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  • Articles  (53)
  • Cell Line  (53)
  • 2000-2004  (53)
  • 1980-1984
  • 1925-1929
  • 2003  (53)
  • Science. 299(5603): 31. doi: 10.1126/science.299.5603.31a.  (1)
  • Science. 299(5605): 363. doi: 10.1126/science.1077838.  (1)
  • Science. 299(5605): 392-6. doi: 10.1126/science.1077813.  (1)
  • Science. 299(5606): 493-5. doi: 10.1126/science.299.5606.493b.  (1)
  • Science. 299(5608): 838-9. doi: 10.1126/science.1082028.  (1)
  • Science. 299(5608): 884-7. doi: 10.1126/science.1079085.  (1)
  • Science. 299(5611): 1394-7. doi: 10.1126/science.1079181.  (1)
  • Science. 299(5611): 1397-400. doi: 10.1126/science.1079474.  (1)
  • Science. 299(5611): 1410-3. doi: 10.1126/science.1081578.  (1)
  • Science. 299(5613): 1713-6. doi: 10.1126/science.1080115.  (1)
  • Science. 299(5614): 1830-1. doi: 10.1126/science.299.5614.1830.  (1)
  • Science. 299(5615): 2054-8. doi: 10.1126/science.1080376.  (1)
  • Science. 300(5617): 329-32. doi: 10.1126/science.1082095.  (1)
  • Science. 300(5619): 592-4. doi: 10.1126/science.1084976.  (1)
  • Science. 300(5619): 653-6. doi: 10.1126/science.1080273.  (1)
  • Science. 300(5620): 763. doi: 10.1126/science.1078395.  (1)
  • Science. 300(5621): 911-2. doi: 10.1126/science.1084819.  (1)
  • Science. 300(5622): 1112. doi: 10.1126/science.1083338.  (1)
  • Science. 300(5622): 1148-51. doi: 10.1126/science.1081315.  (1)
  • Science. 300(5623): 1288-91. doi: 10.1126/science.1082588.  (1)
  • 25
Collection
  • Articles  (53)
Source
Keywords
Publisher
Years
  • 2000-2004  (53)
  • 1980-1984
  • 1925-1929
Year
Journal
Topic
  • 1
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    Reversing the inactivation of peroxiredoxins caused by cysteine sulfinic acid formation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-26
    Description: The active-site cysteine of peroxiredoxins is selectively oxidized to cysteine sulfinic acid during catalysis, which leads to inactivation of peroxidase activity. This oxidation was thought to be irreversible. However, by metabolic labeling of mammalian cells with 35S, we show that the sulfinic form of peroxiredoxin I, produced during the exposure of cells to H2O2, is rapidly reduced to the catalytically active thiol form. The mammalian cells' ability to reduce protein sulfinic acid might serve as a mechanism to repair oxidatively damaged proteins or represent a new type of cyclic modification by which the function of various proteins is regulated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woo, Hyun Ae -- Chae, Ho Zoon -- Hwang, Sung Chul -- Yang, Kap-Seok -- Kang, Sang Won -- Kim, Kanghwa -- Rhee, Sue Goo -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):653-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cell Signaling Research and Division of Molecular Life Sciences, Ewha Womans University, Seoul 120-750, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12714748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalysis ; Cell Line ; Cycloheximide/pharmacology ; Cysteine/*analogs & derivatives/*metabolism ; Dimerization ; HeLa Cells ; Humans ; Hydrogen Peroxide/*metabolism ; Methionine/metabolism ; Mice ; Neurotransmitter Agents ; Oxidation-Reduction ; Peroxidases/chemistry/*metabolism ; Peroxiredoxins ; Protein Synthesis Inhibitors/pharmacology ; Spectrometry, Mass, Electrospray Ionization ; Sulfhydryl Compounds/metabolism ; Sulfinic Acids/metabolism ; Tumor Cells, Cultured
    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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    Insulin staining of ES cell progeny from insulin uptake (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajagopal, Jayaraj -- Anderson, William J -- Kume, Shoen -- Martinez, Olga I -- Melton, Douglas A -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):363.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Howard Hughes Medical Institute, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Apoptosis ; Cell Differentiation ; Cell Line ; Embryo, Mammalian/*cytology ; Humans ; Insulin/*analysis/genetics/immunology/*metabolism ; Islets of Langerhans/*cytology/metabolism ; Mice ; Microscopy, Confocal ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Stem Cells/*cytology/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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  • 3
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    Single molecule profiling of alternative pre-mRNA splicing (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-09
    Description: Alternative pre-messenger RNA splicing is an important mechanism for generating protein diversity and may explain in part how mammalian complexity arises from a surprisingly small complement of genes. Here, we describe "digital polony exon profiling,"a single molecule-based technology for studying complex alternative pre-messenger RNA splicing. This technology allows researchers to monitor the combinatorial diversity of exon inclusion in individual transcripts. A minisequencing strategy provides single nucleotide resolution, and the digital nature of the technology allows quantitation of individual splicing variants. Digital polony exon profiling can be used to investigate the physiological and pathological roles of alternately spliced messenger RNAs, as well as the mechanisms by which these messenger RNAs are produced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Jun -- Shendure, Jay -- Mitra, Robi D -- Church, George M -- 5U54GM62119/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):836-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907803" target="_blank"〉PubMed〈/a〉
    Keywords: Acrylamide ; *Alternative Splicing ; Animals ; Antigens, CD44/genetics ; Brain/metabolism ; Cell Line ; Cell Line, Transformed ; Cyclic AMP Response Element-Binding Protein ; *Exons ; Humans ; Mice ; Microtubule-Associated Proteins/genetics ; Nerve Tissue Proteins/genetics ; Polymerase Chain Reaction/*methods ; Polymorphism, Single Nucleotide ; Protein Isoforms ; RNA Precursors/*genetics/metabolism ; RNA-Binding Proteins ; SMN Complex Proteins
    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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    Role of EDEM in the release of misfolded glycoproteins from the calnexin cycle (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: The mechanisms that determine how folding attempts are interrupted to target folding-incompetent proteins for endoplasmic reticulum-associated degradation (ERAD) are poorly defined. Here the alpha-mannosidase I-like protein EDEM was shown to extract misfolded glycoproteins, but not glycoproteins undergoing productive folding, from the calnexin cycle. EDEM overexpression resulted in faster release of folding-incompetent proteins from the calnexin cycle and earlier onset of degradation, whereas EDEM down-regulation prolonged folding attempts and delayed ERAD. Up-regulation of EDEM during ER stress may promote cell recovery by clearing the calnexin cycle and by accelerating ERAD of terminally misfolded polypeptides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Molinari, Maurizio -- Calanca, Verena -- Galli, Carmela -- Lucca, Paola -- Paganetti, Paolo -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1397-400.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Research in Biomedicine, CH-6500 Bellinzona, Switzerland. Maurizio.molinari@irb.unisi.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610306" target="_blank"〉PubMed〈/a〉
    Keywords: Aspartic Acid Endopeptidases/chemistry/*metabolism ; Calnexin/*metabolism ; Cell Line ; Down-Regulation ; Electrophoresis, Polyacrylamide Gel ; Endoplasmic Reticulum/*metabolism ; Glycoproteins/chemistry/*metabolism ; Glycosylation ; Humans ; Kinetics ; Membrane Proteins/*metabolism ; Molecular Weight ; Polysaccharides/metabolism ; Protein Conformation ; Protein Folding ; RNA Interference ; Transfection ; 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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  • 5
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    A B cell-based sensor for rapid identification of pathogens (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-12
    Description: We report the use of genetically engineered cells in a pathogen identification sensor. This sensor uses B lymphocytes that have been engineered to emit light within seconds of exposure to specific bacteria and viruses. We demonstrated rapid screening of relevant samples and identification of a variety of pathogens at very low levels. Because of its speed, sensitivity, and specificity, this pathogen identification technology could prove useful for medical diagnostics, biowarfare defense, food- and water-quality monitoring, and other applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rider, Todd H -- Petrovick, Martha S -- Nargi, Frances E -- Harper, James D -- Schwoebel, Eric D -- Mathews, Richard H -- Blanchard, David J -- Bortolin, Laura T -- Young, Albert M -- Chen, Jianzhu -- Hollis, Mark A -- New York, N.Y. -- Science. 2003 Jul 11;301(5630):213-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts Institute of Technology Lincoln Laboratory, Lexington, MA 02420, USA. thor@ll.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855808" target="_blank"〉PubMed〈/a〉
    Keywords: Aequorin/biosynthesis ; Antibodies, Bacterial/immunology ; Antibodies, Viral/immunology ; *B-Lymphocytes/immunology ; Bacillus anthracis/immunology/isolation & purification ; Bacteria/immunology/*isolation & purification ; *Bacteriological Techniques ; *Biosensing Techniques ; Cell Line ; Colony Count, Microbial ; Encephalitis Virus, Venezuelan Equine/immunology/isolation & purification ; Escherichia coli O157/immunology/isolation & purification ; Foot-and-Mouth Disease Virus/immunology/isolation & purification ; Immunoglobulin Variable Region/immunology ; Light ; Receptors, Antigen, B-Cell/immunology ; Sensitivity and Specificity ; Time Factors ; Transfection ; Viruses/immunology/*isolation & purification ; Yersinia pestis/immunology/isolation & purification
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  • 6
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    TRB3: a tribbles homolog that inhibits Akt/PKB activation by insulin in liver (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-07
    Description: Insulin resistance is a major hallmark in the development of type II diabetes, which is characterized by the failure of insulin to promote glucose uptake in muscle and to suppress glucose production in liver. The serine-threonine kinase Akt (PKB) is a principal target of insulin signaling that inhibits hepatic glucose output when glucose is available from food. Here we show that TRB3, a mammalian homolog of Drosophila tribbles, functions as a negative modulator of Akt. TRB3 expression is induced in liver under fasting conditions, and TRB3 disrupts insulin signaling by binding directly to Akt and blocking activation of the kinase. Amounts of TRB3 RNA and protein were increased in livers of db/db diabetic mice compared with those in wild-type mice. Hepatic overexpression of TRB3 in amounts comparable to those in db/db mice promoted hyperglycemia and glucose intolerance. Our results suggest that, by interfering with Akt activation, TRB3 contributes to insulin resistance in individuals with susceptibility to type II diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Du, Keyong -- Herzig, Stephan -- Kulkarni, Rohit N -- Montminy, Marc -- New York, N.Y. -- Science. 2003 Jun 6;300(5625):1574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Peptide Biology Laboratories, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037-1002, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12791994" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/physiology ; Amino Acid Substitution ; Animals ; Blood Glucose/metabolism ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Diabetes Mellitus/genetics/metabolism ; Enzyme Activation ; Fasting ; Genetic Vectors ; Glucose/metabolism ; Glucose Intolerance ; Glycogen Synthase Kinase 3/metabolism ; Humans ; Insulin/blood/*metabolism ; Insulin Resistance ; Insulin-Like Growth Factor I/pharmacology ; Liver/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; RNA Interference ; Rats ; Repressor Proteins ; Signal Transduction ; Transfection ; Transgenes ; Tumor Cells, Cultured ; Two-Hybrid System Techniques
    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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    Control of nutrient-sensitive transcription programs by the unconventional prefoldin URI (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-15
    Description: Prefoldins (PFDs) are members of a recently identified, small-molecular weight protein family able to assemble into molecular chaperone complexes. Here we describe an unusually large member of this family, termed URI, that forms complexes with other small-molecular weight PFDs and with RPB5, a shared subunit of all three RNA polymerases. Functional analysis of the yeast and human orthologs of URI revealed that both are targets of nutrient signaling and participate in gene expression controlled by the TOR kinase. Thus, URI is a component of a signaling pathway that coordinates nutrient availability with gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gstaiger, Matthias -- Luke, Brian -- Hess, Daniel -- Oakeley, Edward J -- Wirbelauer, Christiane -- Blondel, Marc -- Vigneron, Marc -- Peter, Matthias -- Krek, Wilhelm -- New York, N.Y. -- Science. 2003 Nov 14;302(5648):1208-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institut, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14615539" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/*metabolism ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; DNA-Binding Proteins/metabolism ; DNA-Directed RNA Polymerases/metabolism ; GATA Transcription Factors ; *Gene Expression Regulation/drug effects ; Humans ; *Intracellular Signaling Peptides and Proteins ; Molecular Sequence Data ; Phosphorylation ; Protein Kinases/metabolism ; Protein Subunits/metabolism ; RNA Interference ; Repressor Proteins/metabolism ; Saccharomyces cerevisiae/*genetics/metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; *Signal Transduction ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases ; Trans-Activators/metabolism ; Transcription Factors/metabolism ; *Transcription, Genetic/drug effects ; 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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  • 8
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    A conserved domain in axonal targeting of Kv1 (Shaker) voltage-gated potassium channels (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-02
    Description: Axonal voltage-gated potassium (Kv1) channels regulate action-potential invasion and hence transmitter release. Although evolutionarily conserved, what mediates their axonal targeting is not known. We found that Kv1 axonal targeting required its T1 tetramerization domain. When fused to unpolarized CD4 or dendritic transferrin receptor, T1 promoted their axonal surface expression. Moreover, T1 mutations eliminating Kvbeta association compromised axonal targeting, but not surface expression, of CD4-T1 fusion proteins. Thus, proper association of Kvbeta with the Kv1 T1 domain is essential for axonal targeting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, Chen -- Jan, Yuh Nung -- Jan, Lily Yeh -- New York, N.Y. -- Science. 2003 Aug 1;301(5633):646-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Departments of Physiology and Biochemistry, University of California, San Francisco, CA 94143-0725, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12893943" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Substitution ; Animals ; Antigens, CD4/metabolism ; Axons/*metabolism ; Biopolymers ; COS Cells ; Cell Line ; Cell Membrane/metabolism ; Cell Polarity ; Cells, Cultured ; Dendrites/metabolism ; Endocytosis ; Hippocampus/cytology ; Humans ; Kv1.2 Potassium Channel ; Models, Molecular ; Mutagenesis ; Neurons/metabolism ; Potassium Channels/*chemistry/*metabolism ; *Potassium Channels, Voltage-Gated ; *Protein Structure, Tertiary ; Receptors, Transferrin/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Shaker Superfamily of Potassium Channels ; Shal Potassium Channels ; 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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  • 9
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    Cell therapy of alpha-sarcoglycan null dystrophic mice through intra-arterial delivery of mesoangioblasts (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-12
    Description: Preclinical or clinical trials for muscular dystrophies have met with modest success, mainly because of inefficient delivery of viral vectors or donor cells to dystrophic muscles. We report here that intra-arterial delivery of wild-type mesoangioblasts, a class of vessel-associated stem cells, corrects morphologically and functionally the dystrophic phenotype of virtually all downstream muscles in adult immunocompetent alpha-sarcoglycan (alpha-SG) null mice, a model organism for limb-girdle muscular dystrophy. When mesoangioblasts isolated from juvenile dystrophic mice and transduced with a lentiviral vector expressing alpha-SG were injected into the femoral artery of dystrophic mice, they reconstituted skeletal muscle in a manner similar to that seen in wild-type cells. The success of this protocol was mainly due to widespread distribution of donor stem cells through the capillary network, a distinct advantage of this strategy over previous approaches.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sampaolesi, Maurilio -- Torrente, Yvan -- Innocenzi, Anna -- Tonlorenzi, Rossana -- D'Antona, Giuseppe -- Pellegrino, M Antonietta -- Barresi, Rita -- Bresolin, Nereo -- De Angelis, M Gabriella Cusella -- Campbell, Kevin P -- Bottinelli, Roberto -- Cossu, Giulio -- 1322/Telethon/Italy -- 463/BI/Telethon/Italy -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):487-92. Epub 2003 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Research Institute, H. S. Raffaele, Via Olgettina 58, 20132 Milan, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/cytology/embryology ; Cell Differentiation ; Cell Line ; Cell Movement ; Cytoskeletal Proteins/*genetics/*metabolism ; Dystrophin/metabolism ; Endothelium, Vascular/physiology ; Female ; Femoral Artery ; Genetic Vectors ; Lentivirus/genetics ; Locomotion ; Male ; Membrane Glycoproteins/*genetics/*metabolism ; Mesoderm/cytology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Muscle Contraction ; Muscle Fibers, Skeletal/cytology/physiology ; Muscle, Skeletal/cytology/metabolism/pathology/*physiology ; Muscular Dystrophy, Animal/metabolism/pathology/*therapy ; Regeneration ; Sarcoglycans ; *Stem Cell Transplantation ; Stem Cells/*physiology ; Transfection
    Print ISSN: 0036-8075
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  • 10
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    Dishevelled 2 recruits beta-arrestin 2 to mediate Wnt5A-stimulated endocytosis of Frizzled 4 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-06
    Description: Wnt proteins, regulators of development in many organisms, bind to seven transmembrane-spanning (7TMS) receptors called frizzleds, thereby recruiting the cytoplasmic molecule dishevelled (Dvl) to the plasma membrane.Frizzled-mediated endocytosis of Wg (a Drosophila Wnt protein) and lysosomal degradation may regulate the formation of morphogen gradients. Endocytosis of Frizzled 4 (Fz4) in human embryonic kidney 293 cells was dependent on added Wnt5A protein and was accomplished by the multifunctional adaptor protein beta-arrestin 2 (betaarr2), which was recruited to Fz4 by binding to phosphorylated Dvl2. These findings provide a previously unrecognized mechanism for receptor recruitment of beta-arrestin and demonstrate that Dvl plays an important role in the endocytosis of frizzled, as well as in promoting signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Wei -- ten Berge, Derk -- Brown, Jeff -- Ahn, Seungkirl -- Hu, Liaoyuan A -- Miller, William E -- Caron, Marc G -- Barak, Larry S -- Nusse, Roel -- Lefkowitz, Robert J -- HL 16037/HL/NHLBI NIH HHS/ -- HL 61365/HL/NHLBI NIH HHS/ -- NS 19576/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Departments of Medicine and Biochemistry, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12958364" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Arrestins/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Clathrin/metabolism ; Cytoplasm/metabolism ; *Endocytosis ; Frizzled Receptors ; Humans ; Mice ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Kinase C/antagonists & inhibitors/metabolism ; Proteins/genetics/*metabolism ; Proto-Oncogene Proteins/*metabolism/pharmacology ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Wnt Proteins
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  • 11
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    The BRCT domain is a phospho-protein binding domain (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-25
    Description: The carboxyl-terminal domain (BRCT) of the Breast Cancer Gene 1 (BRCA1) protein is an evolutionarily conserved module that exists in a large number of proteins from prokaryotes to eukaryotes. Although most BRCT domain-containing proteins participate in DNA-damage checkpoint or DNA-repair pathways, or both, the function of the BRCT domain is not fully understood. We show that the BRCA1 BRCT domain directly interacts with phosphorylated BRCA1-Associated Carboxyl-terminal Helicase (BACH1). This specific interaction between BRCA1 and phosphorylated BACH1 is cell cycle regulated and is required for DNA damage-induced checkpoint control during the transition from G2 to M phase of the cell cycle. Further, we show that two other BRCT domains interact with their respective physiological partners in a phosphorylation-dependent manner. Thirteen additional BRCT domains also preferentially bind phospho-peptides rather than nonphosphorylated control peptides. These data imply that the BRCT domain is a phospho-protein binding domain involved in cell cycle control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Xiaochun -- Chini, Claudia Christiano Silva -- He, Miao -- Mer, Georges -- Chen, Junjie -- CA89239/CA/NCI NIH HHS/ -- CA92312/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 24;302(5645):639-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, Mayo Clinic and Foundation, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576433" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; BRCA1 Protein/*chemistry/*metabolism ; Carrier Proteins/chemistry/metabolism ; Cell Cycle ; *Cell Cycle Proteins ; Cell Line ; DNA Damage ; DNA Repair ; *DNA-Binding Proteins ; E2F Transcription Factors ; G2 Phase ; Humans ; Mitosis ; Mutation ; Nuclear Proteins ; Peptide Library ; Phosphoprotein Phosphatases/chemistry/metabolism ; Phosphoproteins/chemistry/genetics/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein Binding ; Protein Structure, Tertiary ; RNA Helicases/chemistry/genetics/*metabolism ; RNA Polymerase II/metabolism ; RNA, Small Interfering ; Recombinant Fusion Proteins/chemistry/metabolism ; Transcription Factors/metabolism ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    VDAC2 inhibits BAK activation and mitochondrial apoptosis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-26
    Description: The multidomain proapoptotic molecules BAK or BAX are required to initiate the mitochondrial pathway of apoptosis. How cells maintain the potentially lethal proapoptotic effector BAK in a monomeric inactive conformation at mitochondria is unknown. In viable cells, we found BAK complexed with mitochondrial outer-membrane protein VDAC2, a VDAC isoform present in low abundance that interacts specifically with the inactive conformer of BAK. Cells deficient in VDAC2, but not cells lacking the more abundant VDAC1, exhibited enhanced BAK oligomerization and were more susceptible to apoptotic death. Conversely, overexpression of VDAC2 selectively prevented BAK activation and inhibited the mitochondrial apoptotic pathway. Death signals activate "BH3-only" molecules such as tBID, BIM, or BAD, which displace VDAC2 from BAK, enabling homo-oligomerization of BAK and apoptosis. Thus, VDAC2, an isoform restricted to mammals, regulates the activity of BAK and provides a connection between mitochondrial physiology and the core apoptotic pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, Emily H Y -- Sheiko, Tatiana V -- Fisher, Jill K -- Craigen, William J -- Korsmeyer, Stanley J -- NS42319/NS/NINDS NIH HHS/ -- R37CA50239/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):513-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, 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/12881569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; BH3 Interacting Domain Death Agonist Protein ; Biopolymers ; Carrier Proteins/metabolism/pharmacology ; Cell Line ; Cells, Cultured ; Etoposide/pharmacology ; Humans ; Intracellular Membranes/metabolism ; Jurkat Cells ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Mitochondria/*metabolism ; Mitochondria, Liver/metabolism ; Porins/genetics/isolation & purification/*metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; Proto-Oncogene Proteins/metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; Recombinant Proteins/pharmacology ; Staurosporine/pharmacology ; Voltage-Dependent Anion Channel 1 ; Voltage-Dependent Anion Channel 2 ; Voltage-Dependent Anion Channels ; bcl-2 Homologous Antagonist-Killer Protein ; bcl-2-Associated X Protein
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    LRP: role in vascular wall integrity and protection from atherosclerosis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-12
    Description: Vascular smooth muscle cell (SMC) proliferation and migration are important events in the development of atherosclerosis. The low-density lipoprotein receptor-related protein (LRP1) mediates suppression of SMC migration induced by platelet-derived growth factor (PDGF). Here we show that LRP1 forms a complex with the PDGF receptor (PDGFR). Inactivation of LRP1 in vascular SMCs of mice causes PDGFR overexpression and abnormal activation of PDGFR signaling, resulting in disruption of the elastic layer, SMC proliferation, aneurysm formation, and marked susceptibility to cholesterol-induced atherosclerosis. The development of these abnormalities was reduced by treatment with Gleevec, an inhibitor of PDGF signaling. Thus, LRP1 has a pivotal role in protecting vascular wall integrity and preventing atherosclerosis by controlling PDGFR activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boucher, Philippe -- Gotthardt, Michael -- Li, Wei-Ping -- Anderson, Richard G W -- Herz, Joachim -- GM 52016/GM/NIGMS NIH HHS/ -- HL20948/HL/NHLBI NIH HHS/ -- HL63762/HL/NHLBI NIH HHS/ -- NS43408/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 11;300(5617):329-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9046, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690199" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/cytology/metabolism/*pathology ; Arteriosclerosis/*pathology/physiopathology/*prevention & control ; Benzamides ; Cattle ; Cell Division ; Cell Line ; Cholesterol, Dietary/administration & dosage ; Diet, Atherogenic ; Elastin/analysis ; Enzyme Inhibitors/pharmacology ; Imatinib Mesylate ; Ligands ; Low Density Lipoprotein Receptor-Related ; Protein-1/genetics/metabolism/*physiology ; Mesenteric Arteries/cytology/pathology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Muscle, Smooth, Vascular/cytology/*metabolism/pathology ; Myocytes, Smooth Muscle/*metabolism/physiology ; Phosphorylation ; Piperazines/pharmacology ; Platelet-Derived Growth Factor/metabolism/pharmacology ; Proto-Oncogene Proteins c-sis ; Pyrimidines/pharmacology ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Signal Transduction
    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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  • 14
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    Glycosylation restores survival of chilled blood platelets (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-13
    Description: Cooling of blood platelets clusters the von Willebrand factor receptor complex. Macrophage alphaMbeta2 integrins bind to the GPIbalpha subunit of the clustered complex, resulting in rapid clearance of transfused, cooled platelets. This precludes refrigeration of platelets for transfusion, but the current practice of room temperature storage has major drawbacks. We document that alphaMbeta2 is a lectin that recognizes exposed beta-N-acetylglucosamine residues of N-linked glycans on GPIbalpha. Enzymatic galactosylation of chilled platelets blocks alphaMbeta2 recognition, prolonging the circulation of functional cooled platelets. Platelet-associated galactosyltransferase produces efficient galactosylation when uridine diphosphate-galactose is added, affording a potentially simple method for storing platelets in the cold.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffmeister, Karin M -- Josefsson, Emma C -- Isaac, Natasha A -- Clausen, Henrik -- Hartwig, John H -- Stossel, Thomas P -- HL19429/HL/NHLBI NIH HHS/ -- HL56949/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 12;301(5639):1531-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. khoffmeister@rics.bwh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12970565" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylglucosamine/metabolism/pharmacology ; Animals ; Blood Platelets/metabolism/*physiology ; Blood Preservation ; Carbohydrate Conformation ; Cell Line ; Cell Survival ; *Cold Temperature ; Female ; Galactose/*metabolism ; Galactosyltransferases/metabolism ; Glycosylation ; Humans ; Lectins/metabolism ; Ligands ; Macrophage-1 Antigen/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Monosaccharides/pharmacology ; Phagocytosis/drug effects ; Platelet Aggregation ; Platelet Glycoprotein GPIb-IX Complex/metabolism ; *Platelet Membrane Glycoproteins ; Platelet Transfusion ; Refrigeration ; Uridine Diphosphate Galactose/metabolism ; von Willebrand Factor/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Induction of APOBEC3G ubiquitination and degradation by an HIV-1 Vif-Cul5-SCF complex (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: Human immunodeficiency virus-1 (HIV-1) Vif is essential for viral evasion of host antiviral factor CEM15/APOBEC3G. We report that Vif interacts with cellular proteins Cul5, elongins B and C, and Rbx1 to form an Skp1-cullin-F-box (SCF)-like complex. The ability of Vif to suppress antiviral activity of APOBEC3G was specifically dependent on Cul5-SCF function, allowing Vif to interact with APOBEC3G and induce its ubiquitination and degradation. A Vif mutant that interacted with APOBEC3G but not with Cul5-SCF was functionally inactive. The Cul5-SCF was also required for Vif function in distantly related simian immunodeficiency virus mac. These results indicate that the conserved Cul5-SCF pathway used by Vif is a potential target for antiviral development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Xianghui -- Yu, Yunkai -- Liu, Bindong -- Luo, Kun -- Kong, Wei -- Mao, Panyong -- Yu, Xiao-Fang -- 1S10-RR14702/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 7;302(5647):1056-60. Epub 2003 Oct 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/metabolism ; Cell Line ; Cullin Proteins/genetics/*metabolism ; Cytidine Deaminase ; Gene Products, vif/genetics/*metabolism ; HIV-1/genetics/*physiology ; Humans ; Mutation ; Nucleoside Deaminases ; Proteins/*metabolism ; Repressor Proteins ; Transcription Factors/genetics/metabolism ; Transfection ; Ubiquitin/*metabolism ; Virus Replication ; vif Gene Products, Human Immunodeficiency Virus
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Embryonic stem cells. Stem cell programs (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-10
    Description: The availability of human embryonic stem cell lines provides an important tool for scientists to explore the fundamental mechanisms that regulate differentiation into specific cell types. When more is known about the mechanisms that govern these processes, human embryonic stem cells may be clinically useful in generating cell types that have been damaged or depleted by a variety of human diseases. The NIH is actively pursuing a variety of initiatives to promote this developing research field, while continuing and expanding its long-standing investment in adult stem cells and research.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zerhouni, Elias -- New York, N.Y. -- Science. 2003 May 9;300(5621):911-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12738840" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Cell Culture Techniques ; Cell Line ; Education ; *Embryo Research ; Embryo, Mammalian/*cytology ; Expressed Sequence Tags ; Financing, Government ; Humans ; Internet ; *National Institutes of Health (U.S.) ; Patents as Topic ; Research Support as Topic ; *Stem Cells/cytology/physiology ; United States
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  • 17
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    Disruption of the epithelial apical-junctional complex by Helicobacter pylori CagA (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-31
    Description: Helicobacter pylori translocates the protein CagA into gastric epithelial cells and has been linked to peptic ulcer disease and gastric carcinoma. We show that injected CagA associates with the epithelial tight-junction scaffolding protein ZO-1 and the transmembrane protein junctional adhesion molecule, causing an ectopic assembly of tight-junction components at sites of bacterial attachment, and altering the composition and function of the apical-junctional complex. Long-term CagA delivery to polarized epithelia caused a disruption of the epithelial barrier function and dysplastic alterations in epithelial cell morphology. CagA appears to target H. pylori to host cell intercellular junctions and to disrupt junction-mediated functions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3369828/" 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/PMC3369828/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amieva, Manuel R -- Vogelmann, Roger -- Covacci, Antonello -- Tompkins, Lucy S -- Nelson, W James -- Falkow, Stanley -- AI38459/AI/NIAID NIH HHS/ -- CA92229/CA/NCI NIH HHS/ -- DDC DK56339/DC/NIDCD NIH HHS/ -- R01 GM035527/GM/NIGMS NIH HHS/ -- R01GM35227/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 May 30;300(5624):1430-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. amieva@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12775840" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/genetics/*metabolism ; Bacterial Adhesion ; Bacterial Proteins/genetics/*metabolism ; Cell Adhesion Molecules/metabolism ; Cell Line ; Cell Polarity ; Cell Size ; Dogs ; Epithelial Cells/cytology/metabolism/*microbiology/ultrastructure ; Gastric Mucosa ; Helicobacter pylori/*pathogenicity/physiology ; Humans ; Intracellular Signaling Peptides and Proteins ; Junctional Adhesion Molecules ; Membrane Proteins/metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; Protein Tyrosine Phosphatases/metabolism ; Tight Junctions/*microbiology/physiology/*ultrastructure ; Tumor Cells, Cultured ; Zonula Occludens-1 Protein
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  • 18
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    Talin binding to integrin beta tails: a final common step in integrin activation (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-10-04
    Description: Control of integrin affinity for ligands (integrin activation) is essential for normal cell adhesion, migration, and assembly of an extracellular matrix. Integrin activation is usually mediated through the integrin beta subunit cytoplasmic tail and can be regulated by many different biochemical signaling pathways. We report that specific binding of the cytoskeletal protein talin to integrin beta subunit cytoplasmic tails leads to the conformational rearrangements of integrin extracellular domains that increase their affinity. Thus, regulated binding of talin to integrin beta tails is a final common element of cellular signaling cascades that control integrin activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tadokoro, Seiji -- Shattil, Sanford J -- Eto, Koji -- Tai, Vera -- Liddington, Robert C -- de Pereda, Jose M -- Ginsberg, Mark H -- Calderwood, David A -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, The Burnham Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526080" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD29/chemistry/metabolism ; Cell Line ; Fibronectins/metabolism ; Humans ; Integrin beta Chains/chemistry/*metabolism ; Integrin beta3/chemistry/metabolism ; Molecular Sequence Data ; Mutation ; Platelet Glycoprotein GPIIb-IIIa Complex/chemistry/immunology/metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; RNA, Small Interfering ; Recombinant Proteins/metabolism ; *Signal Transduction ; Talin/*metabolism ; Transfection
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  • 19
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    Dilated cardiomyopathy and heart failure caused by a mutation in phospholamban (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-03-01
    Description: Molecular etiologies of heart failure, an emerging cardiovascular epidemic affecting 4.7 million Americans and costing 17.8 billion health-care dollars annually, remain poorly understood. Here we report that an inherited human dilated cardiomyopathy with refractory congestive heart failure is caused by a dominant Arg --〉 Cys missense mutation at residue 9 (R9C) in phospholamban (PLN), a transmembrane phosphoprotein that inhibits the cardiac sarcoplasmic reticular Ca2+-adenosine triphosphatase (SERCA2a) pump. Transgenic PLN(R9C) mice recapitulated human heart failure with premature death. Cellular and biochemical studies revealed that, unlike wild-type PLN, PLN(R9C) did not directly inhibit SERCA2a. Rather, PLN(R9C) trapped protein kinase A (PKA), which blocked PKA-mediated phosphorylation of wild-type PLN and in turn delayed decay of calcium transients in myocytes. These results indicate that myocellular calcium dysregulation can initiate human heart failure-a finding that may lead to therapeutic opportunities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmitt, Joachim P -- Kamisago, Mitsuhiro -- Asahi, Michio -- Li, Guo Hua -- Ahmad, Ferhaan -- Mende, Ulrike -- Kranias, Evangelia G -- MacLennan, David H -- Seidman, J G -- Seidman, Christine E -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1410-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School and Howard Hughes Medical Institute, 200 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610310" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Calcium/metabolism ; Calcium Signaling ; Calcium-Binding Proteins/chemistry/*genetics/*physiology ; Calcium-Transporting ATPases/antagonists & inhibitors/metabolism ; Cardiomegaly ; Cardiomyopathy, Dilated/*genetics/pathology/physiopathology ; Cell Line ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Female ; Heart Failure/*genetics/pathology/physiopathology ; Heart Ventricles/metabolism/pathology ; Humans ; Lod Score ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Muscle Cells/metabolism/physiology ; *Mutation, Missense ; Myocardial Contraction ; Myocardium/pathology ; Pedigree ; Phosphorylation ; Sarcoplasmic Reticulum Calcium-Transporting ATPases
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  • 20
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    Listeria intracellular growth and virulence require host-derived lipoic acid (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: Listeria monocytogenes is a Gram-positive intracytosolic pathogen that causes severe disease in pregnant and immunocompromised individuals. We found that L. monocytogenes lacking the lipoate protein ligase LplA1 was defective for growth specifically in the host cytosol and was less virulent in animals by a factor of 300. A major target for LplA1, the E2 subunit of pyruvate dehydrogenase (PDH), lacked a critical lipoyl modification when the DeltalplA1 strain was grown intracellularly, which suggests that abortive growth was due to loss of PDH function. Thus, the use of host-derived lipoic acid may be a critical process for in vivo replication of bacterial pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Riordan, Mary -- Moors, Marlena A -- Portnoy, Daniel A -- AI29619/AI/NIAID NIH HHS/ -- R01 AI027655/AI/NIAID NIH HHS/ -- R01 AI27655/AI/NIAID NIH HHS/ -- R37 AI029619/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):462-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, School of Public Health, University of California, Berkeley, CA 94720-3202, USA. oriordan@umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Culture Media ; Cytosol/microbiology ; Dihydrolipoyllysine-Residue Acetyltransferase ; Gene Deletion ; Lethal Dose 50 ; Listeria monocytogenes/genetics/*growth & development/metabolism/*pathogenicity ; Listeriosis/microbiology ; Macrophages/metabolism/*microbiology ; Mice ; Mice, Inbred BALB C ; Mutation ; Open Reading Frames ; Peptide Synthases/genetics/metabolism ; Pyruvate Dehydrogenase Complex/metabolism ; Thioctic Acid/*metabolism ; Virulence
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  • 21
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    Requirement of mammalian Timeless for circadian rhythmicity (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-10-18
    Description: Despite a central circadian role in Drosophila for the transcriptional regulator Timeless (dTim), the relevance of mammalian Timeless (mTim) remains equivocal. Conditional knockdown of mTim protein expression in the rat suprachiasmatic nucleus (SCN) disrupted SCN neuronal activity rhythms, and altered levels of known core clock elements. Full-length mTim protein (mTIM-fl) exhibited a 24-hour oscillation, where as a truncated isoform (mTIM-s) was constitutively expressed. mTIM-fl associated with the mammalian clock Period proteins (mPERs) in oscillating SCN cells. These data suggest that mTim is required for rhythmicity and is a functional homolog of dTim on the negative-feedback arm of the mammalian molecular clockwork.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, Jessica W -- Tischkau, Shelley A -- Barnes, Jeffrey A -- Mitchell, Jennifer W -- Burgoon, Penny W -- Hickok, Jason R -- Gillette, Martha U -- GM07143/GM/NIGMS NIH HHS/ -- HL67007/HL/NHLBI NIH HHS/ -- NS10170/NS/NINDS NIH HHS/ -- NS11134/NS/NINDS NIH HHS/ -- NS11158/NS/NINDS NIH HHS/ -- NS22155/NS/NINDS NIH HHS/ -- NS35859/NS/NINDS NIH HHS/ -- R01 HL067007/HL/NHLBI NIH HHS/ -- R01 NS022155/NS/NINDS NIH HHS/ -- R01 NS035859/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):439-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Structural Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564007" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks ; Cell Cycle Proteins ; Cell Line ; *Circadian Rhythm ; Cryptochromes ; *Drosophila Proteins ; Electrophysiology ; *Eye Proteins ; Flavoproteins/metabolism ; Humans ; In Vitro Techniques ; Intracellular Signaling Peptides and Proteins ; Neurons/physiology ; Nuclear Proteins/metabolism ; Oligonucleotides, Antisense/pharmacology ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; RNA Interference ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, G-Protein-Coupled ; Reverse Transcriptase Polymerase Chain Reaction ; Suprachiasmatic Nucleus/*physiology ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection
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    Biotechnology. Stem cells lose market luster (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2003 Mar 21;299(5614):1830-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12649456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Australia ; Biotechnology/*economics/manpower ; Cell Line ; Clinical Trials as Topic ; Cloning, Organism/*economics ; Commerce ; Embryo Research/*economics ; Embryo, Mammalian/*cytology ; Financing, Government ; Humans ; *Investments ; Research Personnel ; Research Support as Topic ; *Stem Cells ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cleavage of Arabidopsis PBS1 by a bacterial type III effector (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-30
    Description: Plant disease-resistance (R) proteins are thought to function as receptors for ligands produced directly or indirectly by pathogen avirulence (Avr) proteins. The biochemical functions of most Avr proteins are unknown, and the mechanisms by which they activate R proteins have not been determined. In Arabidopsis, resistance to Pseudomonas syringae strains expressing AvrPphB requires RPS5, a member of the class of R proteins that have a predicted nucleotide-binding site and leucine-rich repeats, and PBS1, a protein kinase. AvrPphB was found to proteolytically cleave PBS1, and this cleavage was required for RPS5-mediated resistance, which indicates that AvrPphB is detected indirectly via its enzymatic activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shao, Feng -- Golstein, Catherine -- Ade, Jules -- Stoutemyer, Mark -- Dixon, Jack E -- Innes, Roger W -- DK18849/DK/NIDDK NIH HHS/ -- GM46451/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 29;301(5637):1230-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Medical School and Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12947197" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/genetics/*metabolism/microbiology ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Bacterial Proteins/chemistry/genetics/*metabolism ; Carrier Proteins/genetics/metabolism ; Cell Line ; Cysteine Endopeptidases/chemistry/genetics/*metabolism ; Genes, Bacterial ; Genes, Plant ; Genetic Complementation Test ; Humans ; Models, Biological ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Plant Diseases/*microbiology ; Plant Extracts/metabolism ; Plant Proteins/genetics/metabolism ; Plants, Genetically Modified ; Precipitin Tests ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Pseudomonas/*metabolism ; Recombinant Proteins/metabolism ; Tobacco/genetics/metabolism ; Transformation, Genetic
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    Hypermutation of HIV-1 DNA in the absence of the Vif protein (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lecossier, Denise -- Bouchonnet, Francine -- Clavel, Francois -- Hance, Allan J -- New York, N.Y. -- Science. 2003 May 16;300(5622):1112.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U552, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12750511" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Cytidine Deaminase ; DNA Mutational Analysis ; DNA, Viral/biosynthesis/*genetics ; Gene Products, vif/*physiology ; HIV-1/genetics/*physiology ; HeLa Cells ; Humans ; Molecular Sequence Data ; *Mutation ; Nucleoside Deaminases ; Proteins/physiology ; Repressor Proteins ; Virion/genetics/physiology ; Virus Replication ; vif Gene Products, Human Immunodeficiency Virus
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    Nod1 detects a unique muropeptide from gram-negative bacterial peptidoglycan (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-07
    Description: Although the role of Toll-like receptors in extracellular bacterial sensing has been investigated intensively, intracellular detection of bacteria through Nod molecules remains largely uncharacterized. Here, we show that human Nod1 specifically detects a unique diaminopimelate-containing N-acetylglucosamine-N-acetylmuramic acid (GlcNAc-MurNAc) tripeptide motif found in Gram-negative bacterial peptidoglycan, resulting in activation of the transcription factor NF-kappaB pathway. Moreover, we show that in epithelial cells (which represent the first line of defense against invasive pathogens), Nod1is indispensable for intracellular Gram-negative bacterial sensing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Girardin, Stephen E -- Boneca, Ivo G -- Carneiro, Leticia A M -- Antignac, Aude -- Jehanno, Muguette -- Viala, Jerome -- Tedin, Karsten -- Taha, Muhamed-Kheir -- Labigne, Agnes -- Zahringer, Ulrich -- Coyle, Anthony J -- DiStefano, Peter S -- Bertin, John -- Sansonetti, Philippe J -- Philpott, Dana J -- New York, N.Y. -- Science. 2003 Jun 6;300(5625):1584-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite de Pathogenie Microbienne Moleculaire, INSERM U389, Institut Pasteur, 28, Rue du Dr. Roux, 75724Paris Cedex 15, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12791997" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Motifs ; Animals ; Antigens, Differentiation/metabolism ; Carrier Proteins/chemistry/metabolism/*physiology ; Cell Line ; Cytoplasm/microbiology ; Epithelial Cells/metabolism/microbiology ; Gram-Negative Bacteria/*chemistry/immunology ; Gram-Positive Bacteria/chemistry/immunology ; Humans ; Immunity, Innate ; Interleukin-8/metabolism ; *Intracellular Signaling Peptides and Proteins ; Lipopolysaccharides/pharmacology ; Mice ; Myeloid Differentiation Factor 88 ; NF-kappa B/chemistry/metabolism ; Nod1 Signaling Adaptor Protein ; Nod2 Signaling Adaptor Protein ; Oligopeptides/*analysis/chemistry ; Peptidoglycan/*chemistry/pharmacology ; Protein Structure, Tertiary ; Receptors, Immunologic/metabolism ; Signal Transduction ; Trisaccharides/*analysis/chemistry
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  • 26
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    Selective trafficking of non-cell-autonomous proteins mediated by NtNCAPP1 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: In plants, cell-to-cell communication is mediated by plasmodesmata and involves the trafficking of non-cell-autonomous proteins (NCAPs). A component in this pathway, Nicotiana tabacum NON-CELL-AUTONOMOUS PATHWAY PROTEIN1 (NtNCAPP1), was affinity purified and cloned. Protein overlay assays and in vivo studies showed that NtNCAPP1 is located on the endoplasmic reticulum at the cell periphery and displays specificity in its interaction with NCAPs. Deletion of the NtNCAPP1 amino-terminal transmembrane domain produced a dominant-negative mutant that blocked the trafficking of specific NCAPs. Transgenic tobacco plants expressing this mutant form of NtNCAPP1 and plants in which the NtNCAPP1 gene was silenced were compromised in their ability to regulate leaf and floral development. These results support a model in which NCAP delivery to plasmodesmata is both selective and regulated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Jung-Youn -- Yoo, Byung-Chun -- Rojas, Maria R -- Gomez-Ospina, Natalia -- Staehelin, L Andrew -- Lucas, William J -- GM18639/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):392-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Plant Biology, Division of Biological Sciences, University of California, 1 Shields Avenue, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532017" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Communication ; Cell Line ; Cloning, Molecular ; Cytoplasm/metabolism ; Endoplasmic Reticulum/metabolism ; Flowers/growth & development ; Gene Silencing ; Green Fluorescent Proteins ; Immunohistochemistry ; Luminescent Proteins/metabolism ; Molecular Sequence Data ; Mutation ; Phenotype ; Plant Leaves/growth & development ; Plant Proteins/chemistry/genetics/*isolation & purification/*metabolism ; Plants, Genetically Modified ; Plasmodesmata/*metabolism ; Protein Transport ; Recombinant Fusion Proteins/metabolism ; Tobacco/genetics/growth & development/*metabolism ; Tobacco Mosaic Virus ; Viral Proteins/metabolism
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    Chimeric nucleases stimulate gene targeting in human cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porteus, Matthew H -- Baltimore, David -- R01-GM39458/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 May 2;300(5620):763.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, California Institute of Technology, Pasadena CA 91125, USA. matthew.porteus@UTSouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730593" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; DNA/metabolism ; Deoxyribonucleases, Type II Site-Specific/chemistry/genetics/*metabolism ; Dimerization ; Gene Targeting/*methods ; Green Fluorescent Proteins ; Humans ; Luminescent Proteins/genetics ; Mutation ; Nuclear Localization Signals ; Recombinant Fusion Proteins/chemistry/*metabolism ; Recombination, Genetic ; Saccharomyces cerevisiae Proteins ; Transfection ; *Zinc Fingers
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    Predominant autoantibody production by early human B cell precursors (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-16
    Description: During B lymphocyte development, antibodies are assembled by random gene segment reassortment to produce a vast number of specificities. A potential disadvantage of this process is that some of the antibodies produced are self-reactive. We determined the prevalence of self-reactive antibody formation and its regulation in human B cells. A majority (55 to 75%) of all antibodies expressed by early immature B cells displayed self-reactivity, including polyreactive and anti-nuclear specificities. Most of these autoantibodies were removed from the population at two discrete checkpoints during B cell development. Inefficient checkpoint regulation would lead to substantial increases in circulating autoantibodies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wardemann, Hedda -- Yurasov, Sergey -- Schaefer, Anne -- Young, James W -- Meffre, Eric -- Nussenzweig, Michel C -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1374-7. Epub 2003 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920303" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Antinuclear/biosynthesis/immunology ; Antibody Diversity ; Antibody Specificity ; Autoantibodies/*biosynthesis/immunology ; B-Lymphocytes/cytology/*immunology/physiology ; Cell Differentiation ; Cell Line ; Complementarity Determining Regions/chemistry/immunology ; Cytosol/immunology ; Genes, Immunoglobulin ; Humans ; Immunoglobulin Heavy Chains/chemistry/immunology ; Recombination, Genetic ; Selection, Genetic ; Tumor Cells, Cultured
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    The birth of an alternatively spliced exon: 3' splice-site selection in Alu exons (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-24
    Description: Alu repetitive elements can be inserted into mature messenger RNAs via a splicing-mediated process termed exonization. To understand the molecular basis and the regulation of the process of turning intronic Alus into new exons, we compiled and analyzed a data set of human exonized Alus. We revealed a mechanism that governs 3' splice-site selection in these exons during alternative splicing. On the basis of these findings, we identified mutations that activated the exonization of a silent intronic Alu.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lev-Maor, Galit -- Sorek, Rotem -- Shomron, Noam -- Ast, Gil -- New York, N.Y. -- Science. 2003 May 23;300(5623):1288-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics and Molecular Medicine, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12764196" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/genetics ; *Alternative Splicing ; Alu Elements/*genetics ; Cell Line ; Cloning, Molecular ; DNA, Antisense ; Dinucleoside Phosphates/genetics ; *Exons ; Genome, Human ; Glucosyltransferases/genetics ; Humans ; Introns ; Mutagenesis, Site-Directed ; Point Mutation ; Polymerase Chain Reaction ; RNA-Binding Proteins ; Ribonucleoproteins, Small Nuclear/genetics/physiology ; Spliceosomes/metabolism ; Transfection ; Tumor Cells, Cultured
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    Inhibition of neuroepithelial patched-induced apoptosis by sonic hedgehog (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-09
    Description: During early development in vertebrates, Sonic hedgehog (Shh) is produced by the notochord and the floor plate. A ventrodorsal gradient of Shh directs ventrodorsal patterning of the neural tube. However, Shh is also required for the survival of neuroepithelial cells. We show that Patched (Ptc) induces apoptotic cell death unless its ligand Shh is present to block the signal. Moreover, the blockade of Ptc-induced cell death partly rescues the chick spinal cord defect provoked by Shh deprivation. Thus, the proapoptotic activity of unbound Ptc and the positive effect of Shh-bound Ptc on cell differentiation probably cooperate to achieve the appropriate spinal cord development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thibert, Chantal -- Teillet, Marie-Aimee -- Lapointe, Francoise -- Mazelin, Laetitia -- Le Douarin, Nicole M -- Mehlen, Patrick -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):843-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Apoptosis/Differentiation Laboratory, "La Ligue," Molecular and Cellular Genetic Center, CNRS Unite Mixte Recherche (UMR) 5534, University of Lyon, 69622 Villeurbanne, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907805" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 3 ; Caspases/metabolism ; Cell Differentiation ; Cell Line ; Central Nervous System/cytology/*embryology/metabolism ; Chick Embryo ; Electroporation ; Epithelial Cells/cytology/metabolism ; Hedgehog Proteins ; Humans ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mutation ; Protein Binding ; Protein Structure, Tertiary ; Rats ; Receptors, Cell Surface ; Signal Transduction ; Spinal Cord/cytology/embryology ; Trans-Activators/genetics/*metabolism ; Transfection
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  • 31
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    Screening for nitric oxide-dependent protein-protein interactions (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-02
    Description: Because nitric oxide (NO) may be a ubiquitous regulator of cellular signaling, we have modified the yeast two-hybrid system to explore the possibility of NO-dependent protein-protein interactions. We screened for binding partners of procaspase-3, a protein implicated in apoptotic signaling pathways, and identified multiple NO-dependent interactions.Two such interactions, with acid sphingomyelinase and NO synthase, were shown to occur in mammalian cells dependent on endogenous NO. Nitrosylation may thus provide a broad-based mechanism for regulating interactions between proteins. If so, systematic proteomic analyses in which redox state and NO bioavailability are carefully controlled will reveal a large array of novel interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsumoto, Akio -- Comatas, Karrie E -- Liu, Limin -- Stamler, Jonathan S -- New York, N.Y. -- Science. 2003 Aug 1;301(5633):657-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12893946" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Caspase 3 ; Caspases/*metabolism ; Cell Line ; Enzyme Inhibitors/pharmacology ; Enzyme Precursors/*metabolism ; Escherichia coli/genetics/growth & development ; Gene Library ; Humans ; Hydrogen Peroxide/metabolism ; Lysosomes/enzymology ; Mitochondria/enzymology ; Nitric Oxide/*metabolism/pharmacology ; Nitric Oxide Donors/pharmacology ; Nitric Oxide Synthase/antagonists & inhibitors/*metabolism ; Nitric Oxide Synthase Type I ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Oxidation-Reduction ; Precipitin Tests ; *Protein Binding ; Signal Transduction ; Sphingomyelin Phosphodiesterase/*metabolism ; Transfection ; Transformation, Bacterial ; Triazenes/pharmacology ; Two-Hybrid System Techniques ; beta-Galactosidase/metabolism ; omega-N-Methylarginine/pharmacology
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    European Union. E.U. stem cell debate ends in a draw (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1872-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671253" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Embryo Research/economics/legislation & jurisprudence ; Embryo, Mammalian/*cytology ; *European Union ; *Guidelines as Topic ; Humans ; Research Support as Topic ; *Stem Cells
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    Stem cells. Visiting German profs could face jail (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2003 Aug 1;301(5633):577.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12893913" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Embryo Research/*legislation & jurisprudence ; Embryo, Mammalian/*cytology ; *Faculty ; Germany ; Government ; Humans ; Jurisprudence ; Private Sector ; Public Sector ; Research Personnel/*legislation & jurisprudence ; *Stem Cells
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    Genome-wide survey of human alternative pre-mRNA splicing with exon junction microarrays (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: Alternative pre-messenger RNA (pre-mRNA) splicing plays important roles in development, physiology, and disease, and more than half of human genes are alternatively spliced. To understand the biological roles and regulation of alternative splicing across different tissues and stages of development, systematic methods are needed. Here, we demonstrate the use of microarrays to monitor splicing at every exon-exon junction in more than 10,000 multi-exon human genes in 52 tissues and cell lines. These genome-wide data provide experimental evidence and tissue distributions for thousands of known and novel alternative splicing events. Adding to previous studies, the results indicate that at least 74% of human multi-exon genes are alternatively spliced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, Jason M -- Castle, John -- Garrett-Engele, Philip -- Kan, Zhengyan -- Loerch, Patrick M -- Armour, Christopher D -- Santos, Ralph -- Schadt, Eric E -- Stoughton, Roland -- Shoemaker, Daniel D -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2141-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rosetta Inpharmatics LLC, Merck & Co., Inc., 12040 115th Avenue N.E., Kirkland, WA 98034, USA. jason_johnson@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684825" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Amyloid beta-Protein Precursor/analysis/genetics ; Cell Line ; DNA, Complementary ; *Exons ; Expressed Sequence Tags ; *Genome, Human ; Humans ; Hydroxymethylglutaryl CoA Reductases/analysis/genetics ; Molecular Sequence Data ; *Oligonucleotide Array Sequence Analysis ; *Phosphoric Monoester Hydrolases ; Protein Isoforms/analysis ; Proteins/analysis/genetics ; RNA Precursors/*genetics ; ROC Curve ; Reverse Transcriptase Polymerase Chain Reaction ; Tissue Distribution
    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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    Triggering the interferon antiviral response through an IKK-related pathway (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-19
    Description: Rapid induction of type I interferon expression, a central event in establishing the innate antiviral response, requires cooperative activation of numerous transcription factors. Although signaling pathways that activate the transcription factors nuclear factor kappaB and ATF-2/c-Jun have been well characterized, activation of the interferon regulatory factors IRF-3 and IRF-7 has remained a critical missing link in understanding interferon signaling. We report here that the IkappaB kinase (IKK)-related kinases IKKepsilon and TANK-binding kinase 1 are components of the virus-activated kinase that phosphorylate IRF-3 and IRF-7. These studies illustrate an essential role for an IKK-related kinase pathway in triggering the host antiviral response to viral infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharma, Sonia -- tenOever, Benjamin R -- Grandvaux, Nathalie -- Zhou, Guo-Ping -- Lin, Rongtuan -- Hiscott, John -- New York, N.Y. -- Science. 2003 May 16;300(5622):1148-51. Epub 2003 Apr 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lady Davis Institute for Medical Research-Jewish General Hospital, Departments of Microbiology and Immunology and Medicine, McGill University, Montreal, Quebec H3T 1E2, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702806" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; Gene Expression Regulation, Viral ; Hepacivirus/immunology/*physiology ; Humans ; I-kappa B Kinase ; Interferon Regulatory Factor-3 ; Interferon Regulatory Factor-7 ; Interferon Type I/*biosynthesis/genetics ; Phosphorylation ; Promoter Regions, Genetic ; Protein-Serine-Threonine Kinases/*metabolism ; RNA, Small Interfering/metabolism ; Transcription Factors/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Regulation of cell polarity and protrusion formation by targeting RhoA for degradation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-06
    Description: The Rho family of small guanosine triphosphatases regulates actin cytoskeleton dynamics that underlie cellular functions such as cell shape changes, migration, and polarity. We found that Smurf1, a HECT domain E3 ubiquitin ligase, regulated cell polarity and protrusive activity and was required to maintain the transformed morphology and motility of a tumor cell. Atypical protein kinase C zeta (PKCzeta), an effector of the Cdc42/Rac1-PAR6 polarity complex, recruited Smurf1 to cellular protrusions, where it controlled the local level of RhoA. Smurf1 thus links the polarity complex to degradation of RhoA in lamellipodia and filopodia to prevent RhoA signaling during dynamic membrane movements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Hong-Rui -- Zhang, Yue -- Ozdamar, Barish -- Ogunjimi, Abiodun A -- Alexandrova, Evguenia -- Thomsen, Gerald H -- Wrana, Jeffrey L -- HD32429/HD/NICHD NIH HHS/ -- R01 HD032429/HD/NICHD NIH HHS/ -- R01 HD032429-06/HD/NICHD NIH HHS/ -- R01 HD032429-07/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1775-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto M56 1x5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14657501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism/physiology ; *Cell Movement ; *Cell Polarity ; Cell Size ; Cell Transformation, Neoplastic ; Cytoskeleton/ultrastructure ; Guanine Nucleotide Exchange Factors/metabolism ; Humans ; Intercellular Junctions/metabolism ; Mice ; NIH 3T3 Cells ; Protein Kinase C/metabolism ; Protein Structure, Tertiary ; Pseudopodia/*metabolism/ultrastructure ; RNA, Small Interfering ; Signal Transduction ; Transfection ; Ubiquitin-Protein Ligases/chemistry/genetics/*metabolism ; cdc42 GTP-Binding Protein/metabolism ; rhoA GTP-Binding Protein/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    RNA leaching of transcription factors disrupts transcription in myotonic dystrophy (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-06
    Description: Myotonic dystrophy type 1 (DM1) is caused by a CUGn expansion (n approximately 50 to 5000) in the 3' untranslated region of the mRNA of the DM protein kinase gene. We show that mutant RNA binds and sequesters transcription factors (TFs), with up to 90% depletion of selected TFs from active chromatin. Diverse genes are consequently reduced in expression, including the ion transporter CIC-1, which has been implicated in myotonia. When TF specificity protein 1 (Sp1) was overexpressed in DM1-affected cells, low levels of messenger RNA for CIC-1 were restored to normal. Transcription factor leaching from chromatin by mutant RNA provides a potentially unifying pathomechanistic explanation for this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebralidze, A -- Wang, Y -- Petkova, V -- Ebralidse, K -- Junghans, R P -- New York, N.Y. -- Science. 2004 Jan 16;303(5656):383-7. Epub 2003 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotherapeutics Development Lab, Harvard Institute of Human Genetics, Harvard Medical School and Division of Hematology-Oncology, Beth Israel Deaconess Medical Center, 4 Blackfan Circle, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14657503" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cell Line ; Cell Nucleus/metabolism ; Chloride Channels/genetics ; Chromatin/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Humans ; Muscle Cells/*metabolism ; Mutation ; Myotonic Dystrophy/*genetics ; Myotonin-Protein Kinase ; Promoter Regions, Genetic ; Protein-Serine-Threonine Kinases/*genetics ; RNA/genetics/*metabolism ; RNA Splicing ; RNA, Messenger/genetics/metabolism ; Receptors, IgG/genetics ; Receptors, Retinoic Acid/genetics/metabolism ; Ribonucleoproteins/metabolism ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; Sp1 Transcription Factor/genetics/metabolism ; Sp3 Transcription Factor ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic
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    EDEM as an acceptor of terminally misfolded glycoproteins released from calnexin (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: Terminally misfolded proteins in the endoplasmic reticulum (ER) are retrotranslocated to the cytoplasm and degraded by proteasomes through a mechanism known as ER-associated degradation (ERAD). EDEM, a postulated Man8B-binding protein, accelerates the degradation of misfolded proteins in the ER. Here, EDEM was shown to interact with calnexin, but not with calreticulin, through its transmembrane region. Both binding of substrates to calnexin and their release from calnexin were required for ERAD to occur. Overexpression of EDEM accelerated ERAD by promoting the release of terminally misfolded proteins from calnexin. Thus, EDEM appeared to function in the ERAD pathway by accepting substrates from calnexin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oda, Yukako -- Hosokawa, Nobuko -- Wada, Ikuo -- Nagata, Kazuhiro -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1394-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610305" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/*analogs & derivatives/pharmacology ; Calnexin/*metabolism ; Calreticulin/metabolism ; Cell Line ; Endoplasmic Reticulum/*metabolism ; Glycoproteins/chemistry/*metabolism ; Humans ; Indolizines/pharmacology ; Membrane Proteins/*metabolism ; Precipitin Tests ; Protein Binding ; Protein Conformation ; Protein Folding ; Protein Transport ; Recombinant Fusion Proteins/metabolism ; Transfection ; alpha 1-Antitrypsin/chemistry/*metabolism
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    Design and chemical synthesis of a homogeneous polymer-modified erythropoiesis protein (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-08
    Description: We report the design and total chemical synthesis of "synthetic erythropoiesis protein" (SEP), a 51-kilodalton protein-polymer construct consisting of a 166-amino-acid polypeptide chain and two covalently attached, branched, and monodisperse polymer moieties that are negatively charged. The ability to control the chemistry allowed us to synthesize a macromolecule of precisely defined covalent structure. SEP was homogeneous as shown by high-resolution analytical techniques, with a mass of 50,825 +/-10 daltons by electrospray mass spectrometry, and with a pI of 5.0. In cell and animal assays for erythropoiesis, SEP displayed potent biological activity and had significantly prolonged duration of action in vivo. These chemical methods are a powerful tool in the rational design of protein constructs with potential therapeutic applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kochendoerfer, Gerd G -- Chen, Shiah-Yun -- Mao, Feng -- Cressman, Sonya -- Traviglia, Stacey -- Shao, Haiyan -- Hunter, Christie L -- Low, Donald W -- Cagle, E Neil -- Carnevali, Maia -- Gueriguian, Vincent -- Keogh, Peter J -- Porter, Heather -- Stratton, Stephen M -- Wiedeke, M Con -- Wilken, Jill -- Tang, Jie -- Levy, Jay J -- Miranda, Les P -- Crnogorac, Milan M -- Kalbag, Suresh -- Botti, Paolo -- Schindler-Horvat, Janice -- Savatski, Laura -- Adamson, John W -- Kung, Ada -- Kent, Stephen B H -- Bradburne, James A -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):884-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gryphon Therapeutics, 250 East Grand Avenue, Suite 90, South San Francisco, CA 94080, USA. Gkochendoerfer@gryphonRX.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574628" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Circular Dichroism ; *Drug Design ; Drug Stability ; Electrophoresis, Polyacrylamide Gel ; *Erythropoiesis ; Erythropoietin/chemistry/pharmacology ; Hematocrit ; Humans ; Isoelectric Point ; Mice ; Molecular Sequence Data ; Molecular Structure ; Molecular Weight ; *Polymers/*chemical synthesis/*chemistry/pharmacokinetics/pharmacology ; Protein Folding ; Proteins/*chemical synthesis/*chemistry/pharmacokinetics/pharmacology ; Rats ; Receptors, Erythropoietin/drug effects/metabolism ; Recombinant Proteins ; Spectrometry, Mass, Electrospray Ionization
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    FACT facilitates transcription-dependent nucleosome alteration (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-23
    Description: The FACT (facilitates chromatin transcription) complex is required for transcript elongation through nucleosomes by RNA polymerase II (Pol II) in vitro. Here, we show that FACT facilitates Pol II-driven transcription by destabilizing nucleosomal structure so that one histone H2A-H2B dimer is removed during enzyme passage. We also demonstrate that FACT possesses intrinsic histone chaperone activity and can deposit core histones onto DNA. Importantly, FACT activity requires both of its constituent subunits and is dependent on the highly acidic C terminus of its larger subunit, Spt16. These findings define the mechanism by which Pol II can transcribe through chromatin without disrupting its epigenetic status.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Belotserkovskaya, Rimma -- Oh, Sangtaek -- Bondarenko, Vladimir A -- Orphanides, George -- Studitsky, Vasily M -- Reinberg, Danny -- GM37120/GM/NIGMS NIH HHS/ -- GM58650/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 22;301(5636):1090-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry, Division of Nucleic Acids Enzymology, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12934006" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Cycle Proteins/chemistry/metabolism ; Cell Line ; DNA/metabolism ; DNA-Binding Proteins/chemistry/metabolism ; Dimerization ; HeLa Cells ; High Mobility Group Proteins/chemistry/metabolism ; Histones/metabolism ; Humans ; Models, Genetic ; Molecular Chaperones/chemistry/metabolism ; Molecular Sequence Data ; Nucleosomes/*metabolism ; Protein Binding ; Protein Subunits ; RNA Polymerase II/*metabolism ; Recombinant Proteins/chemistry/metabolism ; Templates, Genetic ; Transcription Factors/chemistry/metabolism ; *Transcription, Genetic ; Transcriptional Elongation Factors/chemistry/*metabolism
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    Biochemistry. An overoxidation journey with a return ticket (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Georgiou, George -- Masip, Lluis -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):592-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Engineering, Biomedical Engineering and Institute for Cell and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA. gg@che.utexas.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12714731" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Antioxidants/*metabolism ; Bacteria/enzymology ; Catalysis ; Cell Line ; Cysteine/*analogs & derivatives/metabolism ; Erythrocytes/enzymology ; Evolution, Molecular ; Humans ; Hydrogen Peroxide/*metabolism ; Models, Biological ; Neurotransmitter Agents ; Oxidation-Reduction ; Peroxidases/*chemistry/*metabolism ; Peroxiredoxins ; Protein Conformation ; Protein Structure, Secondary ; *Signal Transduction ; Sulfenic Acids/metabolism ; Sulfinic Acids/metabolism
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    Embryonic stem cells. Key questions loom over effort to energize research (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- Holden, Constance -- New York, N.Y. -- Science. 2003 Jan 24;299(5606):493-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12543947" target="_blank"〉PubMed〈/a〉
    Keywords: Access to Information ; Advisory Committees ; Animals ; Biological Specimen Banks ; Cell Culture Techniques ; Cell Line ; Chimera ; *Embryo Research/ethics ; Embryo, Mammalian/*cytology ; Guidelines as Topic ; Humans ; International Cooperation ; Internet ; Mice ; Pluripotent Stem Cells ; *Stem Cells
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    Transport of dsRNA into cells by the transmembrane protein SID-1 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-13
    Description: RNA interference (RNAi) spreads systemically in plants and nematodes to silence gene expression distant from the site of initiation. We previously identified a gene, sid-1, essential for systemic but not cell-autonomous RNAi in Caenorhabditis elegans. Here, we demonstrate that SID-1 is a multispan transmembrane protein that sensitizes Drosophila cells to soaking RNAi with a potency that is dependent on double-stranded RNA (dsRNA) length. Further analyses revealed that SID-1 enables passive cellular uptake of dsRNA. These data indicate that systemic RNAi in C. elegans involves SID-1-mediated intercellular transport of dsRNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feinberg, Evan H -- Hunter, Craig P -- R01 GM069891/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 12;301(5639):1545-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12970568" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Biological Transport ; Caenorhabditis elegans/*genetics ; Caenorhabditis elegans Proteins/chemistry/*metabolism ; Cell Line ; Diffusion ; Drosophila ; Membrane Proteins/chemistry/*metabolism ; *RNA Interference ; RNA, Double-Stranded/chemistry/genetics/*metabolism ; Recombinant Proteins/metabolism ; Transfection
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    Spread of HTLV-I between lymphocytes by virus-induced polarization of the cytoskeleton (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-18
    Description: Cell contact is required for efficient transmission of human T cell leukemia virus- type 1 (HTLV-I) between cells and between individuals, because naturally infected lymphocytes produce virtually no cell-free infectious HTLV-I particles. However, the mechanism of cell-to-cell spread of HTLV-I is not understood. We show here that cell contact rapidly induces polarization of the cytoskeleton of the infected cell to the cell-cell junction. HTLV-I core (Gag protein) complexes and the HTLV-I genome accumulate at the cell-cell junction and are then transferred to the uninfected cell. Other lymphotropic viruses, such as HIV-1, may similarly subvert normal T cell physiology to allow efficient propagation between cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Igakura, Tadahiko -- Stinchcombe, Jane C -- Goon, Peter K C -- Taylor, Graham P -- Weber, Jonathan N -- Griffiths, Gillian M -- Tanaka, Yuetsu -- Osame, Mitsuhiro -- Bangham, Charles R M -- New York, N.Y. -- Science. 2003 Mar 14;299(5613):1713-6. Epub 2003 Feb 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Imperial College London, St. Mary's Campus, Norfolk Place, London W2 1PG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12589003" target="_blank"〉PubMed〈/a〉
    Keywords: CD4-Positive T-Lymphocytes/immunology/ultrastructure/virology ; CD8-Positive T-Lymphocytes/immunology/ultrastructure/virology ; Cell Adhesion Molecules/metabolism ; Cell Communication ; Cell Line ; *Cell Polarity ; Extracellular Space/virology ; Gene Products, env/metabolism ; Gene Products, gag/metabolism ; Genome, Viral ; HTLV-I Infections/virology ; Human T-lymphotropic virus 1/genetics/*physiology ; Humans ; In Situ Hybridization, Fluorescence ; Intercellular Junctions/*physiology/ultrastructure/virology ; Microscopy, Confocal ; Microtubule-Organizing Center/*physiology/ultrastructure ; Microtubules/physiology ; Nucleocapsid Proteins/metabolism ; Peptide Nucleic Acids ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/immunology/*ultrastructure/*virology ; Talin/metabolism ; Virion/physiology
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    Identification of a testicular odorant receptor mediating human sperm chemotaxis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-29
    Description: Although it has been known for some time that olfactory receptors (ORs) reside in spermatozoa, the function of these ORs is unknown. Here, we identified, cloned, and functionally expressed a previously undescribed human testicular OR, hOR17-4. With the use of ratiofluorometric imaging, Ca2+ signals were induced by a small subset of applied chemical stimuli, establishing the molecular receptive fields for the recombinantly expressed receptor in human embryonic kidney (HEK) 293 cells and the native receptor in human spermatozoa. Bourgeonal was a powerful agonist for both recombinant and native receptor types, as well as a strong chemoattractant in subsequent behavioral bioassays. In contrast, undecanal was a potent OR antagonist to bourgeonal and related compounds. Taken together, these results indicate that hOR17-4 functions in human sperm chemotaxis and may be a critical component of the fertilization process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spehr, Marc -- Gisselmann, Gunter -- Poplawski, Alexandra -- Riffell, Jeffrey A -- Wetzel, Christian H -- Zimmer, Richard K -- Hatt, Hanns -- New York, N.Y. -- Science. 2003 Mar 28;299(5615):2054-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Physiology, Ruhr University Bochum, 150 University Street, D-44780 Bochum, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12663925" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Aldehydes/chemistry/metabolism/pharmacology ; Binding Sites ; Calcium/metabolism ; Calcium Signaling ; Cell Line ; Chemotactic Factors/chemistry/metabolism/*pharmacology ; *Chemotaxis ; Cloning, Molecular ; Dose-Response Relationship, Drug ; Fertilization ; Gene Expression Profiling ; Humans ; Ligands ; Male ; Molecular Structure ; Odors ; Receptors, Odorant/chemistry/genetics/*physiology ; Recombinant Fusion Proteins/metabolism ; Seminal Plasma Proteins/genetics/*physiology ; *Sperm Motility/drug effects ; Spermatozoa/drug effects/*physiology ; Testis/*metabolism ; Type C Phospholipases/metabolism
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    Cell signaling. beta-arrestin--not just for G protein-coupled receptors (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spiegel, Allen -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1338-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892, USA. spiegela@extra.niddk.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12958351" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Arrestins/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Clathrin/metabolism ; Coated Pits, Cell-Membrane/metabolism ; Down-Regulation ; Drosophila ; *Endocytosis ; Frizzled Receptors ; GTP-Binding Proteins/metabolism ; Humans ; Mice ; Phosphoproteins/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases ; Proteins/*metabolism ; Proteoglycans/metabolism ; Proto-Oncogene Proteins/metabolism ; Receptors, Cell Surface/*metabolism ; Receptors, Transforming Growth Factor beta/metabolism ; *Signal Transduction ; Transforming Growth Factor beta/metabolism ; Wnt Proteins
    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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    Cell biology. NO says yes to mitochondria (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Guy C -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):838-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Cambridge University, Cambridge CB2 1QW, UK. gcb@mole.bio.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574611" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/metabolism/ultrastructure ; Adipose Tissue, Brown/cytology/metabolism/ultrastructure ; Animals ; Cell Differentiation ; Cell Line ; Cyclic GMP/metabolism ; Energy Metabolism ; Gene Expression Regulation ; Mice ; Mice, Transgenic ; Mitochondria/*metabolism ; Muscles/metabolism/ultrastructure ; Nitric Oxide/*physiology ; Nitric Oxide Synthase/*metabolism ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Oxygen Consumption ; Rats ; Transcription Factors/metabolism ; Up-Regulation ; Weight Gain
    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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  • 48
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    Redistribution of intracellular oxygen in hypoxia by nitric oxide: effect on HIF1alpha (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: Cells exposed to low oxygen concentrations respond by initiating defense mechanisms, including the stabilization of hypoxia-inducible factor (HIF) 1alpha, a transcription factor that upregulates genes such as those involved in glycolysis and angiogenesis. Nitric oxide and other inhibitors of mitochondrial respiration prevent the stabilization of HIF1alpha during hypoxia. In studies of cultured cells, we show that this effect is a result of an increase in prolyl hydroxylase-dependent degradation of HIF1alpha. With the use of Renilla luciferase to detect intracellular oxygen concentrations, we also demonstrate that, upon inhibition of mitochondrial respiration in hypoxia, oxygen is redistributed toward nonrespiratory oxygen-dependent targets such as prolyl hydroxylases so that they do not register hypoxia. Thus, the signaling consequences of hypoxia may be profoundly modified by nitric oxide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagen, Thilo -- Taylor, Cormac T -- Lam, Francis -- Moncada, Salvador -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1975-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671307" target="_blank"〉PubMed〈/a〉
    Keywords: Antioxidants/pharmacology ; *Cell Hypoxia ; Cell Line ; *Cell Respiration/drug effects ; Cycloheximide/pharmacology ; Cysteine Proteinase Inhibitors/pharmacology ; HeLa Cells ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; Leupeptins/*pharmacology ; Luciferases/metabolism ; Methacrylates ; Mitochondria/*metabolism ; Nitric Oxide/pharmacology/*physiology ; Nitric Oxide Donors/pharmacology ; Oxygen/*metabolism ; Procollagen-Proline Dioxygenase/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Reactive Oxygen Species/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Thiazoles/pharmacology ; Transcription Factors/*metabolism ; Transfection ; Triazenes/pharmacology
    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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  • 49
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    R2D2, a bridge between the initiation and effector steps of the Drosophila RNAi pathway (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: The RNA interference (RNAi) pathway is initiated by processing long double-stranded RNA into small interfering RNA (siRNA). The siRNA-generating enzyme was purified from Drosophila S2cells and consists of two stoichiometric subunits: Dicer-2(DCR-2) and a previously unknown protein that we named R2D2. R2D2 is homologous to the Caenorhabditis elegans RNAi protein RDE-4. Association with R2D2 does not affect the enzymatic activity of DCR-2. Rather, the DCR-2/R2D2 complex, but not DCR-2 alone, binds to siRNA and enhances sequence-specific messenger RNA degradation mediated by the RNA-initiated silencing complex (RISC). These results indicate that R2D2 bridges the initiation and effector steps of the Drosophila RNAi pathway by facilitating siRNA passage from Dicer to RISC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Qinghua -- Rand, Tim A -- Kalidas, Savitha -- Du, Fenghe -- Kim, Hyun-Eui -- Smith, Dean P -- Wang, Xiaodong -- DC02539/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1921-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512631" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Argonaute Proteins ; Biotinylation ; Caenorhabditis elegans/genetics/metabolism ; Caenorhabditis elegans Proteins/chemistry ; Cell Line ; Chemical Precipitation ; Drosophila Proteins/chemistry/genetics/*isolation & purification/*metabolism ; Drosophila melanogaster/*genetics/metabolism ; Electrophoretic Mobility Shift Assay ; Endoribonucleases/genetics/isolation & purification/*metabolism ; Kinetics ; Molecular Sequence Data ; Mutation ; Protein Structure, Tertiary ; RNA Helicases/genetics/*isolation & purification/*metabolism ; *RNA Interference ; RNA, Double-Stranded/metabolism ; RNA, Messenger/metabolism ; RNA, Small Interfering/*metabolism ; RNA-Binding Proteins/chemistry/genetics/isolation & purification/*metabolism ; RNA-Induced Silencing Complex/isolation & purification/metabolism ; Recombinant Proteins/metabolism ; Ribonuclease III
    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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  • 50
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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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    German science. Stem cell project wins final approval (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steghaus-Kovac, Sabine -- New York, N.Y. -- Science. 2003 Jan 3;299(5603):31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12511625" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Embryo Research ; Embryo, Mammalian/*cytology ; Germany ; Humans ; Research Support as Topic ; *Stem Cells
    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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  • 52
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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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    Beta-arrestin 2 mediates endocytosis of type III TGF-beta receptor and down-regulation of its signaling (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-06
    Description: beta-Arrestins bind to activated seven transmembrane-spanning (7TMS) receptors (G protein-coupled receptors) after the receptors are phosphorylated by G protein-coupled receptor kinases (GRKs), thereby regulating their signaling and internalization. Here, we demonstrate an unexpected and analogous role of beta-arrestin 2 (betaarr2) for the single transmembrane-spanning type III transforming growth factor-beta (TGF-beta) receptor (TbetaRIII, also referred to as betaglycan). Binding of betaarr2 to TbetaRIII was also triggered by phosphorylation of the receptor on its cytoplasmic domain (likely at threonine 841). However, such phosphorylation was mediated by the type II TGF-beta receptor (TbetaRII), which is itself a kinase, rather than by a GRK. Association with betaarr2 led to internalization of both receptors and down-regulation of TGF-beta signaling. Thus, the regulatory actions of beta-arrestins are broader than previously appreciated, extending to the TGF-beta receptor family as well.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Wei -- Kirkbride, Kellye C -- How, Tam -- Nelson, Christopher D -- Mo, Jinyao -- Frederick, Joshua P -- Wang, Xiao-Fan -- Lefkowitz, Robert J -- Blobe, Gerard C -- CA 75368/CA/NCI NIH HHS/ -- CA 91816/CA/NCI NIH HHS/ -- HL 16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1394-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Duke University Medical Center, Departments of Medicine and Biochemistry, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12958365" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Arrestins/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; Down-Regulation ; *Endocytosis ; Humans ; Keratinocytes/metabolism ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutagenesis ; Phosphorylation ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases ; Proteoglycans/chemistry/genetics/*metabolism ; RNA, Small Interfering ; Receptors, Transforming Growth Factor beta/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Transfection ; Transforming Growth Factor beta ; Transforming Growth Factor beta1
    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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