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  • Binding Sites  (206)
  • Rats  (186)
  • American Association for the Advancement of Science (AAAS)  (382)
  • Springer Nature
  • 2000-2004  (189)
  • 1995-1999  (193)
  • 1940-1944
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  • American Association for the Advancement of Science (AAAS)  (382)
  • Springer Nature
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  • 1
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    A physical map of 30,000 human genes (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-23
    Description: A map of 30,181 human gene-based markers was assembled and integrated with the current genetic map by radiation hybrid mapping. The new gene map contains nearly twice as many genes as the previous release, includes most genes that encode proteins of known function, and is twofold to threefold more accurate than the previous version. A redesigned, more informative and functional World Wide Web site (www.ncbi.nlm.nih.gov/genemap) provides the mapping information and associated data and annotations. This resource constitutes an important infrastructure and tool for the study of complex genetic traits, the positional cloning of disease genes, the cross-referencing of mammalian genomes, and validated human transcribed sequences for large-scale studies of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deloukas, P -- Schuler, G D -- Gyapay, G -- Beasley, E M -- Soderlund, C -- Rodriguez-Tome, P -- Hui, L -- Matise, T C -- McKusick, K B -- Beckmann, J S -- Bentolila, S -- Bihoreau, M -- Birren, B B -- Browne, J -- Butler, A -- Castle, A B -- Chiannilkulchai, N -- Clee, C -- Day, P J -- Dehejia, A -- Dibling, T -- Drouot, N -- Duprat, S -- Fizames, C -- Fox, S -- Gelling, S -- Green, L -- Harrison, P -- Hocking, R -- Holloway, E -- Hunt, S -- Keil, S -- Lijnzaad, P -- Louis-Dit-Sully, C -- Ma, J -- Mendis, A -- Miller, J -- Morissette, J -- Muselet, D -- Nusbaum, H C -- Peck, A -- Rozen, S -- Simon, D -- Slonim, D K -- Staples, R -- Stein, L D -- Stewart, E A -- Suchard, M A -- Thangarajah, T -- Vega-Czarny, N -- Webber, C -- Wu, X -- Hudson, J -- Auffray, C -- Nomura, N -- Sikela, J M -- Polymeropoulos, M H -- James, M R -- Lander, E S -- Hudson, T J -- Myers, R M -- Cox, D R -- Weissenbach, J -- Boguski, M S -- Bentley, D R -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):744-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sanger Centre, Hinxton Hall, Hinxton, Cambridge CB10 1SA UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784132" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human/*genetics ; Expressed Sequence Tags ; Gene Expression ; Genetic Markers ; *Genome, Human ; Human Genome Project ; Humans ; Internet ; *Physical Chromosome Mapping ; Rats ; Sequence Tagged Sites
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    A receptor in pituitary and hypothalamus that functions in growth hormone release (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-16
    Description: Small synthetic molecules termed growth hormone secretagogues (GHSs) act on the pituitary gland and the hypothalamus to stimulate and amplify pulsatile growth hormone (GH) release. A heterotrimeric GTP-binding protein (G protein)-coupled receptor (GPC-R) of the pituitary and arcuate ventro-medial and infundibular hypothalamus of swine and humans was cloned and was shown to be the target of the GHSs. On the basis of its pharmacological and molecular characterization, this GPC-R defines a neuroendocrine pathway for the control of pulsatile GH release and supports the notion that the GHSs mimic an undiscovered hormone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howard, A D -- Feighner, S D -- Cully, D F -- Arena, J P -- Liberator, P A -- Rosenblum, C I -- Hamelin, M -- Hreniuk, D L -- Palyha, O C -- Anderson, J -- Paress, P S -- Diaz, C -- Chou, M -- Liu, K K -- McKee, K K -- Pong, S S -- Chaung, L Y -- Elbrecht, A -- Dashkevicz, M -- Heavens, R -- Rigby, M -- Sirinathsinghji, D J -- Dean, D C -- Melillo, D G -- Patchett, A A -- Nargund, R -- Griffin, P R -- DeMartino, J A -- Gupta, S K -- Schaeffer, J M -- Smith, R G -- Van der Ploeg, L H -- New York, N.Y. -- Science. 1996 Aug 16;273(5277):974-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Merck Research Laboratories, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8688086" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Codon ; DNA, Complementary/genetics ; GTP-Binding Proteins/metabolism ; Growth Hormone/*secretion ; Hormones/*metabolism ; Humans ; Hypothalamus, Middle/chemistry ; Indoles/*metabolism/pharmacology ; Macaca mulatta ; Molecular Sequence Data ; Oligopeptides/*metabolism ; Pituitary Gland/chemistry ; RNA, Complementary/genetics ; Rats ; Receptors, Cell Surface/analysis/chemistry/genetics/*metabolism ; *Receptors, G-Protein-Coupled ; Receptors, Ghrelin ; Spiro Compounds/*metabolism/pharmacology ; Swine
    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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    Prevention of chemotherapy-induced alopecia in rats by CDK inhibitors (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-01-06
    Description: Most traditional cytotoxic anticancer agents ablate the rapidly dividing epithelium of the hair follicle and induce alopecia (hair loss). Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator of eukaryotic cell cycle progression, may represent a therapeutic strategy for prevention of chemotherapy-induced alopecia (CIA) by arresting the cell cycle and reducing the sensitivity of the epithelium to many cell cycle-active antitumor agents. Potent small-molecule inhibitors of CDK2 were developed using structure-based methods. Topical application of these compounds in a neonatal rat model of CIA reduced hair loss at the site of application in 33 to 50% of the animals. Thus, inhibition of CDK2 represents a potentially useful approach for the prevention of CIA in cancer patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S T -- Benson, B G -- Bramson, H N -- Chapman, D E -- Dickerson, S H -- Dold, K M -- Eberwein, D J -- Edelstein, M -- Frye, S V -- Gampe Jr, R T -- Griffin, R J -- Harris, P A -- Hassell, A M -- Holmes, W D -- Hunter, R N -- Knick, V B -- Lackey, K -- Lovejoy, B -- Luzzio, M J -- Murray, D -- Parker, P -- Rocque, W J -- Shewchuk, L -- Veal, J M -- Walker, D H -- Kuyper, L F -- New York, N.Y. -- Science. 2001 Jan 5;291(5501):134-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Glaxo Wellcome Research and Development, Research Triangle Park, NC 27709, USA. std41085@glaxowellcome.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11141566" target="_blank"〉PubMed〈/a〉
    Keywords: Alopecia/*chemically induced/*prevention & control ; Animals ; Animals, Newborn ; Antineoplastic Agents/*toxicity ; Antineoplastic Combined Chemotherapy Protocols/toxicity ; Apoptosis/drug effects ; *CDC2-CDC28 Kinases ; Cell Cycle/drug effects ; Cell Line ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/*antagonists & inhibitors/metabolism ; Cyclophosphamide/toxicity ; Cytoprotection/drug effects ; DNA/biosynthesis ; Doxorubicin/toxicity ; Drug Design ; Enzyme Inhibitors/chemical synthesis/chemistry/*pharmacology ; Epithelium/drug effects ; Etoposide/toxicity ; Hair Follicle/cytology/*drug effects ; Humans ; Indoles/chemical synthesis/chemistry/*pharmacology ; Mice ; Mice, SCID ; Phosphorylation ; Protein-Serine-Threonine Kinases/*antagonists & inhibitors/metabolism ; Rats ; Retinoblastoma Protein/metabolism ; Scalp/transplantation ; Sulfonamides/chemical synthesis/chemistry/*pharmacology ; Transplantation, Heterologous
    Print ISSN: 0036-8075
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  • 4
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    Peptide antagonists of the human estrogen receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Estrogen receptor alpha transcriptional activity is regulated by distinct conformational states that are the result of ligand binding. Phage display was used to identify peptides that interact specifically with either estradiol- or tamoxifen-activated estrogen receptor alpha. When these peptides were coexpressed with estrogen receptor alpha in cells, they functioned as ligand-specific antagonists, indicating that estradiol-agonist and tamoxifen-partial agonist activities do not occur by the same mechanism. The ability to regulate estrogen receptor alpha transcriptional activity by targeting sites outside of the ligand-binding pocket has implications for the development of estrogen receptor alpha antagonists for the treatment of tamoxifen-refractory breast cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norris, J D -- Paige, L A -- Christensen, D J -- Chang, C Y -- Huacani, M R -- Fan, D -- Hamilton, P T -- Fowlkes, D M -- McDonnell, D P -- DK48807/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):744-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Duke University Medical Center, Department of Pharmacology and Cancer Biology, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426998" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Estradiol/metabolism/*pharmacology ; Estrogen Antagonists/*pharmacology ; Estrogen Receptor alpha ; Humans ; Ligands ; Mifepristone/pharmacology ; Molecular Sequence Data ; Peptide Library ; Peptides/metabolism/*pharmacology ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Estrogen/agonists/*antagonists & inhibitors/chemistry/*metabolism ; Recombinant Fusion Proteins/pharmacology ; Tamoxifen/metabolism/*pharmacology ; Transcription Factor AP-1/genetics/metabolism ; Transcription, Genetic/drug effects
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Receptor for motilin identified in the human gastrointestinal system (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: Motilin is a 22-amino acid peptide hormone expressed throughout the gastrointestinal (GI) tract of humans and other species. It affects gastric motility by stimulating interdigestive antrum and duodenal contractions. A heterotrimeric guanosine triphosphate-binding protein (G protein)-coupled receptor for motilin was isolated from human stomach, and its amino acid sequence was found to be 52 percent identical to the human receptor for growth hormone secretagogues. The macrolide antibiotic erythromycin also interacted with the cloned motilin receptor, providing a molecular basis for its effects on the human GI tract. The motilin receptor is expressed in enteric neurons of the human duodenum and colon. Development of motilin receptor agonists and antagonists may be useful in the treatment of multiple disorders of GI motility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feighner, S D -- Tan, C P -- McKee, K K -- Palyha, O C -- Hreniuk, D L -- Pong, S S -- Austin, C P -- Figueroa, D -- MacNeil, D -- Cascieri, M A -- Nargund, R -- Bakshi, R -- Abramovitz, M -- Stocco, R -- Kargman, S -- O'Neill, G -- Van Der Ploeg, L H -- Evans, J -- Patchett, A A -- Smith, R G -- Howard, A D -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2184-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Metabolic Disorders, Department of Medicinal Chemistry, Merck Research Laboratories, Building RY-80Y-265, 126 East Lincoln Avenue, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381885" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amino Acid Sequence ; Base Sequence ; Binding Sites ; Calcium/metabolism ; Cell Line ; Chromosome Mapping ; Chromosomes, Human, Pair 13 ; Cloning, Molecular ; Colon/*metabolism ; Erythromycin/metabolism ; GTP-Binding Proteins/metabolism ; Humans ; In Situ Hybridization ; Intestine, Small/*metabolism ; Ligands ; Molecular Sequence Data ; Motilin/analogs & derivatives/*metabolism ; Receptors, Gastrointestinal Hormone/*chemistry/*genetics/metabolism ; Receptors, Neuropeptide/*chemistry/*genetics/metabolism ; Stomach/*metabolism ; Thyroid Gland/metabolism ; Transfection
    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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  • 6
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    Embryonic stem cell-derived glial precursors: a source of myelinating transplants (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Self-renewing, totipotent embryonic stem (ES) cells may provide a virtually unlimited donor source for transplantation. A protocol that permits the in vitro generation of precursors for oligodendrocytes and astrocytes from ES cells was devised. Transplantation in a rat model of a human myelin disease shows that these ES cell-derived precursors interact with host neurons and efficiently myelinate axons in brain and spinal cord. Thus, ES cells can serve as a valuable source of cell type-specific somatic precursors for neural transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brustle, O -- Jones, K N -- Learish, R D -- Karram, K -- Choudhary, K -- Wiestler, O D -- Duncan, I D -- McKay, R D -- NS33710/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):754-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuropathology, University of Bonn Medical Center, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany. brustle@uni-bonn.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10427001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*cytology ; Brain/embryology/metabolism ; Cell Differentiation ; Cell Line ; Cell Movement ; Cerebral Ventricles/embryology/surgery ; Diffuse Cerebral Sclerosis of Schilder/genetics/*therapy ; Embryo, Mammalian/cytology ; Growth Substances/pharmacology ; Humans ; Male ; Mice ; Myelin Basic Protein/biosynthesis ; Myelin Proteolipid Protein/biosynthesis/genetics ; Myelin Sheath/*physiology ; Oligodendroglia/*cytology/metabolism/*transplantation/ultrastructure ; Rats ; Spinal Cord ; Stem Cell Transplantation ; Stem Cells/*cytology
    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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    A natural product that lowers cholesterol as an antagonist ligand for FXR (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-04
    Description: Extracts of the resin of the guggul tree (Commiphora mukul) lower LDL (low-density lipoprotein) cholesterol levels in humans. The plant sterol guggulsterone [4,17(20)-pregnadiene-3,16-dione] is the active agent in this extract. We show that guggulsterone is a highly efficacious antagonist of the farnesoid X receptor (FXR), a nuclear hormone receptor that is activated by bile acids. Guggulsterone treatment decreases hepatic cholesterol in wild-type mice fed a high-cholesterol diet but is not effective in FXR-null mice. Thus, we propose that inhibition of FXR activation is the basis for the cholesterol-lowering activity of guggulsterone. Other natural products with specific biologic effects may modulate the activity of FXR or other relatively promiscuous nuclear hormone receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Urizar, Nancy L -- Liverman, Amy B -- Dodds, D'Nette T -- Silva, Frank Valentin -- Ordentlich, Peter -- Yan, Yingzhuo -- Gonzalez, Frank J -- Heyman, Richard A -- Mangelsdorf, David J -- Moore, David D -- New York, N.Y. -- Science. 2002 May 31;296(5573):1703-6. Epub 2002 May 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Caco-2 Cells ; Carrier Proteins/genetics/metabolism ; Cells, Cultured ; Chenodeoxycholic Acid/pharmacology ; Cholesterol/*metabolism ; Cholesterol, Dietary/administration & dosage ; DNA/metabolism ; DNA-Binding Proteins/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Hepatocytes/metabolism ; Histone Acetyltransferases ; Humans ; *Hydroxysteroid Dehydrogenases ; Hypolipidemic Agents/metabolism/*pharmacology ; Ligands ; Liver/metabolism ; *Membrane Glycoproteins ; Mice ; Nuclear Receptor Coactivator 1 ; Pregnenediones/metabolism/*pharmacology ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors/genetics/metabolism ; Receptors, Steroid/antagonists & inhibitors/metabolism ; Transcription Factors/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Transcriptional Activation/drug effects ; Transfection ; Tumor Cells, Cultured
    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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  • 8
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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
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  • 9
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    Two-state allosteric behavior in a single-domain signaling protein (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-27
    Description: Protein actions are usually discussed in terms of static structures, but function requires motion. We find a strong correlation between phosphorylation-driven activation of the signaling protein NtrC and microsecond time-scale backbone dynamics. Using nuclear magnetic resonance relaxation, we characterized the motions of NtrC in three functional states: unphosphorylated (inactive), phosphorylated (active), and a partially active mutant. These dynamics are indicative of exchange between inactive and active conformations. Both states are populated in unphosphorylated NtrC, and phosphorylation shifts the equilibrium toward the active species. These results support a dynamic population shift between two preexisting conformations as the underlying mechanism of activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Volkman, B F -- Lipson, D -- Wemmer, D E -- Kern, D -- GM62117/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2001 Mar 23;291(5512):2429-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Magnetic Resonance Facility at Madison (NMRFAM), Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11264542" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; *Bacterial Proteins ; Binding Sites ; DNA-Binding Proteins/*chemistry/genetics/*metabolism ; Models, Molecular ; Motion ; Mutation ; Nuclear Magnetic Resonance, Biomolecular ; PII Nitrogen Regulatory Proteins ; Phosphorylation ; *Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Signal Transduction ; Time ; *Trans-Activators ; *Transcription Factors
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  • 10
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    The influence of the proinflammatory cytokine, osteopontin, on autoimmune demyelinating disease (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-11-27
    Description: Multiple sclerosis is a demyelinating disease, characterized by inflammation in the brain and spinal cord, possibly due to autoimmunity. Large-scale sequencing of cDNA libraries, derived from plaques dissected from brains of patients with multiple sclerosis (MS), indicated an abundance of transcripts for osteopontin (OPN). Microarray analysis of spinal cords from rats paralyzed by experimental autoimmune encephalomyelitis (EAE), a model of MS, also revealed increased OPN transcripts. Osteopontin-deficient mice were resistant to progressive EAE and had frequent remissions, and myelin-reactive T cells in OPN-/- mice produced more interleukin 10 and less interferon-gamma than in OPN+/+ mice. Osteopontin thus appears to regulate T helper cell-1 (TH1)-mediated demyelinating disease, and it may offer a potential target in blocking development of progressive MS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chabas, D -- Baranzini, S E -- Mitchell, D -- Bernard, C C -- Rittling, S R -- Denhardt, D T -- Sobel, R A -- Lock, C -- Karpuj, M -- Pedotti, R -- Heller, R -- Oksenberg, J R -- Steinman, L -- New York, N.Y. -- Science. 2001 Nov 23;294(5547):1731-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, B002, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11721059" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Encephalomyelitis, Autoimmune, ; Experimental/genetics/immunology/metabolism/pathology ; Expressed Sequence Tags ; Gene Deletion ; *Gene Expression Profiling ; Gene Library ; Humans ; Inflammation/genetics/immunology/metabolism/pathology ; Interferon-gamma/genetics/metabolism ; Interleukin-10/genetics/metabolism ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Multiple Sclerosis/*genetics/immunology/*metabolism/pathology ; Oligonucleotide Array Sequence Analysis ; Osteopontin ; RNA, Messenger/genetics/metabolism ; Rats ; Sialoglycoproteins/deficiency/genetics/*metabolism ; Spinal Cord/metabolism ; Th1 Cells/immunology
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