Laboratory, Department of Animal and Veterinary Science, University of Idaho, Moscow, ID 83844, USA. gwoods@uidaho.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12775846" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Cell Line ; *Cloning, Organism ; Embryo Transfer ; Embryo, Mammalian ; Embryonic and Fetal Development ; Equidae/*embryology/*genetics ; Female ; Fibroblasts ; Horses ; Male ; *Nuclear Transfer Techniques ; Oocytes/metabolism ; Pregnancy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Pyogenic bacterial infections in humans with IRAK-4 deficiency (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-15
    Description: Members of the Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) superfamily share an intracytoplasmic Toll-IL-1 receptor (TIR) domain, which mediates recruitment of the interleukin-1 receptor-associated kinase (IRAK) complex via TIR-containing adapter molecules. We describe three unrelated children with inherited IRAK-4 deficiency. Their blood and fibroblast cells did not activate nuclear factor kappaB and mitogen-activated protein kinase (MAPK) and failed to induce downstream cytokines in response to any of the known ligands of TIR-bearing receptors. The otherwise healthy children developed infections caused by pyogenic bacteria. These findings suggest that, in humans, the TIR-IRAK signaling pathway is crucial for protective immunity against specific bacteria but is redundant against most other microorganisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Picard, Capucine -- Puel, Anne -- Bonnet, Marion -- Ku, Cheng-Lung -- Bustamante, Jacinta -- Yang, Kun -- Soudais, Claire -- Dupuis, Stephanie -- Feinberg, Jacqueline -- Fieschi, Claire -- Elbim, Carole -- Hitchcock, Remi -- Lammas, David -- Davies, Graham -- Al-Ghonaium, Abdulaziz -- Al-Rayes, Hassan -- Al-Jumaah, Sulaiman -- Al-Hajjar, Sami -- Al-Mohsen, Ibrahim Zaid -- Frayha, Husn H -- Rucker, Rajivi -- Hawn, Thomas R -- Aderem, Alan -- Tufenkeji, Haysam -- Haraguchi, Soichi -- Day, Noorbibi K -- Good, Robert A -- Gougerot-Pocidalo, Marie-Anne -- Ozinsky, Adrian -- Casanova, Jean-Laurent -- New York, N.Y. -- Science. 2003 Mar 28;299(5615):2076-9. Epub 2003 Mar 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Humaine des Maladies Infectieuses, Universite Rene Descartes-INSERM U550, Faculte Necker, 156 rue de Vaugirard, 75015 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12637671" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Child ; Codon, Terminator ; Cytokines/secretion ; *Drosophila Proteins ; Female ; Fibroblasts/immunology ; Humans ; Interleukin-1 Receptor-Associated Kinases ; Interleukins/immunology/secretion ; Lipopolysaccharides/immunology ; Male ; Membrane Glycoproteins/chemistry/immunology/metabolism ; Monocytes/immunology ; Mutation ; Neutrophils/immunology ; Pedigree ; Phosphotransferases (Alcohol Group Acceptor)/*deficiency/*genetics/metabolism ; Pneumococcal Infections/*immunology/metabolism ; Protein Structure, Tertiary ; Receptors, Cell Surface/chemistry/immunology/metabolism ; Receptors, Interleukin/immunology ; Receptors, Interleukin-1/chemistry ; Signal Transduction ; Staphylococcal Infections/*immunology/metabolism ; Toll-Like Receptors ; Tumor Necrosis Factor-alpha/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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  • 6
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    Myc-induced T cell leukemia in transgenic zebrafish (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-08
    Description: The zebrafish is an attractive model organism for studying cancer development because of its genetic accessibility. Here we describe the induction of clonally derived T cell acute lymphoblastic leukemia in transgenic zebrafish expressing mouse c-myc under control of the zebrafish Rag2 promoter. Visualization of leukemic cells expressing a chimeric transgene encoding Myc fused to green fluorescent protein (GFP) revealed that leukemias arose in the thymus, spread locally into gill arches and retro-orbital soft tissue, and then disseminated into skeletal muscle and abdominal organs. Leukemic cells homed back to the thymus in irradiated fish transplanted with GFP-labeled leukemic lymphoblasts. This transgenic model provides a platform for drug screens and for genetic screens aimed at identifying mutations that suppress or enhance c-myc- induced carcinogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Langenau, David M -- Traver, David -- Ferrando, Adolfo A -- Kutok, Jeffery L -- Aster, Jon C -- Kanki, John P -- Lin, Shuo -- Prochownik, Ed -- Trede, Nikolaus S -- Zon, Leonard I -- Look, A Thomas -- CA-06516/CA/NCI NIH HHS/ -- CA-68484/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):887-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574629" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Cell Lineage ; *Cell Transformation, Neoplastic ; Clone Cells ; DNA-Binding Proteins/genetics ; *Disease Models, Animal ; Female ; Fertilization in Vitro ; Gene Expression Profiling ; *Genes, myc ; Green Fluorescent Proteins ; Kidney/pathology ; *Leukemia-Lymphoma, Adult T-Cell/genetics/pathology ; Leukemic Infiltration ; Luminescent Proteins/metabolism ; Male ; Mice ; Mutation ; Neoplasm Transplantation ; Olfactory Bulb/pathology ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/metabolism ; Spleen/pathology ; T-Lymphocytes/immunology/*pathology/physiology ; Thymus Gland/pathology ; Transgenes ; *Zebrafish/embryology/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Inhibited and uninhibited infants "grown up": adult amygdalar response to novelty (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-21
    Description: Infants with an inhibited temperament tend to develop into children who avoid people, objects, and situations that are novel or unfamiliar, whereas uninhibited children spontaneously approach novel persons, objects, and situations. Behavioral and physiological features of these two temperamental categories are moderately stable from infancy into early adolescence and have been hypothesized to be due, in part, to variation in amygdalar responses to novelty. We found that adults who had been categorized in the second year of life as inhibited, compared with those previously categorized as uninhibited, showed greater functional MRI signal response within the amygdala to novel versus familiar faces.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwartz, Carl E -- Wright, Christopher I -- Shin, Lisa M -- Kagan, Jerome -- Rauch, Scott L -- New York, N.Y. -- Science. 2003 Jun 20;300(5627):1952-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Psychopathology Research Group, Department of Psychiatry, Massachusetts General Hospital (MGH), Harvard Medical School, 13th Street, Building 149, CNY-9, Charlestown, MA 02129, USA. carl_schwartz@hms.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12817151" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Amygdala/*physiology ; Exploratory Behavior ; Face ; Female ; Humans ; *Inhibition (Psychology) ; Magnetic Resonance Imaging ; Male ; *Recognition (Psychology) ; *Temperament
    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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    Trophoblast L-selectin-mediated adhesion at the maternal-fetal interface (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: Trophoblast adhesion to the uterine wall is the requisite first step of implantation and, subsequently, placentation. At the maternal-fetal interface, we investigated the expression of selectin adhesion systems that enable leukocyte capture from the bloodstream. On the maternal side, human uterine epithelial cells up-regulated selectin oligosaccharide-based ligands during the window of receptivity. On the fetal side, human trophoblasts expressed L-selectin. This ligand-receptor system was functional, because beads coated with the selectin ligand 6-sulfo sLe(x) bound to trophoblasts, and trophoblasts bound to ligand-expressing uterine luminal epithelium in tissue sections. These results suggest that trophoblast L-selectin mediates interactions with the uterus and that this adhesion mechanism may be critical to establishing human pregnancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Genbacev, Olga D -- Prakobphol, Akraporn -- Foulk, Russell A -- Krtolica, Ana R -- Ilic, Dusko -- Singer, Mark S -- Yang, Zhi-Qiang -- Kiessling, Laura L -- Rosen, Steven D -- Fisher, Susan J -- DE 07244/DE/NIDCR NIH HHS/ -- HL 64597/HL/NHLBI NIH HHS/ -- R37GM23547/GM/NIGMS NIH HHS/ -- U01 HD 42283/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):405-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Stomatology, Anatomy, and Pharmaceutical Chemistry, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532021" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Blastocyst/physiology ; Cell Adhesion ; Cells, Cultured ; *Embryo Implantation ; Endometrium/cytology/metabolism/*physiology ; Epithelial Cells/metabolism ; Female ; Follicular Phase ; Humans ; Immunoblotting ; Jurkat Cells ; L-Selectin/immunology/*metabolism ; Ligands ; Luteal Phase ; Mice ; Microspheres ; Oligosaccharides/*metabolism ; Organ Culture Techniques ; Pregnancy ; Trophoblasts/metabolism/*physiology ; Up-Regulation
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Mitochondrial dysfunction in the elderly: possible role in insulin resistance (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-17
    Description: Insulin resistance is a major factor in the pathogenesis of type 2 diabetes in the elderly. To investigate how insulin resistance arises, we studied healthy, lean, elderly and young participants matched for lean body mass and fat mass. Elderly study participants were markedly insulin-resistant as compared with young controls, and this resistance was attributable to reduced insulin-stimulated muscle glucose metabolism. These changes were associated with increased fat accumulation in muscle and liver tissue assessed by 1H nuclear magnetic resonance (NMR) spectroscopy, and with a approximately 40% reduction in mitochondrial oxidative and phosphorylation activity, as assessed by in vivo 13C/31P NMR spectroscopy. These data support the hypothesis that an age-associated decline in mitochondrial function contributes to insulin resistance in the elderly.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004429/" 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/PMC3004429/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petersen, Kitt Falk -- Befroy, Douglas -- Dufour, Sylvie -- Dziura, James -- Ariyan, Charlotte -- Rothman, Douglas L -- DiPietro, Loretta -- Cline, Gary W -- Shulman, Gerald I -- K-23 DK-02347/DK/NIDDK NIH HHS/ -- K23 DK002734/DK/NIDDK NIH HHS/ -- K23 DK002734-04/DK/NIDDK NIH HHS/ -- M01 RR-00125/RR/NCRR NIH HHS/ -- P30 DK-45735/DK/NIDDK NIH HHS/ -- P60 AG-10469/AG/NIA NIH HHS/ -- R01 AG-09872/AG/NIA NIH HHS/ -- R01 AG023686/AG/NIA NIH HHS/ -- R01 AG023686-01A1/AG/NIA NIH HHS/ -- R01 DK-49230/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 May 16;300(5622):1140-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12750520" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Aging/metabolism ; Blood Glucose/metabolism ; Body Mass Index ; Female ; Humans ; Insulin/metabolism ; *Insulin Resistance ; Liver/metabolism ; Male ; Middle Aged ; Mitochondria/*metabolism ; Mitochondrial Diseases/blood/*complications/metabolism ; Muscle, Skeletal/metabolism ; Nuclear Magnetic Resonance, Biomolecular ; Oxidation-Reduction ; Oxygen Consumption ; Phosphorylation ; Triglycerides/*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
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    Inactivation of TNF signaling by rationally designed dominant-negative TNF variants (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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