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  • Articles  (249)
  • Latest Papers from Table of Contents or Articles in Press  (249)
  • Cells, Cultured
  • 2000-2004  (249)
  • Computer Science  (249)
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  • Latest Papers from Table of Contents or Articles in Press  (249)
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  • 1
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    Neuroscience. NAD to the rescue (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bedalov, Antonio -- Simon, Julian A -- New York, N.Y. -- Science. 2004 Aug 13;305(5686):954-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clinical Research Division and J. A. Simon is in the Clinical Research and Human Biology Divisions, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. abedalov@fhcrc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15310883" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cell Nucleus/metabolism ; Cell Survival ; Cells, Cultured ; Ganglia, Spinal/cytology ; Mice ; Mutation ; NAD/biosynthesis/*metabolism ; Nerve Tissue Proteins/genetics/*metabolism ; Neurodegenerative Diseases/drug therapy/physiopathology ; Neuroprotective Agents/therapeutic use ; Nicotinamide-Nucleotide Adenylyltransferase/metabolism ; RNA, Small Interfering ; Sirtuin 1 ; Sirtuins/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Wallerian Degeneration/metabolism/*physiopathology
    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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    Cancer research. Proposed leukemia stem cell encounters a blast of scrutiny (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2004 Aug 13;305(5686):929.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15310869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blast Crisis/*pathology ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Cytoskeletal Proteins/metabolism ; Granulocytes/cytology ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/blood/*pathology ; Macrophages/cytology ; Mice ; Myeloid Progenitor Cells/pathology/*physiology ; Stem Cells/physiology ; Trans-Activators/metabolism ; beta Catenin
    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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    Uridine addition after microRNA-directed cleavage (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-06
    Description: One of the important roles of microRNA (miRNA) is to direct the cleavage of messenger RNA (mRNA). However, the mechanisms of decay of the cleaved mRNA products is not well understood. We show that miRNA-directed cleavage products in organisms as diverse as Arabidopsis, mouse, and Epstein-Barr virus have at their 3' ends a stretch (1 to 24 nucleotides) of oligouridine posttranscriptionally added downstream of the cleavage site. This 3' uridine addition, as shown for Arabidopsis, is correlated with decapping and 5' shortening of the cleaved products, suggesting a mechanistic step in the miRNA-directed mRNA decay mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Binzhang -- Goodman, Howard M -- New York, N.Y. -- Science. 2004 Nov 5;306(5698):997.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts General Hospital, 50 Blossom Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15528436" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arabidopsis ; Cells, Cultured ; Cloning, Molecular ; Herpesvirus 4, Human/metabolism ; Humans ; Mice ; MicroRNAs/*metabolism ; Poly U/metabolism ; RNA, Messenger/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Uridine/*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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  • 4
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    TGF-beta signaling in fibroblasts modulates the oncogenic potential of adjacent epithelia (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-07
    Description: Stromal cells can have a significant impact on the carcinogenic process in adjacent epithelia. The role of transforming growth factor-beta (TGF-beta) signaling in such epithelial-mesenchymal interactions was determined by conditional inactivation of the TGF-beta type II receptor gene in mouse fibroblasts (Tgfbr2fspKO). The loss of TGF-beta responsiveness in fibroblasts resulted in intraepithelial neoplasia in prostate and invasive squamous cell carcinoma of the forestomach, both associated with an increased abundance of stromal cells. Activation of paracrine hepatocyte growth factor (HGF) signaling was identified as one possible mechanism for stimulation of epithelial proliferation. Thus, TGF-beta signaling in fibroblasts modulates the growth and oncogenic potential of adjacent epithelia in selected tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhowmick, Neil A -- Chytil, Anna -- Plieth, David -- Gorska, Agnieszka E -- Dumont, Nancy -- Shappell, Scott -- Washington, M Kay -- Neilson, Eric G -- Moses, Harold L -- AR41943/AR/NIAMS NIH HHS/ -- CA102162/CA/NCI NIH HHS/ -- CA68485/CA/NCI NIH HHS/ -- CA85492/CA/NCI NIH HHS/ -- DK46282/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 6;303(5659):848-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14764882" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Squamous Cell/etiology/metabolism/pathology ; Cell Division ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Epithelial Cells/*physiology ; Female ; Fibroblasts/*physiology ; Hepatocyte Growth Factor/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Neoplasms, Glandular and Epithelial/*etiology/metabolism/pathology ; Prostate/cytology/metabolism/pathology ; Prostatic Intraepithelial Neoplasia/etiology/metabolism/pathology ; Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins c-met/metabolism ; Receptors, Transforming Growth Factor beta/genetics/metabolism ; Recombination, Genetic ; *Signal Transduction ; Stomach/cytology/metabolism/pathology ; Stomach Neoplasms/etiology/metabolism/pathology ; Stromal Cells/*physiology ; Transforming Growth Factor beta/*physiology
    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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    Derivatives of erythropoietin that are tissue protective but not erythropoietic (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-13
    Description: Erythropoietin (EPO) is both hematopoietic and tissue protective, putatively through interaction with different receptors. We generated receptor subtype-selective ligands allowing the separation of EPO's bioactivities at the cellular level and in animals. Carbamylated EPO (CEPO) or certain EPO mutants did not bind to the classical EPO receptor (EPOR) and did not show any hematopoietic activity in human cell signaling assays or upon chronic dosing in different animal species. Nevertheless, CEPO and various nonhematopoietic mutants were cytoprotective in vitro and conferred neuroprotection against stroke, spinal cord compression, diabetic neuropathy, and experimental autoimmune encephalomyelitis at a potency and efficacy comparable to EPO.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leist, Marcel -- Ghezzi, Pietro -- Grasso, Giovanni -- Bianchi, Roberto -- Villa, Pia -- Fratelli, Maddalena -- Savino, Costanza -- Bianchi, Marina -- Nielsen, Jacob -- Gerwien, Jens -- Kallunki, Pekka -- Larsen, Anna Kirstine -- Helboe, Lone -- Christensen, Soren -- Pedersen, Lars O -- Nielsen, Mette -- Torup, Lars -- Sager, Thomas -- Sfacteria, Alessandra -- Erbayraktar, Serhat -- Erbayraktar, Zubeyde -- Gokmen, Necati -- Yilmaz, Osman -- Cerami-Hand, Carla -- Xie, Qiao-Wen -- Coleman, Thomas -- Cerami, Anthony -- Brines, Michael -- New York, N.Y. -- Science. 2004 Jul 9;305(5681):239-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉H. Lundbeck A/S, 2500 Valby, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15247477" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Binding Sites ; Cells, Cultured ; Diabetic Neuropathies/drug therapy ; Drug Design ; Encephalomyelitis, Autoimmune, Experimental/drug therapy ; Erythropoiesis ; Erythropoietin/*analogs & ; derivatives/chemistry/genetics/metabolism/pharmacology/*therapeutic use ; Female ; Hematocrit ; Humans ; Ligands ; Mice ; Mice, Inbred C3H ; Mutagenesis ; Nervous System Diseases/*drug therapy ; Neurons/metabolism ; Neuroprotective Agents/chemistry/metabolism/pharmacology/*therapeutic use ; Rats ; Rats, Sprague-Dawley ; Receptors, Erythropoietin/metabolism ; Recombinant Proteins ; Signal Transduction ; Spinal Cord Compression/drug therapy ; Stroke/drug therapy ; Structure-Activity Relationship
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Medicine. A wily recruiter in the battle against toxic beta amyloid aggregation (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, Ingrid -- New York, N.Y. -- Science. 2004 Oct 29;306(5697):791-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15514121" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid beta-Peptides/*chemistry/metabolism/toxicity ; Animals ; Cell Death/drug effects ; Cells, Cultured ; Congo Red/*analogs & derivatives/*chemical ; synthesis/chemistry/*metabolism/*pharmacology ; Ligands ; Neurons/cytology/*drug effects ; Piperidines/*chemical synthesis/chemistry/metabolism/*pharmacology ; Protein Conformation ; Rats ; Tacrolimus Binding Proteins/*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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  • 7
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    Biomedicine. Insulin resistance takes a trip through the ER (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muoio, Deborah M -- Newgard, Christopher B -- New York, N.Y. -- Science. 2004 Oct 15;306(5695):425-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sarah W. Stedman Nutrition and Metabolism Center, 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/15486283" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Animals ; Cells, Cultured ; DNA-Binding Proteins/genetics/metabolism ; Endoplasmic Reticulum/*metabolism ; Endoribonucleases ; Enzyme Activation ; Homeostasis ; Humans ; Insulin/*metabolism ; Insulin Receptor Substrate Proteins ; Insulin Resistance/*physiology ; Islets of Langerhans/metabolism ; Liver/metabolism ; Membrane Proteins/metabolism ; Mice ; Mitogen-Activated Protein Kinase 8 ; Mitogen-Activated Protein Kinases/*metabolism ; Muscle, Skeletal/metabolism ; Nuclear Proteins/genetics/metabolism ; Obesity/*metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; Transcription Factors ; eIF-2 Kinase/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    ABAD directly links Abeta to mitochondrial toxicity in Alzheimer's disease (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-17
    Description: Mitochondrial dysfunction is a hallmark of beta-amyloid (Abeta)-induced neuronal toxicity in Alzheimer's disease (AD). Here, we demonstrate that Abeta-binding alcohol dehydrogenase (ABAD) is a direct molecular link from Abeta to mitochondrial toxicity. Abeta interacts with ABAD in the mitochondria of AD patients and transgenic mice. The crystal structure of Abeta-bound ABAD shows substantial deformation of the active site that prevents nicotinamide adenine dinucleotide (NAD) binding. An ABAD peptide specifically inhibits ABAD-Abeta interaction and suppresses Abeta-induced apoptosis and free-radical generation in neurons. Transgenic mice overexpressing ABAD in an Abeta-rich environment manifest exaggerated neuronal oxidative stress and impaired memory. These data suggest that the ABAD-Abeta interaction may be a therapeutic target in AD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lustbader, Joyce W -- Cirilli, Maurizio -- Lin, Chang -- Xu, Hong Wei -- Takuma, Kazuhiro -- Wang, Ning -- Caspersen, Casper -- Chen, Xi -- Pollak, Susan -- Chaney, Michael -- Trinchese, Fabrizio -- Liu, Shumin -- Gunn-Moore, Frank -- Lue, Lih-Fen -- Walker, Douglas G -- Kuppusamy, Periannan -- Zewier, Zay L -- Arancio, Ottavio -- Stern, David -- Yan, Shirley ShiDu -- Wu, Hao -- 1K07AG00959/AG/NIA NIH HHS/ -- AG16736/AG/NIA NIH HHS/ -- AG17490/AG/NIA NIH HHS/ -- NS42855/NS/NINDS NIH HHS/ -- P50AG08702/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2004 Apr 16;304(5669):448-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Reproductive Sciences and Department of Obstetrics and Gynecology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15087549" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Hydroxyacyl CoA Dehydrogenases/chemistry/*metabolism ; Aged ; Aged, 80 and over ; Alzheimer Disease/*metabolism ; Amino Acid Sequence ; Amyloid beta-Peptides/chemistry/genetics/*metabolism ; Animals ; Binding Sites ; Brain/*metabolism ; Brain Chemistry ; Carrier Proteins/chemistry/*metabolism ; Cells, Cultured ; Cerebral Cortex/chemistry/metabolism ; Crystallization ; DNA Fragmentation ; Hippocampus/physiology ; Humans ; Learning ; Memory ; Mice ; Mice, Transgenic ; Microscopy, Confocal ; Microscopy, Immunoelectron ; Mitochondria/chemistry/*metabolism ; Models, Molecular ; Molecular Sequence Data ; Mutation ; NAD/metabolism ; Neurons/metabolism ; Protein Binding ; Protein Conformation ; Reactive Oxygen Species/metabolism
    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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    Gene targeting in stem cells from individuals with osteogenesis imperfecta (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-21
    Description: Adult stem cells offer the potential to treat many diseases through a combination of ex vivo genetic manipulation and autologous transplantation. Mesenchymal stem cells (MSCs, also referred to as marrow stromal cells) are adult stem cells that can be isolated as proliferating, adherent cells from bones. MSCs can differentiate into multiple cell types present in several tissues, including bone, fat, cartilage, and muscle, making them ideal candidates for a variety of cell-based therapies. Here, we have used adeno-associated virus vectors to disrupt dominant-negative mutant COL1A1 collagen genes in MSCs from individuals with the brittle bone disorder osteogenesis imperfecta, demonstrating successful gene targeting in adult human stem cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chamberlain, Joel R -- Schwarze, Ulrike -- Wang, Pei-Rong -- Hirata, Roli K -- Hankenson, Kurt D -- Pace, James M -- Underwood, Robert A -- Song, Kit M -- Sussman, Michael -- Byers, Peter H -- Russell, David W -- New York, N.Y. -- Science. 2004 Feb 20;303(5661):1198-201.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle, WA 98195-7720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14976317" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Bone Marrow Cells/physiology ; Cell Differentiation ; Cells, Cultured ; Collagen Type I/chemistry/*genetics/metabolism ; Dependovirus/genetics ; *Gene Targeting ; Genetic Therapy ; Genetic Vectors ; Humans ; Kanamycin Kinase/genetics ; Male ; Mesenchymal Stromal Cells/*physiology ; Mice ; Osteogenesis ; Osteogenesis Imperfecta/*genetics/*therapy ; Point Mutation ; Recombination, Genetic ; Stem Cell Transplantation
    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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  • 10
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    A process for controlling intracellular bacterial infections induced by membrane injury (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-05
    Description: Strategies for inhibiting phagolysosome fusion are essential for the intracellular survival and replication of many pathogens. We found that the lysosomal synaptotagmin Syt VII is required for a mechanism that promotes phagolysosomal fusion and limits the intracellular growth of pathogenic bacteria. Syt VII was required for a form of Ca2+-dependent phagolysosome fusion that is analogous to Ca2+-regulated exocytosis of lysosomes, which can be triggered by membrane injury. Bacterial type III secretion systems, which permeabilize membranes and cause Ca2+ influx in mammalian cells, promote lysosomal exocytosis and inhibit intracellular survival in Syt VII +/+ but not -/- cells. Thus, the lysosomal repair response can also protect cells against pathogens that trigger membrane permeabilization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roy, Deepannita -- Liston, David R -- Idone, Vincent J -- Di, Anke -- Nelson, Deborah J -- Pujol, Celine -- Bliska, James B -- Chakrabarti, Sabyasachi -- Andrews, Norma W -- AI34867/AI/NIAID NIH HHS/ -- AI43389/AI/NIAID NIH HHS/ -- AI48507/AI/NIAID NIH HHS/ -- GM64625/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Jun 4;304(5676):1515-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Microbial Pathogenesis and Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15178804" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/*growth & development/metabolism ; Bacterial Proteins/genetics/metabolism ; CHO Cells ; Calcium/metabolism ; *Calcium-Binding Proteins ; Cell Membrane/*physiology ; Cells, Cultured ; Cricetinae ; Endocytosis ; Exocytosis ; Listeria monocytogenes/growth & development ; Lysosomes/microbiology/physiology ; Macrophages/microbiology ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mutation ; Nerve Tissue Proteins/genetics/*physiology ; Permeability ; Phagosomes/microbiology/physiology ; Salmonella typhimurium/*growth & development/metabolism ; Synaptotagmins ; Vacuoles/microbiology ; Yersinia pseudotuberculosis/genetics/growth & development
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Direct activation of Bax by p53 mediates mitochondrial membrane permeabilization and apoptosis (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-14
    Description: The tumor suppressor p53 exerts its anti-neoplastic activity primarily through the induction of apoptosis. We found that cytosolic localization of endogenous wild-type or trans-activation-deficient p53 was necessary and sufficient for apoptosis. p53 directly activated the proapoptotic Bcl-2 protein Bax in the absence of other proteins to permeabilize mitochondria and engage the apoptotic program. p53 also released both proapoptotic multidomain proteins and BH3-only proteins [Proapoptotic Bcl-2 family proteins that share only the third Bcl-2 homology domain (BH3)] that were sequestered by Bcl-xL. The transcription-independent activation of Bax by p53 occurred with similar kinetics and concentrations to those produced by activated Bid. We propose that when p53 accumulates in the cytosol, it can function analogously to the BH3-only subset of proapoptotic Bcl-2 proteins to activate Bax and trigger apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chipuk, Jerry E -- Kuwana, Tomomi -- Bouchier-Hayes, Lisa -- Droin, Nathalie M -- Newmeyer, Donald D -- Schuler, Martin -- Green, Douglas R -- AI40646/AI/NIAID NIH HHS/ -- AI47891/AI/NIAID NIH HHS/ -- GM52735/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 13;303(5660):1010-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14963330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; BH3 Interacting Domain Death Agonist Protein ; Carrier Proteins/metabolism ; Cell Line, Transformed ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytochromes c/metabolism ; Cytosol/metabolism ; Gene Expression Regulation ; Genes, p53 ; HeLa Cells ; Humans ; Intracellular Membranes/*physiology ; Liposomes/metabolism ; Mice ; Mitochondria/*physiology ; Mutation ; Permeability ; Protein Conformation ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinant Fusion Proteins/metabolism ; Tumor Suppressor Protein p53/chemistry/*metabolism ; Ultraviolet Rays ; Wheat Germ Agglutinins/pharmacology ; bcl-2-Associated X Protein ; bcl-X Protein
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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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    The Semaphorin 4D receptor Plexin-B1 is a GTPase activating protein for R-Ras (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-07
    Description: Plexins are cell surface receptors for semaphorin molecules, and their interaction governs cell adhesion and migration in a variety of tissues. We report that the Semaphorin 4D (Sema4D) receptor Plexin-B1 directly stimulates the intrinsic guanosine triphosphatase (GTPase) activity of R-Ras, a member of the Ras superfamily of small GTP-binding proteins that has been implicated in promoting cell adhesion and neurite outgrowth. This activity required the interaction of Plexin-B1 with Rnd1, a small GTP-binding protein of the Rho family. Down-regulation of R-Ras activity by the Plexin-B1-Rnd1 complex was essential for the Sema4D-induced growth cone collapse in hippocampal neurons. Thus, Plexin-B1 mediates Sema4D-induced repulsive axon guidance signaling by acting as a GTPase activating protein for R-Ras.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oinuma, Izumi -- Ishikawa, Yukio -- Katoh, Hironori -- Negishi, Manabu -- New York, N.Y. -- Science. 2004 Aug 6;305(5685):862-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neurobiology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15297673" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, CD ; Axons/physiology ; COS Cells ; Cells, Cultured ; Down-Regulation ; GTP Phosphohydrolases/*metabolism ; GTPase-Activating Proteins/chemistry/genetics/*metabolism ; Guanosine Triphosphate/metabolism ; Hippocampus/cytology ; Humans ; Membrane Glycoproteins/*metabolism/pharmacology ; Neurites/physiology ; Neurons/*metabolism ; PC12 Cells ; Protein Structure, Tertiary ; RNA, Small Interfering ; Rats ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Semaphorins ; Signal Transduction ; Transfection ; ras Proteins/*metabolism ; rho GTP-Binding Proteins/genetics/metabolism ; rhoA GTP-Binding Protein/metabolism
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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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    Neuroscience. Vesicular glutamate transporter--shooting blanks (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schuske, Kim -- Jorgensen, Erik M -- New York, N.Y. -- Science. 2004 Jun 18;304(5678):1750-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Utah, 257 South 1400 East, Salt Lake City, UT 84112-0840, USA. jorgensen@biology.utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15205517" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Brain/metabolism ; Carrier Proteins/genetics/*metabolism ; Cell Membrane/physiology ; Cells, Cultured ; Excitatory Postsynaptic Potentials ; Glutamic Acid/metabolism ; Hippocampus/cytology/metabolism ; Membrane Fusion ; *Membrane Transport Proteins ; Mice ; Mice, Knockout ; Models, Neurological ; Mutation ; Neurons/*metabolism ; *Synaptic Transmission ; Synaptic Vesicles/*metabolism/physiology ; Vesicular Glutamate Transport Protein 1 ; Vesicular Glutamate Transport Protein 2 ; *Vesicular Transport 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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  • 14
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    Regulation of bone mass in mice by the lipoxygenase gene Alox15 (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-13
    Description: The development of osteoporosis involves the interaction of multiple environmental and genetic factors. Through combined genetic and genomic approaches, we identified the lipoxygenase gene Alox15 as a negative regulator of peak bone mineral density in mice. Crossbreeding experiments with Alox15 knockout mice confirmed that 12/15-lipoxygenase plays a role in skeletal development. Pharmacologic inhibitors of this enzyme improved bone density and strength in two rodent models of osteoporosis. These results suggest that drugs targeting the 12/15-lipoxygenase pathway merit investigation as a therapy for osteoporosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klein, Robert F -- Allard, John -- Avnur, Zafrira -- Nikolcheva, Tania -- Rotstein, David -- Carlos, Amy S -- Shea, Marie -- Waters, Ruth V -- Belknap, John K -- Peltz, Gary -- Orwoll, Eric S -- AR44659/AR/NIAMS NIH HHS/ -- HG02322/HG/NHGRI NIH HHS/ -- R01 AR044659/AR/NIAMS NIH HHS/ -- R01 AR044659-08/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Jan 9;303(5655):229-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bone and Mineral Research Unit, Department of Medicine, School of Medicine, Oregon Health and Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97239, USA. kleinro@ohsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14716014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonate 12-Lipoxygenase/*genetics/*metabolism ; Arachidonate 15-Lipoxygenase/*genetics/*metabolism ; Bone Density/drug effects/*genetics ; Bone Marrow Cells/metabolism ; Cell Differentiation ; Cells, Cultured ; Crosses, Genetic ; Enzyme Inhibitors/pharmacology ; Female ; Fluorenes/pharmacology ; Gene Expression Profiling ; Genetic Linkage ; Kidney/metabolism ; Lipoxygenase Inhibitors ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mice, Knockout ; Mice, Transgenic ; Oligonucleotide Array Sequence Analysis ; Osteoblasts/cytology/metabolism/physiology ; Osteogenesis ; Osteoporosis/enzymology ; Polymorphism, Genetic ; Quantitative Trait Loci ; Rats ; Receptors, Cytoplasmic and Nuclear/metabolism ; Stromal Cells/metabolism ; Transcription Factors/metabolism
    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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  • 15
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    Cdh1-APC controls axonal growth and patterning in the mammalian brain (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-13
    Description: The anaphase-promoting complex (APC) is highly expressed in postmitotic neurons, but its function in the nervous system was previously unknown. We report that the inhibition of Cdh1-APC in primary neurons specifically enhanced axonal growth. Cdh1 knockdown in cerebellar slice overlay assays and in the developing rat cerebellum in vivo revealed cell-autonomous abnormalities in layer-specific growth of granule neuron axons and parallel fiber patterning. Cdh1 RNA interference in neurons was also found to override the inhibitory influence of myelin on axonal growth. Thus, Cdh1-APC appears to play a role in regulating axonal growth and patterning in the developing brain that may also limit the growth of injured axons in the adult brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Konishi, Yoshiyuki -- Stegmuller, Judith -- Matsuda, Takahiko -- Bonni, Shirin -- Bonni, Azad -- R01NS41021/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 13;303(5660):1026-30. Epub 2004 Jan 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14716021" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase-Promoting Complex-Cyclosome ; Animals ; Axons/*physiology/ultrastructure ; Cell Cycle ; Cell Cycle Proteins/metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Cerebellar Cortex/*cytology/growth & development ; Dendrites/physiology/ultrastructure ; Electroporation ; Morphogenesis ; Mutation ; Myelin Sheath/metabolism ; Neurons/*physiology ; Organ Culture Techniques ; RNA Interference ; Rats ; Rats, Long-Evans ; Transfection ; Ubiquitin-Protein Ligase Complexes/genetics/*metabolism
    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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  • 16
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    The PP2A-associated protein alpha4 is an essential inhibitor of apoptosis (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-23
    Description: Despite evidence that protein kinases are regulators of apoptosis, a specific role for phosphatases in regulating cell survival has not been established. Here we show that alpha4, a noncatalytic subunit of protein phosphatase 2A (PP2A), is required to repress apoptosis in murine cells. alpha4 is a nonredundant regulator of the dephosphorylation of the transcription factors c-Jun and p53. As a result of alpha4 deletion, multiple proapoptotic genes were transcribed. Either inhibition of new protein synthesis or Bcl-xL overexpression suppressed apoptosis initiated by alpha4 deletion. Thus, mammalian cell viability depends on repression of transcription-initiated apoptosis mediated by a component of PP2A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kong, Mei -- Fox, Casey J -- Mu, James -- Solt, Laura -- Xu, Anne -- Cinalli, Ryan M -- Birnbaum, Morris J -- Lindsten, Tullia -- Thompson, Craig B -- New York, N.Y. -- Science. 2004 Oct 22;306(5696):695-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15499020" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology ; Animals ; *Apoptosis ; Cell Differentiation ; Cell Line ; Cell Survival ; Cells, Cultured ; Cycloheximide/pharmacology ; Gene Deletion ; Gene Expression Profiling ; Liver/cytology/metabolism ; Mice ; Mice, Transgenic ; Oligonucleotide Array Sequence Analysis ; PPAR gamma/metabolism ; Phosphoprotein Phosphatases/*metabolism ; Phosphoproteins/*metabolism ; Phosphorylation ; Protein Phosphatase 2 ; Protein Synthesis Inhibitors/pharmacology ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Transcription, Genetic ; Tumor Suppressor Protein p53/metabolism ; bcl-X Protein
    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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  • 17
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    Rescue of cardiac defects in id knockout embryos by injection of embryonic stem cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-09
    Description: We report that Id knockout mouse embryos display multiple cardiac defects, but mid-gestation lethality is rescued by the injection of 15 wild-type embryonic stem (ES) cells into mutant blastocysts. Myocardial markers altered in Id mutant cells are restored to normal throughout the chimeric myocardium. Intraperitoneal injection of ES cells into female mice before conception also partially rescues the cardiac phenotype with no incorporation of ES cells. Insulin-like growth factor 1, a long-range secreted factor, in combination with WNT5a, a locally secreted factor, likely account for complete reversion of the cardiac phenotype. Thus, ES cells have the potential to reverse congenital defects through Id-dependent local and long-range effects in a mammalian embryo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1351017/" 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/PMC1351017/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fraidenraich, Diego -- Stillwell, Elizabeth -- Romero, Elizabeth -- Wilkes, David -- Manova, Katia -- Basson, Craig T -- Benezra, Robert -- K01 HL076568/HL/NHLBI NIH HHS/ -- KO1HL076568/HL/NHLBI NIH HHS/ -- R01 CA107429/CA/NCI NIH HHS/ -- R01CA107429/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2004 Oct 8;306(5694):247-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology and Genetics Program, Department of Medicine, Weill Medical College of Cornell University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15472070" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst ; Cell Division ; Cells, Cultured ; DNA-Binding Proteins/genetics ; Embryo Loss ; Embryo, Mammalian/*cytology ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Heart/*embryology ; Heart Defects, Congenital/embryology/*therapy ; Inhibitor of Differentiation Protein 1 ; Inhibitor of Differentiation Protein 2 ; Insulin-Like Growth Factor I/genetics/physiology ; Maternal-Fetal Exchange ; Mice ; Mice, Knockout ; Myocardium/cytology/metabolism ; Myocytes, Cardiac/cytology ; Oligonucleotide Array Sequence Analysis ; Pericardium/embryology/metabolism ; Pregnancy ; Proto-Oncogene Proteins/genetics/physiology ; Repressor Proteins/genetics ; *Stem Cell Transplantation ; Stem Cells/*physiology ; Transcription Factors/genetics ; Wnt Proteins
    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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  • 18
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    Vesicular glutamate transporters 1 and 2 target to functionally distinct synaptic release sites (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-01
    Description: Vesicular glutamate transporters (VGLUTs) 1 and 2 show a mutually exclusive distribution in the adult brain that suggests specialization for synapses with different properties of release. Consistent with this distribution, inactivation of the VGLUT1 gene silenced a subset of excitatory neurons in the adult. However, the same cell populations exhibited VGLUT1-independent transmission early in life. Developing hippocampal neurons transiently coexpressed VGLUT2 and VGLUT1 at distinct synaptic sites with different short-term plasticity. The loss of VGLUT1 also reduced the reserve pool of synaptic vesicles. Thus, VGLUT1 plays an unanticipated role in membrane trafficking at the nerve terminal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fremeau, Robert T Jr -- Kam, Kaiwen -- Qureshi, Tayyaba -- Johnson, Juliette -- Copenhagen, David R -- Storm-Mathisen, Jon -- Chaudhry, Farrukh A -- Nicoll, Roger A -- Edwards, Robert H -- R01 EY001869/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2004 Jun 18;304(5678):1815-9. Epub 2004 Apr 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Graduate Programs in Neuroscience and Cell Biology, University of California San Francisco School of Medicine, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15118123" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Brain/cytology/*metabolism ; Carrier Proteins/genetics/*metabolism ; Cell Membrane/physiology ; Cells, Cultured ; Cerebellum/metabolism/ultrastructure ; Excitatory Postsynaptic Potentials ; Glutamic Acid/metabolism ; Hippocampus/cytology/metabolism/ultrastructure ; In Situ Hybridization ; *Membrane Transport Proteins ; Mice ; Mice, Knockout ; Nerve Tissue Proteins/metabolism ; Neurons/*metabolism/physiology ; Patch-Clamp Techniques ; Purkinje Cells/physiology ; Pyramidal Cells/metabolism ; Synapses/*metabolism/ultrastructure ; *Synaptic Transmission ; Synaptic Vesicles/*metabolism/physiology ; Vesicular Glutamate Transport Protein 1 ; Vesicular Glutamate Transport Protein 2 ; *Vesicular Transport 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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  • 19
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    Endothelial cells stimulate self-renewal and expand neurogenesis of neural stem cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-03
    Description: Neural stem cells are reported to lie in a vascular niche, but there is no direct evidence for a functional relationship between the stem cells and blood vessel component cells. We show that endothelial cells but not vascular smooth muscle cells release soluble factors that stimulate the self-renewal of neural stem cells, inhibit their differentiation, and enhance their neuron production. Both embryonic and adult neural stem cells respond, allowing extensive production of both projection neuron and interneuron types in vitro. Endothelial coculture stimulates neuroepithelial cell contact, activating Notch and Hes 1 to promote self-renewal. These findings identify endothelial cells as a critical component of the neural stem cell niche.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Qin -- Goderie, Susan K -- Jin, Li -- Karanth, Nithin -- Sun, Yu -- Abramova, Natalia -- Vincent, Peter -- Pumiglia, Kevin -- Temple, Sally -- R01 CA081419/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2004 May 28;304(5675):1338-40. Epub 2004 Apr 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, NY 12208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15060285" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology/physiology ; Cattle ; Cell Adhesion ; *Cell Communication ; Cell Differentiation ; Cell Division ; Cell Line ; Cell Lineage ; Cells, Cultured ; Cerebral Cortex/embryology ; Clone Cells/physiology ; Coculture Techniques ; Embryo, Mammalian/cytology ; Endothelial Cells/cytology/*physiology ; Endothelium, Vascular/cytology ; Fibroblast Growth Factor 2/pharmacology ; Mice ; Muscle, Smooth, Vascular/cytology/physiology ; Myocytes, Smooth Muscle/cytology/physiology ; Neurons/cytology/*physiology ; Oligodendroglia/cytology/physiology ; Signal Transduction ; Stem Cells/cytology/*physiology
    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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  • 20
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    Promotion of B cell immune responses via an alum-induced myeloid cell population (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-19
    Description: Exposure of naive B cells to the cytokine interleukin-4 (IL-4) and/or antigen leads to a state of "priming," in which subsequent aggregation of major histocompatibility complex class II molecules induces the mobilization of calcium ions and cell proliferation. However, it is not clear how critical this priming is for immune responses or how it is normally induced in vivo. Injection of mice with the commonly used adjuvant alum led to priming of splenic B cells and to the accumulation in the spleen of a previously unknown population of IL-4-producing, Gr1+ cells. These cells and IL-4 were both required for in vivo priming and expansion of antigen-specific B cells, as well as for optimal production of antibody. These studies reveal a key role for a previously unknown accessory myeloid cell population in the generation of humoral immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jordan, Michael B -- Mills, David M -- Kappler, John -- Marrack, Philippa -- Cambier, John C -- AI-17134/AI/NIAID NIH HHS/ -- AI-18785/AI/NIAID NIH HHS/ -- AI-20519/AI/NIAID NIH HHS/ -- AI-22295/AI/NIAID NIH HHS/ -- AI-50802/AI/NIAID NIH HHS/ -- AI-52225/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 Jun 18;304(5678):1808-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Integrated Department of Immunology, National Jewish Medical and Research Center, University of Colorado Health Sciences Center, 1400 Jackson Street, Denver, CO 80206, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15205534" target="_blank"〉PubMed〈/a〉
    Keywords: *Adjuvants, Immunologic ; Adoptive Transfer ; *Alum Compounds/administration & dosage ; Animals ; B-Lymphocytes/*immunology ; Calcium/metabolism ; Cell Separation ; Cells, Cultured ; Coculture Techniques ; Eosinophils/cytology/immunology ; Freund's Adjuvant ; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology ; Histocompatibility Antigens Class II/immunology ; Immunization ; Interleukin-4/immunology/metabolism ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Myeloid Cells/*immunology ; Nitrophenols/immunology ; Serum Albumin, Bovine/immunology ; Signal Transduction ; Spleen/cytology/immunology
    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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  • 21
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    Selective differentiation of neural progenitor cells by high-epitope density nanofibers (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-24
    Description: Neural progenitor cells were encapsulated in vitro within a three-dimensional network of nanofibers formed by self-assembly of peptide amphiphile molecules. The self-assembly is triggered by mixing cell suspensions in media with dilute aqueous solutions of the molecules, and cells survive the growth of the nanofibers around them. These nanofibers were designed to present to cells the neurite-promoting laminin epitope IKVAV at nearly van der Waals density. Relative to laminin or soluble peptide, the artificial nanofiber scaffold induced very rapid differentiation of cells into neurons, while discouraging the development of astrocytes. This rapid selective differentiation is linked to the amplification of bioactive epitope presentation to cells by the nanofibers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silva, Gabriel A -- Czeisler, Catherine -- Niece, Krista L -- Beniash, Elia -- Harrington, Daniel A -- Kessler, John A -- Stupp, Samuel I -- NS20013/NS/NINDS NIH HHS/ -- NS20778/NS/NINDS NIH HHS/ -- NS34758/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 27;303(5662):1352-5. Epub 2004 Jan 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Bioengineering and Nanoscience in Advanced Medicine, Northwestern University, Chicago, IL 60611, USA. gsilva@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14739465" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology ; *Cell Differentiation ; Cell Movement ; Cell Survival ; Cells, Cultured ; Diffusion ; Epitopes ; Glial Fibrillary Acidic Protein/analysis ; Hydrogen Bonding ; Hydrophobic and Hydrophilic Interactions ; Laminin/administration & dosage/chemistry/immunology/*metabolism ; Mice ; *Nanotechnology ; Neurites/physiology/ultrastructure ; Neurons/*cytology/physiology ; Peptide Fragments/administration & dosage/chemistry/*metabolism ; Rats ; Spinal Cord ; Stem Cells/*cytology/physiology ; Tubulin/analysis
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  • 22
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    Defective telomere lagging strand synthesis in cells lacking WRN helicase activity (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-14
    Description: Cells from Werner syndrome patients are characterized by slow growth rates, premature senescence, accelerated telomere shortening rates, and genome instability. The syndrome is caused by the loss of the RecQ helicase WRN, but the underlying molecular mechanism is unclear. Here we report that cells lacking WRN exhibit deletion of telomeres from single sister chromatids. Only telomeres replicated by lagging strand synthesis were affected, and prevention of loss of individual telomeres was dependent on the helicase activity of WRN. Telomere loss could be counteracted by telomerase activity. We propose that WRN is necessary for efficient replication of G-rich telomeric DNA, preventing telomere dysfunction and consequent genomic instability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crabbe, Laure -- Verdun, Ramiro E -- Haggblom, Candy I -- Karlseder, Jan -- GM069525/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 10;306(5703):1951-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15591207" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Anaphase ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins ; Cell Line ; Cells, Cultured ; Chromatids/metabolism ; Chromosomes, Human/physiology ; DNA Damage ; DNA Helicases/genetics/*metabolism ; DNA-Binding Proteins ; Exodeoxyribonucleases ; Genomic Instability ; HeLa Cells ; Humans ; In Situ Hybridization, Fluorescence ; Models, Genetic ; Mutation ; Protein-Serine-Threonine Kinases/metabolism ; RecQ Helicases ; S Phase ; Telomerase/metabolism ; Telomere/*metabolism ; Tumor Suppressor Proteins ; Werner Syndrome/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 23
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    Instructive role of Wnt/beta-catenin in sensory fate specification in neural crest stem cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-13
    Description: Wnt signaling has recently emerged as a key factor in controlling stem cell expansion. In contrast, we show here that Wnt/beta-catenin signal activation in emigrating neural crest stem cells (NCSCs) has little effect on the population size and instead regulates fate decisions. Sustained beta-catenin activity in neural crest cells promotes the formation of sensory neural cells in vivo at the expense of virtually all other neural crest derivatives. Moreover, Wnt1 is able to instruct early NCSCs (eNCSCs) to adopt a sensory neuronal fate in a beta-catenin-dependent manner. Thus, the role of Wnt/beta-catenin in stem cells is cell-type dependent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Hye-Youn -- Kleber, Maurice -- Hari, Lisette -- Brault, Veronique -- Suter, Ueli -- Taketo, Makoto M -- Kemler, Rolf -- Sommer, Lukas -- New York, N.Y. -- Science. 2004 Feb 13;303(5660):1020-3. Epub 2004 Jan 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cell Biology, Department of Biology, Swiss Federal Institute of Technology, ETH-Honggerberg, CH-8093 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14716020" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors ; Cadherins/metabolism ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cell Movement ; Cells, Cultured ; Central Nervous System/embryology ; Cytoskeletal Proteins/*metabolism ; DNA-Binding Proteins/metabolism ; Mice ; Models, Neurological ; Multipotent Stem Cells/*physiology ; Mutation ; Nerve Tissue Proteins/metabolism ; Neural Crest/*cytology/embryology/physiology ; Neurons, Afferent/*cytology/physiology ; Proto-Oncogene Proteins/*metabolism ; *Signal Transduction ; Trans-Activators/*metabolism ; Transcription Factor Brn-3 ; Transcription Factors/metabolism ; Wnt Proteins ; Wnt1 Protein ; *Zebrafish Proteins ; beta Catenin
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  • 24
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    Genome-wide RNAi analysis of growth and viability in Drosophila cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-07
    Description: A crucial aim upon completion of whole genome sequences is the functional analysis of all predicted genes. We have applied a high-throughput RNA-interference (RNAi) screen of 19,470 double-stranded (ds) RNAs in cultured cells to characterize the function of nearly all (91%) predicted Drosophila genes in cell growth and viability. We found 438 dsRNAs that identified essential genes, among which 80% lacked mutant alleles. A quantitative assay of cell number was applied to identify genes of known and uncharacterized functions. In particular, we demonstrate a role for the homolog of a mammalian acute myeloid leukemia gene (AML1) in cell survival. Such a systematic screen for cell phenotypes, such as cell viability, can thus be effective in characterizing functionally related genes on a genome-wide scale.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boutros, Michael -- Kiger, Amy A -- Armknecht, Susan -- Kerr, Kim -- Hild, Marc -- Koch, Britta -- Haas, Stefan A -- Paro, Renato -- Perrimon, Norbert -- Heidelberg Fly Array Consortium -- R01 GM078176/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 6;303(5659):832-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14764878" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Cycle ; Cell Survival ; Cells, Cultured ; Computational Biology ; Core Binding Factor Alpha 2 Subunit ; DNA-Binding Proteins/genetics ; Drosophila Proteins/genetics/metabolism/physiology ; Drosophila melanogaster/*genetics/*growth & development ; Genes, Essential ; *Genes, Insect ; *Genome ; Humans ; Inhibitor of Apoptosis Proteins ; Phenotype ; Proteome ; Proto-Oncogene Proteins/genetics ; *RNA Interference ; RNA, Double-Stranded/genetics ; Reproducibility of Results ; Sequence Homology ; Transcription Factors/genetics/metabolism
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    Two distinct actin networks drive the protrusion of migrating cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-18
    Description: Cell migration initiates by extension of the actin cytoskeleton at the leading edge. Computational analysis of fluorescent speckle microscopy movies of migrating epithelial cells revealed this process is mediated by two spatially colocalized but kinematically, kinetically, molecularly, and functionally distinct actin networks. A lamellipodium network assembled at the leading edge but completely disassembled within 1 to 3 micrometers. It was weakly coupled to the rest of the cytoskeleton and promoted the random protrusion and retraction of the leading edge. Productive cell advance was a function of the second colocalized network, the lamella, where actomyosin contraction was integrated with substrate adhesion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ponti, A -- Machacek, M -- Gupton, S L -- Waterman-Storer, C M -- Danuser, G -- GM67230/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Sep 17;305(5691):1782-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Scripps Research Institute (TSRI), La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15375270" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/drug effects/*physiology ; Actins/*physiology ; Animals ; Cell Line ; *Cell Movement ; Cells, Cultured ; Cytochalasin D/pharmacology ; *Depsipeptides ; Epithelial Cells/*physiology/ultrastructure ; Heterocyclic Compounds with 4 or More Rings/pharmacology ; Kinetics ; Macropodidae ; Microscopy, Fluorescence ; Motion Pictures as Topic ; Peptides, Cyclic/pharmacology ; Pseudopodia/*physiology/ultrastructure ; Salamandridae
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    Enhanced dendritic cell antigen capture via toll-like receptor-induced actin remodeling (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-25
    Description: Microbial products are sensed through Toll-like receptors (TLRs) and trigger a program of dendritic cell (DC) maturation that enables DCs to activate T cells. Although an accepted hallmark of this response is eventual down-regulation of DC endocytic capacity, we show that TLR ligands first acutely stimulate antigen macropinocytosis, leading to enhanced presentation on class I and class II major histocompatibility complex molecules. Simultaneously, actin-rich podosomes disappear, which suggests a coordinated redeployment of actin to fuel endocytosis. These reciprocal changes are transient and require p38 and extracellular signal-regulated kinase activation. Thus, the DC actin cytoskeleton can be rapidly mobilized in response to innate immune stimuli to enhance antigen capture and presentation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉West, Michele A -- Wallin, Robert P A -- Matthews, Stephen P -- Svensson, Henrik G -- Zaru, Rossana -- Ljunggren, Hans-Gustaf -- Prescott, Alan R -- Watts, Colin -- G0100536/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2004 Aug 20;305(5687):1153-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology and Immunology, Wellcome Trust Biocentre, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15326355" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*physiology ; Animals ; Antigen Presentation ; Antigens/*immunology ; Cell Membrane/physiology/ultrastructure ; Cells, Cultured ; Cytoskeleton/*physiology/ultrastructure ; Dendritic Cells/*immunology ; Down-Regulation ; Endocytosis ; Ligands ; Lipopolysaccharides/immunology ; Membrane Glycoproteins/*metabolism ; Mice ; Microscopy, Fluorescence ; Microscopy, Video ; Mitogen-Activated Protein Kinases/metabolism ; Pinocytosis ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; Toll-Like Receptors
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    Integrins regulate Rac targeting by internalization of membrane domains (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-07
    Description: Translocation of the small GTP-binding protein Rac1 to the cell plasma membrane is essential for activating downstream effectors and requires integrin-mediated adhesion of cells to extracellular matrix. We report that active Rac1 binds preferentially to low-density, cholesterol-rich membranes, and specificity is determined at least in part by membrane lipids. Cell detachment triggered internalization of plasma membrane cholesterol and lipid raft markers. Preventing internalization maintained Rac1 membrane targeting and effector activation in nonadherent cells. Regulation of lipid rafts by integrin signals may regulate the location of membrane domains such as lipid rafts and thereby control domain-specific signaling events in anchorage-dependent cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉del Pozo, Miguel A -- Alderson, Nazilla B -- Kiosses, William B -- Chiang, Hui-Hsien -- Anderson, Richard G W -- Schwartz, Martin A -- GM52016/GM/NIGMS NIH HHS/ -- HL 20948/HL/NHLBI NIH HHS/ -- R01 GM47214/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 6;303(5659):839-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. mdelpozo@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14764880" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD29/metabolism ; Binding Sites ; Cell Adhesion ; Cell Line ; Cell Membrane/*metabolism ; Cells, Cultured ; Cholera Toxin/metabolism ; Cholesterol/metabolism ; G(M1) Ganglioside/metabolism ; Glycosylphosphatidylinositols/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Integrins/*metabolism ; Liposomes/metabolism ; Membrane Microdomains/*metabolism ; Mice ; NIH 3T3 Cells ; Rats ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection ; rac1 GTP-Binding Protein/genetics/*metabolism
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    Stress-dependent regulation of FOXO transcription factors by the SIRT1 deacetylase (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-21
    Description: The Sir2 deacetylase modulates organismal life-span in various species. However, the molecular mechanisms by which Sir2 increases longevity are largely unknown. We show that in mammalian cells, the Sir2 homolog SIRT1 appears to control the cellular response to stress by regulating the FOXO family of Forkhead transcription factors, a family of proteins that function as sensors of the insulin signaling pathway and as regulators of organismal longevity. SIRT1 and the FOXO transcription factor FOXO3 formed a complex in cells in response to oxidative stress, and SIRT1 deacetylated FOXO3 in vitro and within cells. SIRT1 had a dual effect on FOXO3 function: SIRT1 increased FOXO3's ability to induce cell cycle arrest and resistance to oxidative stress but inhibited FOXO3's ability to induce cell death. Thus, one way in which members of the Sir2 family of proteins may increase organismal longevity is by tipping FOXO-dependent responses away from apoptosis and toward stress resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunet, Anne -- Sweeney, Lora B -- Sturgill, J Fitzhugh -- Chua, Katrin F -- Greer, Paul L -- Lin, Yingxi -- Tran, Hien -- Ross, Sarah E -- Mostoslavsky, Raul -- Cohen, Haim Y -- Hu, Linda S -- Cheng, Hwei-Ling -- Jedrychowski, Mark P -- Gygi, Steven P -- Sinclair, David A -- Alt, Frederick W -- Greenberg, Michael E -- NIHP30-HD18655/HD/NICHD NIH HHS/ -- P01 NS35138-17/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Mar 26;303(5666):2011-5. Epub 2004 Feb 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Center for Blood Research (CBR) Institute for Biomedical Research, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14976264" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Apoptosis ; Cell Cycle ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; Cerebellum/cytology ; Forkhead Transcription Factors ; Gene Expression Profiling ; Gene Expression Regulation ; Histone Deacetylases/genetics/*metabolism ; Humans ; Intracellular Signaling Peptides and Proteins ; Mice ; Mice, Knockout ; Neurons/cytology ; *Oxidative Stress ; Phosphorylation ; Proteins/genetics ; Recombinant Proteins/metabolism ; Sirtuin 1 ; Sirtuins/genetics/*metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
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    Regeneration of peroxiredoxins by p53-regulated sestrins, homologs of bacterial AhpD (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-24
    Description: Acting as a signal, hydrogen peroxide circumvents antioxidant defense by overoxidizing peroxiredoxins (Prxs), the enzymes that metabolize peroxides. We show that sestrins, a family of proteins whose expression is modulated by p53, are required for regeneration of Prxs containing Cys-SO(2)H, thus reestablishing the antioxidant firewall. Sestrins contain a predicted redox-active domain homologous to AhpD, the enzyme catalyzing the reduction of a bacterial Prx, AhpC. Purified Hi95 (sestrin 2) protein supports adenosine triphosphate-dependent reduction of overoxidized PrxI in vitro, indicating that unlike AhpD, which is a disulfide reductase, sestrins are cysteine sulfinyl reductases. As modulators of peroxide signaling and antioxidant defense, sestrins constitute potential therapeutic targets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Budanov, Andrei V -- Sablina, Anna A -- Feinstein, Elena -- Koonin, Eugene V -- Chumakov, Peter M -- New York, N.Y. -- Science. 2004 Apr 23;304(5670):596-600.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15105503" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Cell Division ; Cell Line, Tumor ; Cell Survival ; Cells, Cultured ; Heat-Shock Proteins/chemistry/genetics/*metabolism ; Humans ; Hydrogen Peroxide/metabolism ; Molecular Sequence Data ; Mutation ; Nuclear Proteins/chemistry/genetics/*metabolism ; Oxidation-Reduction ; Oxidoreductases/genetics/metabolism ; Peroxidases/*chemistry/*metabolism ; Peroxiredoxins ; RNA, Small Interfering ; Reactive Oxygen Species/metabolism ; Recombinant Proteins/metabolism ; Tumor Suppressor Protein p53/metabolism
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    Argonaute2 is the catalytic engine of mammalian RNAi (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-31
    Description: Gene silencing through RNA interference (RNAi) is carried out by RISC, the RNA-induced silencing complex. RISC contains two signature components, small interfering RNAs (siRNAs) and Argonaute family proteins. Here, we show that the multiple Argonaute proteins present in mammals are both biologically and biochemically distinct, with a single mammalian family member, Argonaute2, being responsible for messenger RNA cleavage activity. This protein is essential for mouse development, and cells lacking Argonaute2 are unable to mount an experimental response to siRNAs. Mutations within a cryptic ribonuclease H domain within Argonaute2, as identified by comparison with the structure of an archeal Argonaute protein, inactivate RISC. Thus, our evidence supports a model in which Argonaute contributes "Slicer" activity to RISC, providing the catalytic engine for RNAi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Jidong -- Carmell, Michelle A -- Rivas, Fabiola V -- Marsden, Carolyn G -- Thomson, J Michael -- Song, Ji-Joon -- Hammond, Scott M -- Joshua-Tor, Leemor -- Hannon, Gregory J -- New York, N.Y. -- Science. 2004 Sep 3;305(5689):1437-41. Epub 2004 Jul 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Watson School of Biological Sciences, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15284456" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Argonaute Proteins ; Catalysis ; Cell Line ; Cells, Cultured ; Central Nervous System/embryology ; Embryonic and Fetal Development ; Eukaryotic Initiation Factor-2 ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Humans ; In Situ Hybridization ; Mice ; MicroRNAs/metabolism ; Molecular Sequence Data ; Mutagenesis, Insertional ; Oligonucleotide Array Sequence Analysis ; Peptide Initiation Factors/chemistry/*metabolism ; Point Mutation ; *RNA Interference ; RNA, Double-Stranded ; RNA, Messenger/*metabolism ; RNA, Small Interfering/metabolism ; RNA-Induced Silencing Complex/chemistry/*metabolism
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    Innate antiviral responses by means of TLR7-mediated recognition of single-stranded RNA (2004)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2004-02-21
    Description: Interferons (IFNs) are critical for protection from viral infection, but the pathways linking virus recognition to IFN induction remain poorly understood. Plasmacytoid dendritic cells produce vast amounts of IFN-alpha in response to the wild-type influenza virus. Here, we show that this requires endosomal recognition of influenza genomic RNA and signaling by means of Toll-like receptor 7 (TLR7) and MyD88. Single-stranded RNA (ssRNA) molecules of nonviral origin also induce TLR7-dependent production of inflammatory cytokines. These results identify ssRNA as a ligand for TLR7 and suggest that cells of the innate immune system sense endosomal ssRNA to detect infection by RNA viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diebold, Sandra S -- Kaisho, Tsuneyasu -- Hemmi, Hiroaki -- Akira, Shizuo -- Reis e Sousa, Caetano -- New York, N.Y. -- Science. 2004 Mar 5;303(5663):1529-31. Epub 2004 Feb 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Laboratory, Cancer Research UK, London Research Institute, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14976261" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Antigens, Differentiation/metabolism ; Cells, Cultured ; Cytokines/biosynthesis ; Dendritic Cells/*immunology ; Endocytosis ; Endosomes/immunology/virology ; Genome, Viral ; *Immunity, Innate ; Influenza A virus/genetics/*immunology ; Interferon-alpha/biosynthesis ; Ligands ; Membrane Glycoproteins/*metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88 ; Poly U/immunology ; Polyribonucleotides/immunology ; RNA/*immunology ; RNA, Viral/*immunology ; Receptors, Cell Surface/*metabolism ; Receptors, Immunologic/metabolism ; Signal Transduction ; Toll-Like Receptor 7
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    Requirement of JNK2 for scavenger receptor A-mediated foam cell formation in atherogenesis (2004)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2004-11-30
    Description: In vitro studies suggest a role for c-Jun N-terminal kinases (JNKs) in proatherogenic cellular processes. We show that atherosclerosis-prone ApoE-/- mice simultaneously lacking JNK2 (ApoE-/- JNK2-/- mice), but not ApoE-/- JNK1-/- mice, developed less atherosclerosis than do ApoE-/- mice. Pharmacological inhibition of JNK activity efficiently reduced plaque formation. Macrophages lacking JNK2 displayed suppressed foam cell formation caused by defective uptake and degradation of modified lipoproteins and showed increased amounts of the modified lipoprotein-binding and -internalizing scavenger receptor A (SR-A), whose phosphorylation was markedly decreased. Macrophage-restricted deletion of JNK2 was sufficient to decrease atherogenesis. Thus, JNK2-dependent phosphorylation of SR-A promotes uptake of lipids in macrophages, thereby regulating foam cell formation, a critical step in atherogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ricci, Romeo -- Sumara, Grzegorz -- Sumara, Izabela -- Rozenberg, Izabela -- Kurrer, Michael -- Akhmedov, Alexander -- Hersberger, Martin -- Eriksson, Urs -- Eberli, Franz R -- Becher, Burkhard -- Boren, Jan -- Chen, Mian -- Cybulsky, Myron I -- Moore, Kathryn J -- Freeman, Mason W -- Wagner, Erwin F -- Matter, Christian M -- Luscher, Thomas F -- New York, N.Y. -- Science. 2004 Nov 26;306(5701):1558-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research, Institute of Physiology, and Division of Cardiology, University Hospital Zurich, CH-8057 Zurich, Switzerland. romeo.ricci@cell.biol.ethz.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15567863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD36/metabolism ; Aorta/chemistry/pathology ; Apolipoproteins E/genetics ; Arteriosclerosis/*metabolism/pathology ; Bone Marrow Transplantation ; Cells, Cultured ; Cholesterol/metabolism ; Cholesterol, Dietary/administration & dosage ; Diet, Atherogenic ; Endothelial Cells/physiology ; Foam Cells/*metabolism ; Lipoproteins, LDL/metabolism ; Macrophages/*metabolism ; Macrophages, Peritoneal/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitogen-Activated Protein Kinase 8/metabolism ; Mitogen-Activated Protein Kinase 9/genetics/*metabolism ; Muscle, Smooth, Vascular/cytology ; Myocytes, Smooth Muscle/physiology ; Phosphorylation ; Receptors, Immunologic/genetics/*metabolism ; Receptors, Scavenger ; Scavenger Receptors, Class A ; T-Lymphocytes/immunology
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    Neuroscience. Cellular interactions in the stem cell niche (2004)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2004-05-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wurmser, Andrew E -- Palmer, Theo D -- Gage, Fred H -- New York, N.Y. -- Science. 2004 May 28;304(5675):1253-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, Salk Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15166350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology/physiology ; *Cell Communication ; Cell Differentiation ; Cell Division ; Cell Survival ; Cells, Cultured ; Coculture Techniques ; Embryo, Mammalian/cytology ; Endothelial Cells/cytology/*physiology ; Mice ; Neurons/cytology/*physiology ; Signal Transduction ; Stem Cells/cytology/*physiology
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    Regulation of an ATG7-beclin 1 program of autophagic cell death by caspase-8 (2004)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2004-05-08
    Description: Caspases play a central role in apoptosis, a well-studied pathway of programmed cell death. Other programs of death potentially involving necrosis and autophagy may exist, but their relation to apoptosis and mechanisms of regulation remains unclear. We define a new molecular pathway in which activation of the receptor-interacting protein (a serine-threonine kinase) and Jun amino-terminal kinase induced cell death with the morphology of autophagy. Autophagic death required the genes ATG7 and beclin 1 and was induced by caspase-8 inhibition. Clinical therapies involving caspase inhibitors may arrest apoptosis but also have the unanticipated effect of promoting autophagic cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Li -- Alva, Ajjai -- Su, Helen -- Dutt, Parmesh -- Freundt, Eric -- Welsh, Sarah -- Baehrecke, Eric H -- Lenardo, Michael J -- GM59136/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Jun 4;304(5676):1500-2. Epub 2004 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, 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/15131264" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; Apoptosis Regulatory Proteins ; *Autophagy ; Caspase 8 ; *Caspase Inhibitors ; Caspases/genetics/*metabolism ; *Cell Death ; Cell Line ; Cells, Cultured ; Humans ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 7 ; MAP Kinase Signaling System ; Membrane Proteins ; Mice ; Mitogen-Activated Protein Kinase Kinases/genetics/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Proteins/genetics/*metabolism ; RNA Interference ; Receptor-Interacting Protein Serine-Threonine Kinases
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    Increased nuclear NAD biosynthesis and SIRT1 activation prevent axonal degeneration (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-18
    Description: Axonal degeneration is an active program of self-destruction that is observed in many physiological and pathological settings. In Wallerian degeneration slow (wlds) mice, Wallerian degeneration in response to axonal injury is delayed because of a mutation that results in overexpression of a chimeric protein (Wlds) composed of the ubiquitin assembly protein Ufd2a and the nicotinamide adenine dinucleotide (NAD) biosynthetic enzyme Nmnat1. We demonstrate that increased Nmnat activity is responsible for the axon-sparing activity of the Wlds protein. Furthermore, we demonstrate that SIRT1, a mammalian ortholog of Sir2, is the downstream effector of increased Nmnat activity that leads to axonal protection. These findings suggest that novel therapeutic strategies directed at increasing the supply of NAD and/or Sir2 activation may be effective for treatment of diseases characterized by axonopathy and neurodegeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Araki, Toshiyuki -- Sasaki, Yo -- Milbrandt, Jeffrey -- AG05681/AG/NIA NIH HHS/ -- AG13730/AG/NIA NIH HHS/ -- NS40745/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Aug 13;305(5686):1010-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15310905" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Axons/drug effects/*physiology ; Axotomy ; Benzamides/pharmacology ; Cell Line ; Cell Nucleus/metabolism ; Cell Survival ; Cells, Cultured ; Ganglia, Spinal/cytology ; Humans ; Lentivirus/genetics/physiology ; Mice ; Mutation ; NAD/*biosynthesis/pharmacology ; Naphthols/pharmacology ; Nerve Tissue Proteins/*metabolism ; Neuroprotective Agents/pharmacology ; Nicotinamide-Nucleotide Adenylyltransferase/*metabolism ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/metabolism ; RNA, Small Interfering ; Sirtuin 1 ; Sirtuins/antagonists & inhibitors/*metabolism ; Stilbenes/pharmacology ; Ubiquitin-Protein Ligases/genetics/metabolism ; Vincristine/pharmacology ; Wallerian Degeneration/metabolism/*physiopathology
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    Regulation of dendritic protein synthesis by miniature synaptic events (2004)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2004-06-26
    Description: We examined dendritic protein synthesis after a prolonged blockade of action potentials alone and after a blockade of both action potentials and miniature excitatory synaptic events (minis). Relative to controls, dendrites exposed to a prolonged blockade of action potentials showed diminished protein synthesis. Dendrites in which both action potentials and minis were blocked showed enhanced protein synthesis, suggesting that minis inhibit dendritic translation. When minis were acutely blocked or stimulated, an immediate increase or decrease, respectively, in dendritic translation was observed. Taken together, these results reveal a role for miniature synaptic events in the acute regulation of dendritic protein synthesis in neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sutton, Michael A -- Wall, Nicholas R -- Aakalu, Girish N -- Schuman, Erin M -- New York, N.Y. -- Science. 2004 Jun 25;304(5679):1979-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, Howard Hughes Medical Institute (HHMI), California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15218151" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Botulinum Toxins, Type A/pharmacology ; Cells, Cultured ; Dendrites/*metabolism ; *Excitatory Postsynaptic Potentials/drug effects ; Genes, Reporter ; Hippocampus/cytology ; Neurons/metabolism/physiology ; Patch-Clamp Techniques ; *Protein Biosynthesis/drug effects ; Rats ; Receptors, N-Methyl-D-Aspartate/metabolism ; Signal Transduction ; Spider Venoms/pharmacology ; Synapses/*physiology ; *Synaptic Transmission/drug effects ; Synaptic Vesicles/metabolism ; Tetrodotoxin/pharmacology
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    Nicotine activation of alpha4* receptors: sufficient for reward, tolerance, and sensitization (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-06
    Description: The identity of nicotinic receptor subtypes sufficient to elicit both the acute and chronic effects of nicotine dependence is unknown. We engineered mutant mice with a4 nicotinic subunits containing a single point mutation, Leu9' --〉 Ala9' in the pore-forming M2 domain, rendering a4* receptors hypersensitive to nicotine. Selective activation of a4* nicotinic acetylcholine receptors with low doses of agonist recapitulates nicotine effects thought to be important in dependence, including reinforcement in response to acute nicotine administration, as well as tolerance and sensitization elicited by chronic nicotine administration. These data indicate that activation of a4* receptors is sufficient for nicotine-induced reward, tolerance, and sensitization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tapper, Andrew R -- McKinney, Sheri L -- Nashmi, Raad -- Schwarz, Johannes -- Deshpande, Purnima -- Labarca, Cesar -- Whiteaker, Paul -- Marks, Michael J -- Collins, Allan C -- Lester, Henry A -- DA-15663/DA/NIDA NIH HHS/ -- DA-3194/DA/NIDA NIH HHS/ -- MH-49716/MH/NIMH NIH HHS/ -- NS-11756/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Nov 5;306(5698):1029-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15528443" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaloids/metabolism ; Animals ; Azocines/metabolism ; Bicyclo Compounds, Heterocyclic/metabolism ; Brain/drug effects/metabolism ; Calcium/metabolism ; Cells, Cultured ; *Drug Tolerance ; Leucine ; Mice ; Mice, Inbred C57BL ; Motor Activity/drug effects ; Neurons/metabolism ; Nicotine/*pharmacology ; Point Mutation ; Pyridines/metabolism ; Quinolizines/metabolism ; Receptors, Nicotinic/genetics/*physiology ; *Reward ; Serine ; Tobacco Use Disorder/*metabolism ; Up-Regulation
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    Lysosomal glycosphingolipid recognition by NKT cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-13
    Description: NKT cells represent a distinct lineage of T cells that coexpress a conserved alphabeta T cell receptor (TCR) and natural killer (NK) receptors. Although the TCR of NKT cells is characteristically autoreactive to CD1d, a lipid-presenting molecule, endogenous ligands for these cells have not been identified. We show that a lysosomal glycosphingolipid of previously unknown function, isoglobotrihexosylceramide (iGb3), is recognized both by mouse and human NKT cells. Impaired generation of lysosomal iGb3 in mice lacking beta-hexosaminidase b results in severe NKT cell deficiency, suggesting that this lipid also mediates development of NKT cells in the mouse. We suggest that expression of iGb3 in peripheral tissues may be involved in controlling NKT cell responses to infections and malignancy and in autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Dapeng -- Mattner, Jochen -- Cantu, Carlos 3rd -- Schrantz, Nicolas -- Yin, Ning -- Gao, Ying -- Sagiv, Yuval -- Hudspeth, Kelly -- Wu, Yun-Ping -- Yamashita, Tadashi -- Teneberg, Susann -- Wang, Dacheng -- Proia, Richard L -- Levery, Steven B -- Savage, Paul B -- Teyton, Luc -- Bendelac, Albert -- AI053725/AI/NIAID NIH HHS/ -- AI50847/AI/NIAID NIH HHS/ -- P20RR16459/RR/NCRR NIH HHS/ -- R01 AI38339/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 3;306(5702):1786-9. Epub 2004 Nov 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Chicago, Department of Pathology, Chicago, IL 60637, USA. dzhou@midway.uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15539565" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigens, CD1/immunology/metabolism ; Antigens, CD1d ; Autoimmunity ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Dendritic Cells/immunology ; Galactosyltransferases/genetics/metabolism ; Globosides/chemistry/*immunology/metabolism ; Humans ; Hybridomas ; Infection/immunology ; Killer Cells, Natural/*immunology ; Ligands ; Lymphocyte Activation ; Lymphocyte Count ; Lysosomes/*metabolism ; Mice ; Mice, Inbred C57BL ; Neoplasms/immunology ; Plant Lectins/immunology ; Rats ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Saposins/metabolism ; T-Lymphocyte Subsets/*immunology ; beta-N-Acetylhexosaminidases/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Dynamic interaction of stargazin-like TARPs with cycling AMPA receptors at synapses (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-06
    Description: Activity-dependent plasticity in the brain arises in part from changes in the number of synaptic AMPA receptors. Synaptic trafficking of AMPA receptors is controlled by stargazin and homologous transmembrane AMPA receptor regulatory proteins (TARPs). We found that TARPs were stable at the plasma membrane, whereas AMPA receptors were internalized in a glutamate-regulated manner. Interaction with AMPA receptors involved both extra- and intracellular determinants of TARPs. Upon binding to glutamate, AMPA receptors detached from TARPs. This did not require ion flux or intracellular second messengers. This allosteric mechanism for AMPA receptor dissociation from TARPs may participate in glutamate-mediated internalization of receptors in synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tomita, Susumu -- Fukata, Masaki -- Nicoll, Roger A -- Bredt, David S -- New York, N.Y. -- Science. 2004 Mar 5;303(5663):1508-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California, San Francisco, San Francisco, CA 94143-2140, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15001777" target="_blank"〉PubMed〈/a〉
    Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology ; Animals ; Calcium Channels/analysis/*metabolism ; Cell Line ; Cells, Cultured ; Cerebral Cortex/chemistry/cytology ; Endocytosis ; Glutamic Acid/metabolism/pharmacology ; Humans ; Neuronal Plasticity ; Protein Binding ; Protein Structure, Tertiary ; Rats ; Receptors, AMPA/agonists/antagonists & inhibitors/*metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/*metabolism ; Xenopus laevis ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/pharmacology
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    Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-16
    Description: Obesity contributes to the development of type 2 diabetes, but the underlying mechanisms are poorly understood. Using cell culture and mouse models, we show that obesity causes endoplasmic reticulum (ER) stress. This stress in turn leads to suppression of insulin receptor signaling through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptor substrate-1 (IRS-1). Mice deficient in X-box-binding protein-1 (XBP-1), a transcription factor that modulates the ER stress response, develop insulin resistance. These findings demonstrate that ER stress is a central feature of peripheral insulin resistance and type 2 diabetes at the molecular, cellular, and organismal levels. Pharmacologic manipulation of this pathway may offer novel opportunities for treating these common diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ozcan, Umut -- Cao, Qiong -- Yilmaz, Erkan -- Lee, Ann-Hwee -- Iwakoshi, Neal N -- Ozdelen, Esra -- Tuncman, Gurol -- Gorgun, Cem -- Glimcher, Laurie H -- Hotamisligil, Gokhan S -- AI32412/AI/NIAID NIH HHS/ -- DK52539/DK/NIDDK NIH HHS/ -- P05-CA100707/CA/NCI NIH HHS/ -- T32-DK07703/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2004 Oct 15;306(5695):457-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Complex Diseases, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15486293" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Animals ; Cells, Cultured ; DNA-Binding Proteins/genetics/metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Endoplasmic Reticulum/*metabolism ; Glucose/metabolism ; Homeostasis ; Insulin/*metabolism ; Insulin Receptor Substrate Proteins ; *Insulin Resistance ; Liver/metabolism ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Obese ; Mitogen-Activated Protein Kinase 8 ; Mitogen-Activated Protein Kinases/metabolism ; Muscle, Skeletal/metabolism ; Mutation ; Nuclear Proteins/genetics/metabolism ; Obesity/*metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Receptor, Insulin/metabolism ; Signal Transduction ; Transcription Factors ; Tunicamycin/pharmacology ; eIF-2 Kinase/metabolism
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    Recycling endosomes supply AMPA receptors for LTP (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-28
    Description: Long-term potentiation (LTP) of synaptic strength, the most established cellular model of information storage in the brain, is expressed by an increase in the number of postsynaptic AMPA receptors. However, the source of AMPA receptors mobilized during LTP is unknown. We report that AMPA receptors are transported from recycling endosomes to the plasma membrane for LTP. Stimuli that triggered LTP promoted not only AMPA receptor insertion but also generalized recycling of cargo and membrane from endocytic compartments. Thus, recycling endosomes supply AMPA receptors for LTP and provide a mechanistic link between synaptic potentiation and membrane remodeling during synapse modification.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Mikyoung -- Penick, Esther C -- Edwards, Jeffrey G -- Kauer, Julie A -- Ehlers, Michael D -- DA11289/DA/NIDA NIH HHS/ -- MH64748/MH/NIMH NIH HHS/ -- NS39402/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Sep 24;305(5692):1972-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Box 3209, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15448273" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/metabolism ; Cell Membrane/metabolism ; Cells, Cultured ; Endosomes/*metabolism ; Hippocampus/cytology ; *Long-Term Potentiation ; Neurons/metabolism ; Patch-Clamp Techniques ; Protein Transport ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/*metabolism ; Synapses ; Transfection ; rab GTP-Binding Proteins/genetics/metabolism
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    Neuroscience. Calcium and CREST for healthy dendrites (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jefferis, Gregory S X E -- Komiyama, Takaki -- Luo, Liqun -- New York, N.Y. -- Science. 2004 Jan 9;303(5655):179-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences and Neurosciences Program, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14715999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; CREB-Binding Protein ; Calcium/*metabolism ; Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; DNA-Binding Proteins/metabolism ; Dendrites/*physiology/ultrastructure ; Mice ; Neurons/physiology/ultrastructure ; Nuclear Proteins/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Trans-Activators/chemistry/genetics/*metabolism ; Transcription Factors/metabolism ; *Transcription, Genetic ; *Transcriptional Activation ; Transfection
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    Epithelial-to-mesenchymal transition generates proliferative human islet precursor cells (2004)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2004-11-27
    Description: Insulin-expressing beta cells, found in pancreatic islets, are capable of generating more beta cells even in the adult. We show that fibroblast-like cells derived from adult human islets donated postmortem proliferate readily in vitro. These mesenchymal-type cells, which exhibit no hormone expression, can then be induced to differentiate into hormone-expressing islet-like cell aggregates, which reestablishes the epithelial character typical of islet cells. Immunohistochemistry, in situ hybridization, and messenger RNA measurements in single cells and cell populations establish the transition of epithelial cells within islets to mesenchymal cells in culture and then to insulin-expressing epithelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gershengorn, Marvin C -- Hardikar, Anandwardhan A -- Wei, Chiju -- Geras-Raaka, Elizabeth -- Marcus-Samuels, Bernice -- Raaka, Bruce M -- New York, N.Y. -- Science. 2004 Dec 24;306(5705):2261-4. Epub 2004 Nov 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-8029, USA. marving@intra.niddk.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15564314" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; C-Peptide/biosynthesis/genetics ; Cell Aggregation ; Cell Differentiation ; Cell Line, Tumor ; *Cell Proliferation ; Cell Shape ; Cells, Cultured ; Child ; Child, Preschool ; Culture Media, Serum-Free ; Epithelial Cells/*cytology ; Humans ; Immunohistochemistry ; In Situ Hybridization ; Insulin/*biosynthesis/genetics ; Islets of Langerhans/*cytology/metabolism ; Keratins/genetics/metabolism ; Mesoderm/*cytology ; Middle Aged ; Proinsulin/biosynthesis/genetics ; RNA, Messenger/genetics/metabolism ; Vimentin/biosynthesis/genetics
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    Harnessing chaperones to generate small-molecule inhibitors of amyloid beta aggregation (2004)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2004-10-30
    Description: Protein aggregation is involved in the pathogenesis of neurodegenerative diseases and hence is considered an attractive target for therapeutic intervention. However, protein-protein interactions are exceedingly difficult to inhibit. Small molecules lack sufficient steric bulk to prevent interactions between large peptide surfaces. To yield potent inhibitors of beta-amyloid (Abeta) aggregation, we synthesized small molecules that increase their steric bulk by binding to chaperones but also have a moiety available for interaction with Abeta. This strategy yields potent inhibitors of Abeta aggregation and could lead to therapeutics for Alzheimer's disease and other forms of neurodegeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gestwicki, Jason E -- Crabtree, Gerald R -- Graef, Isabella A -- NS046789/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Oct 29;306(5697):865-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Howard Hughes Medical Institute, Stanford University Medical School, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15514157" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/drug therapy ; Amyloid beta-Peptides/*chemistry/metabolism/toxicity ; Animals ; Cell Death/drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Congo Red/*analogs & derivatives/*chemical ; synthesis/chemistry/metabolism/*pharmacology ; Cross-Linking Reagents ; Fluorescence ; Hippocampus/cytology ; In Situ Nick-End Labeling ; Ligands ; Microscopy, Fluorescence ; Molecular Chaperones/*metabolism ; Molecular Structure ; Neurites/ultrastructure ; Neurons/cytology/*drug effects/ultrastructure ; Peptide Fragments/chemistry/metabolism ; Piperidines/*chemical synthesis/chemistry/metabolism/*pharmacology ; Rats ; Tacrolimus Binding Proteins/*metabolism/pharmacology
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    Mammalian tissue oxygen levels modulate iron-regulatory protein activities in vivo (2004)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2004-12-18
    Description: The iron-regulatory proteins (IRPs) posttranscriptionally regulate expression of transferrin receptor, ferritin, and other iron metabolism proteins. Although both IRPs can regulate expression of the same target genes, IRP2-/- mice significantly misregulate iron metabolism and develop neurodegeneration, whereas IRP1-/- mice are spared. We found that IRP2-/- cells misregulated iron metabolism when cultured in 3 to 6% oxygen, which is comparable to physiological tissue concentrations, but not in 21% oxygen, a concentration that activated IRP1 and allowed it to substitute for IRP2. Thus, IRP2 dominates regulation of mammalian iron homeostasis because it alone registers iron concentrations and modulates its RNA-binding activity at physiological oxygen tensions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyron-Holtz, Esther G -- Ghosh, Manik C -- Rouault, Tracey A -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2087-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604406" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Ferritins/biosynthesis/metabolism ; Gene Expression Regulation ; Homeostasis ; Iron/*metabolism ; Iron Regulatory Protein 1/genetics/*metabolism ; Iron Regulatory Protein 2/genetics/*metabolism ; Lymphocytes/*metabolism ; Macrophages/*metabolism ; Mice ; Oxidants/metabolism ; Oxygen/*physiology ; RNA/metabolism ; Receptors, Transferrin/biosynthesis/metabolism ; Response Elements ; Spleen/cytology
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    Abnormal cytokinesis in cells deficient in the breast cancer susceptibility protein BRCA2 (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-18
    Description: Germ-line mutations inactivating BRCA2 predispose to cancer. BRCA2-deficient cells exhibit alterations in chromosome number (aneuploidy), as well as structurally aberrant chromosomes. Here, we show that BRCA2 deficiency impairs the completion of cell division by cytokinesis. BRCA2 inactivation in murine embryo fibroblasts (MEFs) and HeLa cells by targeted gene disruption or RNA interference delays and prevents cell cleavage. Impeded cell separation is accompanied by abnormalities in myosin II organization during the late stages in cytokinesis. BRCA2 may have a role in regulating these events, as it localizes to the cytokinetic midbody. Our findings thus link cytokinetic abnormalities to a hereditary cancer syndrome characterized by chromosomal instability and may help to explain why BRCA2-deficient tumors are frequently aneuploid.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daniels, Matthew J -- Wang, Yunmei -- Lee, Miyoung -- Venkitaraman, Ashok R -- New York, N.Y. -- Science. 2004 Oct 29;306(5697):876-9. Epub 2004 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Cambridge, Cancer Research UK, Department of Oncology and the Medical Research Council (MRC) Cancer Cell Unit, Hutchison/MRC Research Centre, Hills Road, Cambridge CB2 2XZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15375219" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase ; Aneuploidy ; Animals ; BRCA2 Protein/*physiology ; *Cell Division ; Cell Line, Tumor ; Cell Nucleus/physiology ; Cells, Cultured ; Embryo, Mammalian ; Gene Targeting ; Genes, BRCA2 ; HeLa Cells ; Humans ; Mice ; Mitosis ; Myosin Type II/metabolism ; RNA, Small Interfering
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    Impaired degradation of mutant alpha-synuclein by chaperone-mediated autophagy (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-31
    Description: Aberrant alpha-synuclein degradation is implicated in Parkinson's disease pathogenesis because the protein accumulates in the Lewy inclusion bodies associated with the disease. Little is known, however, about the pathways by which wild-type alpha-synuclein is normally degraded. We found that wild-type alpha-synuclein was selectively translocated into lysosomes for degradation by the chaperone-mediated autophagy pathway. The pathogenic A53T and A30P alpha-synuclein mutants bound to the receptor for this pathway on the lysosomal membrane, but appeared to act as uptake blockers, inhibiting both their own degradation and that of other substrates. These findings may underlie the toxic gain-of-function by the mutants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cuervo, Ana Maria -- Stefanis, Leonidas -- Fredenburg, Ross -- Lansbury, Peter T -- Sulzer, David -- AG021904/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2004 Aug 27;305(5688):1292-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Structural Biology, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA. amcuervo@aecom.yu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15333840" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Antigens, CD/metabolism ; *Autophagy ; Cells, Cultured ; Glyceraldehyde-3-Phosphate Dehydrogenases/metabolism/pharmacology ; Half-Life ; Intracellular Membranes/metabolism ; Lysosome-Associated Membrane Glycoproteins ; Lysosomes/*metabolism ; Male ; Mice ; Molecular Chaperones/*metabolism ; Mutation ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neurons/metabolism ; PC12 Cells ; Protein Binding ; Protein Transport ; Rats ; Rats, Wistar ; Synucleins ; alpha-Synuclein
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    Dendrite development regulated by CREST, a calcium-regulated transcriptional activator (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-13
    Description: The lasting effects of neuronal activity on brain development involve calcium-dependent gene expression. Using a strategy called transactivator trap, we cloned a calcium-responsive transactivator called CREST (for calcium-responsive transactivator). CREST is a SYT-related nuclear protein that interacts with adenosine 3',5'-monophosphate (cAMP) response element-binding protein (CREB)-binding protein (CBP) and is expressed in the developing brain. Mice that have a targeted disruption of the crest gene are viable but display defects in cortical and hippocampal dendrite development. Cortical neurons from crest mutant mice are compromised in calcium-dependent dendritic growth. Thus, calcium activation of CREST-mediated transcription helps regulate neuronal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aizawa, Hiroyuki -- Hu, Shu-Ching -- Bobb, Kathryn -- Balakrishnan, Karthik -- Ince, Gulayse -- Gurevich, Inga -- Cowan, Mitra -- Ghosh, Anirvan -- MH60598/MH/NIMH NIH HHS/ -- NS39993/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Jan 9;303(5655):197-202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14716005" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Brain/cytology/embryology/growth & development/metabolism ; CREB-Binding Protein ; Calcium/*metabolism ; Calcium Channels/metabolism ; Cell Line ; Cells, Cultured ; Cerebral Cortex/cytology/embryology/metabolism ; Cloning, Molecular ; Dendrites/*physiology/ultrastructure ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Library ; Gene Targeting ; Humans ; In Situ Hybridization ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; Nervous System/embryology/growth & development/metabolism ; Neurons/*physiology/ultrastructure ; Nuclear Proteins/metabolism ; Protein Structure, Tertiary ; Rats ; Recombinant Fusion Proteins/metabolism ; Trans-Activators/chemistry/genetics/*metabolism ; *Transcription, Genetic ; *Transcriptional Activation ; Transfection
    Print ISSN: 0036-8075
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    Integrase inhibitors and cellular immunity suppress retroviral replication in rhesus macaques (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-13
    Description: We describe the efficacy of L-870812, an inhibitor of HIV-1 and SIV integrase, in rhesus macaques infected with the simian-human immunodeficiency virus (SHIV) 89.6P. When initiated before CD4 cell depletion, L-870812 therapy mediated a sustained suppression of viremia, preserving CD4 levels and permitting the induction of virus-specific cellular immunity. L-870812 was also active in chronic infection; however, the magnitude and durability of the effect varied in conjunction with the pretreatment immune response and viral load. These studies demonstrate integrase inhibitor activity in vivo and suggest that cellular immunity facilitates chemotherapeutic efficacy in retroviral infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hazuda, Daria J -- Young, Steven D -- Guare, James P -- Anthony, Neville J -- Gomez, Robert P -- Wai, John S -- Vacca, Joseph P -- Handt, Larry -- Motzel, Sherri L -- Klein, Hilton J -- Dornadula, Geethanjali -- Danovich, Robert M -- Witmer, Marc V -- Wilson, Keith A A -- Tussey, Lynda -- Schleif, William A -- Gabryelski, Lori S -- Jin, Lixia -- Miller, Michael D -- Casimiro, Danilo R -- Emini, Emilio A -- Shiver, John W -- New York, N.Y. -- Science. 2004 Jul 23;305(5683):528-32. Epub 2004 Jul 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Merck Research Laboratories, Post Office Box 4, West Point, PA 19486, USA. daria_hazuda@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15247437" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*drug therapy/*immunology/virology ; Animals ; Anti-HIV Agents/administration & dosage/blood/pharmacology/therapeutic use ; CD4 Lymphocyte Count ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cells, Cultured ; Drug Resistance, Viral ; HIV Integrase/genetics/metabolism ; HIV Integrase Inhibitors/administration & dosage/blood/pharmacology/therapeutic ; use ; HIV-1/drug effects/enzymology/genetics/*physiology ; Immunity, Cellular ; Integrase Inhibitors/administration & dosage/blood/pharmacology/*therapeutic use ; Integrases/genetics/metabolism ; Leukocytes, Mononuclear/virology ; Macaca mulatta ; Mutation ; Naphthyridines/administration & dosage/blood/pharmacology/*therapeutic use ; Simian Acquired Immunodeficiency Syndrome/*drug therapy/*immunology/virology ; Simian Immunodeficiency Virus/drug effects/enzymology/genetics/*physiology ; Viral Load ; Viremia/drug therapy ; Virus Replication/drug effects
    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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    COX-2-derived prostacyclin confers atheroprotection on female mice (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-20
    Description: Female gender affords relative protection from cardiovascular disease until the menopause. We report that estrogen acts on estrogen receptor subtype alpha to up-regulate the production of atheroprotective prostacyclin, PGI2, by activation of cyclooxygenase 2 (COX-2). This mechanism restrained both oxidant stress and platelet activation that contribute to atherogenesis in female mice. Deletion of the PGI2 receptor removed the atheroprotective effect of estrogen in ovariectomized female mice. This suggests that chronic treatment of patients with selective inhibitors of COX-2 could undermine protection from cardiovascular disease in premenopausal females.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, Karine M -- Lawson, John A -- Fries, Susanne -- Koller, Beverley -- Rader, Daniel J -- Smyth, Emer M -- Fitzgerald, Garret A -- HL62250/HL/NHLBI NIH HHS/ -- HL70128/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 10;306(5703):1954-7. Epub 2004 Nov 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Translational Medicine and Therapeutics, University of Pennsylvania, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15550624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antioxidants/metabolism ; Arteriosclerosis/metabolism/pathology/*prevention & control ; Cardiovascular Diseases/chemically induced ; Cells, Cultured ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors/adverse effects/pharmacology ; Epoprostenol/biosynthesis/metabolism/*physiology ; Estradiol/pharmacology ; Estrogen Receptor alpha/metabolism ; Female ; Hydrogen Peroxide/pharmacology ; Isoenzymes/*metabolism ; Lactones/adverse effects/pharmacology ; Lipid Peroxidation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular/drug effects/metabolism ; Myocytes, Smooth Muscle/cytology/drug effects/metabolism ; Ovariectomy ; Oxidative Stress ; Platelet Activation ; Prostaglandin-Endoperoxide Synthases/*metabolism ; Receptors, Epoprostenol/genetics/physiology ; Receptors, LDL/genetics/physiology ; Sex Characteristics ; Sulfones/adverse effects/pharmacology
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    Cell biology. Oxygen sensing: it's a gas! (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoshi, Toshinori -- Lahiri, Sukhamay -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2050-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. hoshi@hoshi.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604396" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon Monoxide/*metabolism ; Carotid Body/*cytology/*physiology ; Cell Hypoxia ; Cell Membrane/physiology ; Cells, Cultured ; Heme/metabolism/pharmacology ; Heme Oxygenase (Decyclizing)/genetics/*metabolism ; Hemeproteins/metabolism ; Large-Conductance Calcium-Activated Potassium Channels ; Membrane Potentials ; Mitochondria/metabolism ; NADP/pharmacology ; NADPH Oxidase/metabolism ; Oxidation-Reduction ; Oxygen/*physiology ; Potassium Channels, Calcium-Activated ; Proteomics ; RNA, Small Interfering/pharmacology ; Signal Transduction
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    Visfatin: a protein secreted by visceral fat that mimics the effects of insulin (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: Fat tissue produces a variety of secreted proteins (adipocytokines) with important roles in metabolism. We isolated a newly identified adipocytokine, visfatin, that is highly enriched in the visceral fat of both humans and mice and whose expression level in plasma increases during the development of obesity. Visfatin corresponds to a protein identified previously as pre-B cell colony-enhancing factor (PBEF), a 52-kilodalton cytokine expressed in lymphocytes. Visfatin exerted insulin-mimetic effects in cultured cells and lowered plasma glucose levels in mice. Mice heterozygous for a targeted mutation in the visfatin gene had modestly higher levels of plasma glucose relative to wild-type littermates. Surprisingly, visfatin binds to and activates the insulin receptor. Further study of visfatin's physiological role may lead to new insights into glucose homeostasis and/or new therapies for metabolic disorders such as diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukuhara, Atsunori -- Matsuda, Morihiro -- Nishizawa, Masako -- Segawa, Katsumori -- Tanaka, Masaki -- Kishimoto, Kae -- Matsuki, Yasushi -- Murakami, Mirei -- Ichisaka, Tomoko -- Murakami, Hiroko -- Watanabe, Eijiro -- Takagi, Toshiyuki -- Akiyoshi, Megumi -- Ohtsubo, Tsuguteru -- Kihara, Shinji -- Yamashita, Shizuya -- Makishima, Makoto -- Funahashi, Tohru -- Yamanaka, Shinya -- Hiramatsu, Ryuji -- Matsuzawa, Yuji -- Shimomura, Iichiro -- New York, N.Y. -- Science. 2005 Jan 21;307(5708):426-30. Epub 2004 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and Pathophysiology, Graduate School of Medicine, and Department of Organismal Biosystems, Graduate School of Frontier Biosciences, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604363" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/drug effects/metabolism ; Adipose Tissue/*metabolism ; Animals ; Binding Sites ; Blood Glucose/analysis ; Cell Line ; Cells, Cultured ; Cytokines/blood/genetics/*metabolism/pharmacology ; Diabetes Mellitus, Type 2/metabolism ; Dose-Response Relationship, Drug ; Female ; Gene Expression Profiling ; Gene Expression Regulation/drug effects ; Gene Targeting ; Humans ; Insulin/blood/*metabolism ; Insulin Resistance ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Molecular Mimicry ; Muscle Cells/metabolism ; Nicotinamide Phosphoribosyltransferase ; Phosphorylation ; Receptor, Insulin/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; Subcutaneous Tissue ; Viscera
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    Polyubiquitination of p53 by a ubiquitin ligase activity of p300 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-12
    Description: Rapid turnover of the tumor suppressor protein p53 requires the MDM2 ubiquitin ligase, and both interact with p300-CREB-binding protein transcriptional coactivator proteins. p53 is stabilized by the binding of p300 to the oncoprotein E1A, suggesting that p300 regulates p53 degradation. Purified p300 exhibited intrinsic ubiquitin ligase activity that was inhibited by E1A. In vitro, p300 with MDM2 catalyzed p53 polyubiquitination, whereas MDM2 catalyzed p53 monoubiquitination. E1A expression caused a decrease in polyubiquitinated but not monoubiquitinated p53 in cells. Thus, generation of the polyubiquitinated forms of p53 that are targeted for proteasome degradation requires the intrinsic ubiquitin ligase activities of MDM2 and p300.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grossman, Steven R -- Deato, Maria E -- Brignone, Chrystelle -- Chan, Ho Man -- Kung, Andrew L -- Tagami, Hideaki -- Nakatani, Yoshihiro -- Livingston, David M -- CA15751/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 11;300(5617):342-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690203" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus E1A Proteins/metabolism ; Animals ; Catalysis ; Cells, Cultured ; E1A-Associated p300 Protein ; Embryo, Mammalian ; Fibroblasts/metabolism ; Humans ; Ligases/antagonists & inhibitors/metabolism ; Mice ; Nuclear Proteins/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-mdm2 ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Trans-Activators/antagonists & inhibitors/*metabolism ; Transfection ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/*metabolism ; Ubiquitin-Protein Ligases ; Ubiquitins/*metabolism
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    Role of Raf in vascular protection from distinct apoptotic stimuli (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-05
    Description: Raf kinases have been linked to endothelial cell survival. Here, we show that basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) differentially activate Raf, resulting in protection from distinct pathways of apoptosis in human endothelial cells and chick embryo vasculature. bFGF activated Raf-1 via p21-activated protein kinase-1 (PAK-1) phosphorylation of serines 338 and 339, resulting in Raf-1 mitochondrial translocation and endothelial cell protection from the intrinsic pathway of apoptosis, independent of the mitogen-activated protein kinase kinase-1 (MEK1). In contrast, VEGF activated Raf-1 via Src kinase, leading to phosphorylation of tyrosines 340 and 341 and MEK1-dependent protection from extrinsic-mediated apoptosis. These findings implicate Raf-1 as a pivotal regulator of endothelial cell survival during angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alavi, Alireza -- Hood, John D -- Frausto, Ricardo -- Stupack, Dwayne G -- Cheresh, David A -- CA45726/CA/NCI NIH HHS/ -- CA50286/CA/NCI NIH HHS/ -- CA75924/CA/NCI NIH HHS/ -- P01 CA78045/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):94-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Survival ; Cells, Cultured ; Chick Embryo ; Endothelial Growth Factors/pharmacology ; Endothelium, Vascular/*cytology/drug effects ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Fibroblast Growth Factor 2/pharmacology ; Flavonoids/pharmacology ; Humans ; Intercellular Signaling Peptides and Proteins/pharmacology ; Lymphokines/pharmacology ; MAP Kinase Kinase 1 ; Mitochondria/metabolism ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Neovascularization, Pathologic ; *Neovascularization, Physiologic/drug effects ; Phosphorylation ; Point Mutation ; Protein Transport ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins B-raf ; Proto-Oncogene Proteins c-raf/chemistry/genetics/*metabolism ; Signal Transduction ; Umbilical Veins ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; p21-Activated Kinases ; src-Family Kinases/antagonists & inhibitors/metabolism
    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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    Derepression of BDNF transcription involves calcium-dependent phosphorylation of MeCP2 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-01
    Description: Mutations in MeCP2, which encodes a protein that has been proposed to function as a global transcriptional repressor, are the cause of Rett syndrome (RT T), an X-linked progressive neurological disorder. Although the selective inactivation of MeCP2 in neurons is sufficient to confer a Rett-like phenotype in mice, the specific functions of MeCP2 in postmitotic neurons are not known. We find that MeCP2 binds selectively to BDNF promoter III and functions to repress expression of the BDNF gene. Membrane depolarization triggers the calcium-dependent phosphorylation and release of MeCP2 from BDNF promoter III, thereby facilitating transcription. These studies indicate that MeCP2 plays a key role in the control of neuronal activity-dependent gene regulation and suggest that the deregulation of this process may underlie the pathology of RT T.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Wen G -- Chang, Qiang -- Lin, Yingxi -- Meissner, Alexander -- West, Anne E -- Griffith, Eric C -- Jaenisch, Rudolf -- Greenberg, Michael E -- HD 18655/HD/NICHD NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):885-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/*genetics ; Calcium/*metabolism ; Cell Membrane/physiology ; Cells, Cultured ; *Chromosomal Proteins, Non-Histone ; Cloning, Molecular ; CpG Islands ; DNA Methylation ; DNA-Binding Proteins/*metabolism ; Electrophoretic Mobility Shift Assay ; *Gene Expression Regulation ; Gene Silencing ; Histones/metabolism ; Methyl-CpG-Binding Protein 2 ; Methylation ; Mice ; Mice, Knockout ; Neurons/metabolism/physiology ; Phosphorylation ; Potassium Chloride/pharmacology ; Precipitin Tests ; Promoter Regions, Genetic ; Rats ; *Repressor Proteins ; Rett Syndrome/genetics ; *Transcription, Genetic
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    Inflammatory blockade restores adult hippocampal neurogenesis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-15
    Description: Cranial radiation therapy causes a progressive decline in cognitive function that is linked to impaired neurogenesis. Chronic inflammation accompanies radiation injury, suggesting that inflammatory processes may contribute to neural stem cell dysfunction. Here, we show that neuroinflammation alone inhibits neurogenesis and that inflammatory blockade with indomethacin, a common nonsteroidal anti-inflammatory drug, restores neurogenesis after endotoxin-induced inflammation and augments neurogenesis after cranial irradiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monje, Michelle L -- Toda, Hiroki -- Palmer, Theo D -- F30 NS04696701/NS/NINDS NIH HHS/ -- MH20016-05/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1760-5. Epub 2003 Nov 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford University, Department of Neurosurgery, MSLS P309, Mail Code 5487, 1201 Welch Road, Stanford, CA 94305-5487, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14615545" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Antigens, CD/metabolism ; Apoptosis ; Cell Differentiation ; Cells, Cultured ; Coculture Techniques ; Culture Media, Conditioned ; Cytokine Receptor gp130 ; Cytokines/physiology ; Dentate Gyrus/cytology/drug effects/physiology/radiation effects ; Female ; Gamma Rays ; Hippocampus/cytology/drug effects/*physiology/radiation effects ; In Situ Nick-End Labeling ; Indomethacin/*pharmacology ; Inflammation/drug therapy/*physiopathology ; Interleukin-6/pharmacology/physiology ; Lipopolysaccharides/pharmacology ; Membrane Glycoproteins/metabolism ; Mice ; Microglia/*physiology ; Mitotic Index ; Neurons/drug effects/*physiology/radiation effects ; Rats ; Rats, Inbred F344 ; Receptors, Interleukin-6/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; Stem Cells/physiology
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Regulation of NF-kappaB-dependent lymphocyte activation and development by paracaspase (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-25
    Description: Paracaspase (MALT1), a member of an evolutionarily conserved superfamily of caspase-like proteins, has been shown to bind and colocalize with the protein Bcl10 in vitro and, because of this association, has been suggested to be involved in the CARMA1-Bcl10 pathway of antigen-induced nuclear factor kappaB (NF-kappaB) activation. We demonstrate that primary T and B lymphocytes from paracaspase-deficient mice are defective in antigen-receptor-induced NF-kappaB activation, cytokine production, and proliferation. Paracaspase acts downstream of Bcl10 to induce NF-kappaB activation and is required for the normal development of B cells, indicating that paracaspase provides the missing link between Bcl10 and activation of the IkappaB kinase complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruefli-Brasse, Astrid A -- French, Dorothy M -- Dixit, Vishva M -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1581-4. Epub 2003 Oct 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Oncology Department, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576442" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antibody Formation ; Antigens, CD/analysis ; B-Lymphocyte Subsets/immunology/physiology ; B-Lymphocytes/*immunology/metabolism/physiology ; Caspases ; Cell Differentiation ; Cell Division ; Cell Survival ; Cells, Cultured ; Cytokines/metabolism ; Gene Deletion ; Gene Targeting ; Guanylate Kinase ; I-kappa B Kinase ; *Lymphocyte Activation ; Lymphoma, B-Cell, Marginal Zone/chemistry/*metabolism ; Mice ; Mice, Inbred C57BL ; NF-kappa B/*metabolism ; Neoplasm Proteins/chemistry/*metabolism ; Nucleoside-Phosphate Kinase/metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocyte Subsets/immunology/physiology ; T-Lymphocytes/*immunology/metabolism/physiology ; 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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    Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-12
    Description: Stimulation of Toll-like receptors (TLRs) triggers activation of a common MyD88-dependent signaling pathway as well as a MyD88-independent pathway that is unique to TLR3 and TLR4 signaling pathways leading to interferon (IFN)-beta production. Here we disrupted the gene encoding a Toll/IL-1 receptor (TIR) domain-containing adaptor, TRIF. TRIF-deficient mice were defective in both TLR3- and TLR4-mediated expression of IFN-beta and activation of IRF-3. Furthermore, inflammatory cytokine production in response to the TLR4 ligand, but not to other TLR ligands, was severely impaired in TRIF-deficient macrophages. Mice deficient in both MyD88 and TRIF showed complete loss of nuclear factor kappa B activation in response to TLR4 stimulation. These findings demonstrate that TRIF is essential for TLR3- and TLR4-mediated signaling pathways facilitating mammalian antiviral host defense.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamoto, Masahiro -- Sato, Shintaro -- Hemmi, Hiroaki -- Hoshino, Katsuaki -- Kaisho, Tsuneyasu -- Sanjo, Hideki -- Takeuchi, Osamu -- Sugiyama, Masanaka -- Okabe, Masaru -- Takeda, Kiyoshi -- Akira, Shizuo -- New York, N.Y. -- Science. 2003 Aug 1;301(5633):640-3. Epub 2003 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855817" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adaptor Proteins, Vesicular Transport/genetics/*physiology ; Animals ; Antigens, Differentiation/*physiology ; Cells, Cultured ; Cytokines/biosynthesis ; DNA-Binding Proteins/metabolism ; Dimerization ; Embryo, Mammalian ; Fibroblasts/metabolism ; Gene Expression Regulation ; Gene Targeting ; Interferon Regulatory Factor-3 ; Interferon-beta/genetics/*metabolism ; JNK Mitogen-Activated Protein Kinases ; Ligands ; Lipopolysaccharides/immunology/pharmacology ; Macrophages, Peritoneal/immunology/metabolism ; Membrane Glycoproteins/*metabolism ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinases/metabolism ; Myeloid Differentiation Factor 88 ; NF-kappa B/metabolism ; Poly I-C/pharmacology ; Receptors, Cell Surface/*metabolism ; Receptors, Immunologic/*physiology ; *Signal Transduction ; Toll-Like Receptor 3 ; Toll-Like Receptor 4 ; Toll-Like Receptors ; Transcription Factors/metabolism
    Print ISSN: 0036-8075
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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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    Mono- versus polyubiquitination: differential control of p53 fate by Mdm2 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: Although Mdm2-mediated ubiquitination is essential for both degradation and nuclear export of p53, the molecular basis for the differential effects of Mdm2 remains unknown. Here we show that low levels of Mdm2 activity induce monoubiquitination and nuclear export of p53, whereas high levels promote p53's polyubiquitination and nuclear degradation. A p53-ubiquitin fusion protein that mimics monoubiquitinated p53 was found to accumulate in the cytoplasm in an Mdm2-independent manner, indicating that monoubiquitination is critical for p53 trafficking. These results clarify the nature of ubiquitination-mediated p53 regulation and suggest that distinct mechanisms regulate p53 function in accordance with the levels of Mdm2 activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Muyang -- Brooks, Christopher L -- Wu-Baer, Foon -- Chen, Delin -- Baer, Richard -- Gu, Wei -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1972-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Genetics and Department of Pathology, College of Physicians & Surgeons, Columbia University, 1150 St. Nicholas Avenue, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671306" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; Cell Line, Tumor ; Cell Nucleus/*metabolism ; Cells, Cultured ; Cytoplasm/metabolism ; Humans ; Mice ; Mice, Knockout ; Mutation ; *Nuclear Proteins ; Protein Transport ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins c-mdm2 ; Recombinant Fusion Proteins/metabolism ; Transfection ; Tumor Suppressor Protein p53/genetics/*metabolism ; Ubiquitin/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Identification of Hedgehog pathway components by RNAi in Drosophila cultured cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-29
    Description: Classical genetic screens can be limited by the selectivity of mutational targeting, the complexities of anatomically based phenotypic analysis, or difficulties in subsequent gene identification. Focusing on signaling response to the secreted morphogen Hedgehog (Hh), we used RNA interference (RNAi) and a quantitative cultured cell assay to systematically screen functional roles of all kinases and phosphatases, and subsequently 43% of predicted Drosophila genes. Two gene products reported to function in Wingless (Wg) signaling were identified as Hh pathway components: a cell surface protein (Dally-like protein) required for Hh signal reception, and casein kinase 1alpha, a candidate tumor suppressor that regulates basal activities of both Hh and Wg pathways. This type of cultured cell-based functional genomics approach may be useful in the systematic analysis of other biological processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lum, Lawrence -- Yao, Shenqin -- Mozer, Brian -- Rovescalli, Alessandra -- Von Kessler, Doris -- Nirenberg, Marshall -- Beachy, Philip A -- New York, N.Y. -- Science. 2003 Mar 28;299(5615):2039-45.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12663920" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Casein Kinases ; Cells, Cultured ; Computational Biology ; Congenital Abnormalities/genetics ; Cyclic AMP-Dependent Protein Kinases/genetics/metabolism ; Drosophila/embryology/*genetics/metabolism ; Drosophila Proteins/*genetics/metabolism ; Embryo, Nonmammalian/metabolism ; Gene Expression Regulation ; *Genes, Insect ; Genome ; Genomics ; Hedgehog Proteins ; Neoplasms/genetics ; Protein Kinases/genetics/metabolism ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Proteoglycans/chemistry/genetics/metabolism ; Proto-Oncogene Proteins/genetics/metabolism ; *RNA Interference ; RNA, Double-Stranded/genetics ; *Signal Transduction ; Transfection ; Wnt1 Protein
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    Transcription-coupled events associating with immunoglobulin switch region chromatin (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: Class switch recombination (CSR) at the antibody immunoglobulin locus is regulated by germline transcription (GLT)-coupled modifications in the accessibility of the switch region, where CSR takes place. Here we show that histone acetylation of switch regions is linked to CSR but that histone acetylation cannot alone promote CSR or GLT. Activation-induced cytidine deaminase (AID) specifically associates with the CSR target chromatin in a GLT-coupled manner, which may occur potentially by means of physical interaction between AID and the transcription machinery. These data indicate an important role of GLT in the regulation of chromatin accessibility, strongly suggesting that the target of AID is chromatin DNA. Our results give insights on the role of AID and the regulatory mechanism of CSR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nambu, Yukiko -- Sugai, Manabu -- Gonda, Hiroyuki -- Lee, Chung-Gi -- Katakai, Tomoya -- Agata, Yasutoshi -- Yokota, Yoshifumi -- Shimizu, Akira -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2137-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular Biology and Genetics, Kyoto University, 53 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684824" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; B-Lymphocytes/*immunology ; Cells, Cultured ; Chromatin/*metabolism ; Cytidine Deaminase/*metabolism ; DNA/metabolism ; Histone Deacetylase Inhibitors ; Histones/metabolism ; Hydroxamic Acids/pharmacology ; *Immunoglobulin Class Switching ; Immunoglobulin E/biosynthesis ; Immunoglobulin G/biosynthesis ; *Immunoglobulin Switch Region ; Interleukin-4/immunology ; Lipopolysaccharides/immunology ; Lymphocyte Activation ; Mice ; Precipitin Tests ; RNA/metabolism ; RNA Polymerase II/metabolism ; Recombination, Genetic ; *Transcription, Genetic ; Transforming Growth Factor beta/immunology ; Transforming Growth Factor beta1
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    Eppendorf 2003 prize-winning essay. Ubiquitin and the deconstruction of synapses (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ehlers, Michael D -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):800-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA. ehlers@neuro.duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593160" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Awards and Prizes ; Carrier Proteins/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cysteine Endopeptidases/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Multienzyme Complexes/metabolism ; Nerve Tissue Proteins/*metabolism ; Neurons/metabolism ; Proteasome Endopeptidase Complex ; Receptors, N-Methyl-D-Aspartate/metabolism ; Signal Transduction ; Synapses/*metabolism/ultrastructure ; Synaptic Membranes/*metabolism/ultrastructure ; *Synaptic Transmission ; Ubiquitin/*metabolism
    Print ISSN: 0036-8075
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    Maintenance of stable heterochromatin domains by dynamic HP1 binding (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-01
    Description: One function of heterochromatin is the epigenetic silencing by sequestration of genes into transcriptionally repressed nuclear neighborhoods. Heterochromatin protein 1 (HP1) is a major component of heterochromatin and thus is a candidate for establishing and maintaining the transcriptionally repressive heterochromatin structure. Here we demonstrate that maintenance of stable heterochromatin domains in living cells involves the transient binding and dynamic exchange of HP1 from chromatin. HP1 exchange kinetics correlate with the condensation level of chromatin and are dependent on the histone methyltransferase Suv39h. The chromodomain and the chromoshadow domain of HP1 are both required for binding to native chromatin in vivo, but they contribute differentially to binding in euchromatin and heterochromatin. These data argue against HP1 repression of transcription by formation of static, higher order oligomeric networks but support a dynamic competition model, and they demonstrate that heterochromatin is accessible to regulatory factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheutin, Thierry -- McNairn, Adrian J -- Jenuwein, Thomas -- Gilbert, David M -- Singh, Prim B -- Misteli, Tom -- New York, N.Y. -- Science. 2003 Jan 31;299(5607):721-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute, 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/12560555" target="_blank"〉PubMed〈/a〉
    Keywords: Amanitins/pharmacology ; Animals ; Binding Sites ; CHO Cells ; Cell Nucleus/metabolism ; Cells, Cultured ; Chromosomal Proteins, Non-Histone/*chemistry/genetics/*metabolism ; Cricetinae ; Dimerization ; Euchromatin/metabolism ; Fluorescence Recovery After Photobleaching ; HeLa Cells ; Heterochromatin/*chemistry/*metabolism ; Histones/metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Kinetics ; Methyltransferases/metabolism ; Mice ; Mice, Knockout ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/metabolism ; Transfection
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    Requirement of AMPA receptor GluR2 phosphorylation for cerebellar long-term depression (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-14
    Description: Cerebellar long-term depression (LTD) is a model of synaptic memory that requires protein kinase C (PKC) activation and is expressed as a reduction in the number of postsynaptic alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors. LTD was absent in cultured cerebellar Purkinje cells from mutant mice lacking the AMPA receptor GluR2 subunit and could be rescued by transient transfection with the wild-type GluR2 subunit. Transfection with a point mutant that eliminated PKC phosphorylation of Ser880 in the carboxy-terminal PDZ ligand of GluR2 failed to restore LTD. In contrast, transfection with a point mutant that mimicked phosphorylation at Ser880 occluded subsequent LTD. Thus, PKC phosphorylation of GluR2 Ser880 is a critical event in the induction of cerebellar LTD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chung, Hee Jung -- Steinberg, Jordan P -- Huganir, Richard L -- Linden, David J -- MH01590/MH/NIMH NIH HHS/ -- MH51106/MH/NIMH NIH HHS/ -- NS36715/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Jun 13;300(5626):1751-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12805550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Carrier Proteins/metabolism ; Cells, Cultured ; Cerebellar Cortex/cytology/*physiology ; Enzyme Activation ; Excitatory Postsynaptic Potentials ; *Long-Term Synaptic Depression ; Mice ; Mice, Knockout ; Nerve Tissue Proteins/metabolism ; Nuclear Proteins/metabolism ; Nuclear Receptor Coactivator 2 ; Patch-Clamp Techniques ; Phorbol Esters/pharmacology ; Phosphorylation ; Phosphoserine/metabolism ; Point Mutation ; Protein Binding ; Protein Kinase C/metabolism ; Purkinje Cells/*physiology ; Receptors, AMPA/genetics/*metabolism ; Transcription Factors/metabolism ; Transfection
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    Derivation of oocytes from mouse embryonic stem cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: Continuation of mammalian species requires the formation and development of the sexually dimorphic germ cells. Cultured embryonic stem cells are generally considered pluripotent rather than totipotent because of the failure to detect germline cells under differentiating conditions. Here we show that mouse embryonic stem cells in culture can develop into oogonia that enter meiosis, recruit adjacent cells to form follicle-like structures, and later develop into blastocysts. Oogenesis in culture should contribute to various areas, including nuclear transfer and manipulation of the germ line, and advance studies on fertility treatment and germ and somatic cell interaction and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hubner, Karin -- Fuhrmann, Guy -- Christenson, Lane K -- Kehler, James -- Reinbold, Rolland -- De La Fuente, Rabindranath -- Wood, Jennifer -- Strauss, Jerome F 3rd -- Boiani, Michele -- Scholer, Hans R -- 1RO1HD42011-01/HD/NICHD NIH HHS/ -- HD06274/HD/NICHD NIH HHS/ -- T32 HD07305/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 May 23;300(5623):1251-6. Epub 2003 May 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Germline Development Group, Center for Animal Transgenesis and Germ Cell Research, School of Veterinary Medicine, University of Pennsylvania, New Bolton Center, 382 West Street Road, Kennett Square, PA 19348, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730498" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; Blastocyst/cytology/*physiology ; Cell Adhesion ; Cell Aggregation ; *Cell Differentiation ; Cell Lineage ; Cell Separation ; Cells, Cultured ; DNA-Binding Proteins/genetics ; Embryo, Mammalian/*cytology ; Estradiol/metabolism ; Female ; Gene Expression ; Genes, Reporter ; Meiosis ; Mice ; Mice, Transgenic ; Octamer Transcription Factor-3 ; Oocytes/cytology/*physiology ; *Oogenesis ; Ovarian Follicle/cytology/physiology ; Recombinant Fusion Proteins ; Totipotent Stem Cells/*physiology ; *Transcription Factors ; Transfection
    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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    BAX and BAK regulation of endoplasmic reticulum Ca2+: a control point for apoptosis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-08
    Description: BAX and BAK are "multidomain" proapoptotic proteins that initiate mitochondrial dysfunction but also localize to the endoplasmic reticulum (ER). Mouse embryonic fibroblasts deficient for BAX and BAK (DKO cells) were found to have a reduced resting concentration of calcium in the ER ([Ca2+]er) that results in decreased uptake of Ca2+ by mitochondria after Ca2+ release from the ER. Expression of SERCA (sarcoplasmic-endoplasmic reticulum Ca2+ adenosine triphosphatase) corrected [Ca2+]er and mitochondrial Ca2+ uptake in DKO cells, restoring apoptotic death in response to agents that release Ca2+ from intracellular stores (such as arachidonic acid, C2-ceramide, and oxidative stress). In contrast, targeting of BAX to mitochondria selectively restored apoptosis to "BH3-only" signals. A third set of stimuli, including many intrinsic signals, required both ER-released Ca2+ and the presence of mitochondrial BAX or BAK to fully restore apoptosis. Thus, BAX and BAK operate in both the ER and mitochondria as an essential gateway for selected apoptotic signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scorrano, Luca -- Oakes, Scott A -- Opferman, Joseph T -- Cheng, Emily H -- Sorcinelli, Mia D -- Pozzan, Tullio -- Korsmeyer, Stanley J -- R37CA50239/CA/NCI NIH HHS/ -- T32HL07627/HL/NHLBI NIH HHS/ -- TCP02016/Telethon/Italy -- New York, N.Y. -- Science. 2003 Apr 4;300(5616):135-9. Epub 2003 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Department of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12624178" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Arachidonic Acid/pharmacology ; Calcium/*metabolism ; Calcium Signaling ; Calcium-Transporting ATPases/metabolism ; Cell Fractionation ; Cell Line, Transformed ; Cells, Cultured ; Endoplasmic Reticulum/*metabolism ; Histamine/pharmacology ; Hydrogen Peroxide/pharmacology ; Ionomycin/pharmacology ; Membrane Proteins/*metabolism ; Mice ; Mice, Knockout ; Microscopy, Confocal ; Microscopy, Immunoelectron ; Mitochondria/metabolism ; Proto-Oncogene Proteins/*metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; Recombinant Fusion Proteins/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases ; Sphingosine/*analogs & derivatives/pharmacology ; bcl-2 Homologous Antagonist-Killer Protein ; bcl-2-Associated X Protein
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    Toll pathway-dependent blockade of CD4+CD25+ T cell-mediated suppression by dendritic cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: Toll-like receptors (TLRs) control activation of adaptive immune responses by antigen-presenting cells (APCs). However, initiation of adaptive immune responses is also controlled by regulatory T cells (TR cells), which act to prevent activation of autoreactive T cells. Here we describe a second mechanism of immune induction by TLRs, which is independent of effects on costimulation. Microbial induction of the Toll pathway blocked the suppressive effect of CD4+CD25+ TR cells, allowing activation of pathogen-specific adaptive immune responses. This block of suppressor activity was dependent in part on interleukin-6, which was induced by TLRs upon recognition of microbial products.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pasare, Chandrashekhar -- Medzhitov, Ruslan -- New York, N.Y. -- Science. 2003 Feb 14;299(5609):1033-6. Epub 2003 Jan 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532024" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD/immunology/metabolism ; Antigens, Differentiation/metabolism ; Cells, Cultured ; Culture Media, Conditioned ; Dendritic Cells/*immunology/metabolism ; Dinucleoside Phosphates/immunology ; *Drosophila Proteins ; *Immune Tolerance ; Immunization ; Interleukin-6/*physiology/secretion ; Lipopolysaccharides/immunology ; Lymphocyte Activation ; Membrane Glycoproteins/*physiology ; Mice ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88 ; Ovalbumin/immunology ; Receptors, Cell Surface/*physiology ; Receptors, Immunologic/metabolism ; Self Tolerance ; T-Lymphocytes/immunology ; T-Lymphocytes, Regulatory/*immunology ; Toll-Like Receptors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Hirschsprung disease is linked to defects in neural crest stem cell function (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-16
    Description: Genes associated with Hirschsprung disease, a failure to form enteric ganglia in the hindgut, were highly up-regulated in gut neural crest stem cells relative to whole-fetus RNA. One of these genes, the glial cell line-derived neurotrophic factor (GDNF) receptor Ret, was necessary for neural crest stem cell migration in the gut. GDNF promoted the migration of neural crest stem cells in culture but did not affect their survival or proliferation. Gene expression profiling, combined with reverse genetics and analyses of stem cell function, suggests that Hirschsprung disease is caused by defects in neural crest stem cell function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614078/" 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/PMC2614078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwashita, Toshihide -- Kruger, Genevieve M -- Pardal, Ricardo -- Kiel, Mark J -- Morrison, Sean J -- CA46592/CA/NCI NIH HHS/ -- DK58771/DK/NIDDK NIH HHS/ -- NIH5P60-DK20572/DK/NIDDK NIH HHS/ -- P30 AR48310/AR/NIAMS NIH HHS/ -- P60-AR20557/AR/NIAMS NIH HHS/ -- R01 NS040750/NS/NINDS NIH HHS/ -- R01 NS040750-01/NS/NINDS NIH HHS/ -- R01 NS40750-01/NS/NINDS NIH HHS/ -- R21 HD40760-02/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 15;301(5635):972-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109-0934, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920301" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Movement ; Cell Separation ; Cell Survival ; Cells, Cultured ; Digestive System/cytology/*embryology/innervation/metabolism ; Fetus/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Glial Cell Line-Derived Neurotrophic Factor ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Hirschsprung Disease/*etiology/genetics ; Mice ; Multipotent Stem Cells/*physiology ; Nerve Growth Factors/genetics/metabolism/pharmacology ; Neural Crest/*cytology/physiology ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins/*genetics/metabolism ; Proto-Oncogene Proteins c-ret ; Rats ; Rats, Sprague-Dawley ; Receptor Protein-Tyrosine Kinases/*genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; 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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    American Chemical Society meeting. Molecular scaffolding helps raise a crop of neurons (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, Robert F -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):46-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526056" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Differentiation ; Cells, Cultured ; Hydrocarbons ; Mice ; *Nanotechnology ; Neurons/*cytology ; *Peptides/chemistry ; Rats ; Spinal Cord Injuries/therapy ; Stem Cells/*cytology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Embryonic stem cells. Scientists make sperm in a dish (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):1875.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Division ; Cell Separation ; Cells, Cultured ; Embryo, Mammalian/*cytology ; Fertilization ; Genomic Imprinting ; Male ; Mice ; Spermatozoa/*cytology/drug effects/physiology ; Stem Cells/drug effects/*physiology ; Tretinoin/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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    Stem cells. Oocytes spontaneously generated (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2003 May 2;300(5620):721.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730567" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Culture Techniques ; Cell Differentiation ; Cells, Cultured ; Cloning, Organism ; Embryo Research ; Embryo, Mammalian/*cytology ; Estradiol/metabolism ; Ethics, Research ; Humans ; Meiosis ; Mice ; Oocytes/*physiology ; *Oogenesis ; Stem Cells/*physiology
    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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    Toxicity and protection in prions (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LeBlanc, Andrea C -- Roucou, Xavier -- New York, N.Y. -- Science. 2003 Jul 11;301(5630):168-9; author reply 168-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855791" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Death ; Cells, Cultured ; Cytosol/*chemistry/metabolism ; Humans ; Neurons/cytology/*physiology ; PrPC Proteins/chemistry/metabolism/*physiology ; PrPSc Proteins/chemistry/metabolism
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    Pregnancy-stimulated neurogenesis in the adult female forebrain mediated by prolactin (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-04
    Description: Neurogenesis occurs in the olfactory system of the adult brain throughout life, in both invertebrates and vertebrates, but its physiological regulation is not understood. We show that the production of neuronal progenitors is stimulated in the forebrain subventricular zone of female mice during pregnancy and that this effect is mediated by the hormone prolactin. The progenitors then migrate to produce new olfactory interneurons, a process likely to be important for maternal behavior, because olfactory discrimination is critical for recognition and rearing of offspring. Neurogenesis occurs even in females that mate with sterile males. These findings imply that forebrain olfactory neurogenesis may contribute to adaptive behaviors in mating and pregnancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shingo, Tetsuro -- Gregg, Christopher -- Enwere, Emeka -- Fujikawa, Hirokazu -- Hassam, Rozina -- Geary, Colleen -- Cross, James C -- Weiss, Samuel -- New York, N.Y. -- Science. 2003 Jan 3;299(5603):117-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genes & Development Research Group, Department of Cell Biology and Anatomy, University of Calgary Faculty of Medicine, Calgary, Alberta, Canada T2N 4N1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12511652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Movement ; Cells, Cultured ; Choroid Plexus/metabolism ; Dentate Gyrus/cytology ; Epidermal Growth Factor/pharmacology ; Estradiol/administration & dosage/pharmacology ; Female ; Interneurons/cytology/*physiology ; Male ; Mice ; Neurons/cytology/*physiology ; Olfactory Bulb/*cytology ; Pregnancy ; Progesterone/administration & dosage/pharmacology ; Prolactin/administration & dosage/blood/pharmacology/*physiology ; Prosencephalon/*cytology/*physiology ; Pseudopregnancy ; Receptors, Prolactin/genetics/metabolism ; Signal Transduction ; Stem Cells/*cytology
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    Diffusion dynamics of glycine receptors revealed by single-quantum dot tracking (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: Semiconductor quantum dots (QDs) are nanometer-sized fluorescent probes suitable for advanced biological imaging. We used QDs to track individual glycine receptors (GlyRs) and analyze their lateral dynamics in the neuronal membrane of living cells for periods ranging from milliseconds to minutes. We characterized multiple diffusion domains in relation to the synaptic, perisynaptic, or extrasynaptic GlyR localization. The entry of GlyRs into the synapse by diffusion was observed and further confirmed by electron microscopy imaging of QD-tagged receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dahan, Maxime -- Levi, Sabine -- Luccardini, Camilla -- Rostaing, Philippe -- Riveau, Beatrice -- Triller, Antoine -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):442-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire Kastler Brossel, CNRS UMR 8552, Ecole Normale Superieure and Universite Pierre et Marie Curie, 24 rue Lhomond, 75005 Paris, France. maxime.dahan@lkb.ens.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/metabolism/ultrastructure ; Cells, Cultured ; Dendrites/metabolism/ultrastructure ; Diffusion ; Fluorescence ; *Fluorescent Dyes ; Microscopy, Electron ; *Nanotechnology ; Neurites/metabolism/ultrastructure ; Neurons/*metabolism/ultrastructure ; Pyridinium Compounds ; Quaternary Ammonium Compounds ; Rats ; Rats, Sprague-Dawley ; Receptors, Glycine/*metabolism ; Semiconductors ; Spinal Cord/cytology ; Synapses/metabolism/ultrastructure
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    Development. What makes an embryo stick? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fazleabas, Asgerally T -- Kim, J Julie -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):355-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics and Gynecology, University of Illinois, Chicago, IL 60612, USA. asgi@uic.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532005" target="_blank"〉PubMed〈/a〉
    Keywords: Blastocyst/physiology ; Cell Adhesion ; Cell Adhesion Molecules/metabolism ; Cells, Cultured ; Coculture Techniques ; *Embryo Implantation ; Endometrium/cytology/*physiology ; Epithelial Cells/physiology ; Female ; Humans ; L-Selectin/*metabolism ; Ligands ; Oligosaccharides/metabolism ; Pregnancy ; Signal Transduction ; Trophoblasts/*metabolism ; Up-Regulation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Recruitment of HIV and its receptors to dendritic cell-T cell junctions (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-05-06
    Description: Monocyte-derived dendritic cells (MDDCs) can efficiently bind and transfer HIV infectivity without themselves becoming infected. Using live-cell microscopy, we found that HIV was recruited to sites of cell contact in MDDCs. Analysis of conjugates between MDDCs and T cells revealed that, in the absence of antigen-specific signaling, the HIV receptors CD4, CCR5, and CXCR4 on the T cell were recruited to the interface while the MDDCs concentrated HIV to the same region. We propose that contact between dendritic cells and T cells facilitates transmission of HIV by locally concentrating virus, receptor, and coreceptor during the formation of an infectious synapse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, David -- Wu, Li -- Bohks, Stacy M -- KewalRamani, Vineet N -- Unutmaz, Derya -- Hope, Thomas J -- R01 AI052051/AI/NIAID NIH HHS/ -- R01-AI47770/AI/NIAID NIH HHS/ -- R01-AI49131/AI/NIAID NIH HHS/ -- R01-AI52051/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2003 May 23;300(5623):1295-7. Epub 2003 May 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of Illinois, Chicago, IL 60612, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730499" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD4/metabolism ; CD4-Positive T-Lymphocytes/physiology/ultrastructure/*virology ; Cell Adhesion ; Cell Membrane/virology ; Cells, Cultured ; Coculture Techniques ; Dendritic Cells/physiology/ultrastructure/*virology ; Fluorescent Antibody Technique ; Gene Products, vpr/analysis ; Green Fluorescent Proteins ; HIV-1/*physiology ; Humans ; Intercellular Junctions/physiology/*virology ; Lipopolysaccharides/pharmacology ; Luciferases/analysis ; Luminescent Proteins/analysis ; Models, Biological ; Monocytes ; Receptors, CCR5/metabolism ; Receptors, CXCR4/metabolism ; Receptors, HIV/*metabolism ; Virion/physiology ; vpr Gene Products, Human Immunodeficiency Virus
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    RNA interference. New screen nets 'Hedgehog' genes (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2003 Mar 28;299(5615):1961.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12663885" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Casein Kinases ; Cells, Cultured ; Computational Biology ; Drosophila/embryology/*genetics/metabolism ; Drosophila Proteins/*genetics/metabolism ; Embryo, Nonmammalian/metabolism ; *Genes, Insect ; Genomics ; Hedgehog Proteins ; Protein Kinases ; *RNA Interference ; RNA, Double-Stranded/genetics ; *Signal Transduction
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    Stem cell research. Same results, different interpretations (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):324.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12531985" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Cell Differentiation ; Cells, Cultured ; Diabetes Mellitus, Experimental/therapy ; Embryo, Mammalian/*cytology ; Insulin/biosynthesis/genetics/immunology/*metabolism ; Islets of Langerhans/cytology/*metabolism ; Mice ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Stem Cells/*cytology/metabolism
    Print ISSN: 0036-8075
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    Role of histone H3 lysine 27 methylation in X inactivation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-22
    Description: The Polycomb group (PcG) protein Eed is implicated in regulation of imprinted X-chromosome inactivation in extraembryonic cells but not of random X inactivation in embryonic cells. The Drosophila homolog of the Eed-Ezh2 PcG protein complex achieves gene silencing through methylation of histone H3 on lysine 27 (H3-K27), which suggests a role for H3-K27 methylation in imprinted X inactivation. Here we demonstrate that transient recruitment of the Eed-Ezh2 complex to the inactive X chromosome (Xi) occurs during initiation of X inactivation in both extraembryonic and embryonic cells and is accompanied by H3-K27 methylation. Recruitment of the complex and methylation on the Xi depend on Xist RNA but are independent of its silencing function. Together, our results suggest a role for Eed-Ezh2-mediated H3-K27 methylation during initiation of both imprinted and random X inactivation and demonstrate that H3-K27 methylation is not sufficient for silencing of the Xi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plath, Kathrin -- Fang, Jia -- Mlynarczyk-Evans, Susanna K -- Cao, Ru -- Worringer, Kathleen A -- Wang, Hengbin -- de la Cruz, Cecile C -- Otte, Arie P -- Panning, Barbara -- Zhang, Yi -- New York, N.Y. -- Science. 2003 Apr 4;300(5616):131-5. Epub 2003 Mar 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12649488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/metabolism/*physiology ; Cell Differentiation ; Cell Nucleus/metabolism ; Cells, Cultured ; *Dosage Compensation, Genetic ; Female ; Fluorescent Antibody Technique ; Genomic Imprinting ; HeLa Cells ; Histones/*metabolism ; Humans ; In Situ Hybridization, Fluorescence ; Lysine/metabolism ; Male ; Methylation ; Mice ; Mutation ; Polycomb Repressive Complex 2 ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/metabolism ; Stem Cells/metabolism/*physiology ; Transgenes ; Trophoblasts/*physiology ; X Chromosome/*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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  • 82
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    Neuroscience. SPARring with spines (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, Guido -- Brose, Nils -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1341-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Neuroscience, Max Planck Institute for Experimental Medicine, D-37075 Gottingen, Germany. gmeyer@em.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631024" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Cell Cycle ; Cells, Cultured ; Cysteine Endopeptidases/metabolism ; Dendrites/*physiology/ultrastructure ; Down-Regulation ; GTPase-Activating Proteins/chemistry/*metabolism ; Hippocampus/cytology/metabolism ; Multienzyme Complexes/metabolism ; Nerve Tissue Proteins/metabolism ; Neuronal Plasticity/*physiology ; Phosphorylation ; Proteasome Endopeptidase Complex ; Protein Kinases/*metabolism ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases ; Recombinant Proteins/metabolism ; Signal Transduction ; Synapses/*physiology ; Two-Hybrid System Techniques ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/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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  • 83
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    Molecular biology. MeCP2 repression goes nonglobal (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klose, Robert -- Bird, Adrian -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):793-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Centre for Cell Biology, University of Edinburgh, The King's Buildings, Edinburgh EH9 3JR, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593157" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors ; Brain-Derived Neurotrophic Factor/*genetics/physiology ; Cells, Cultured ; Chromatin/metabolism ; *Chromosomal Proteins, Non-Histone ; CpG Islands/*physiology ; *DNA Methylation ; DNA-Binding Proteins/genetics/*metabolism ; *Gene Expression Regulation ; Gene Silencing ; Histones/metabolism ; Humans ; Methyl-CpG-Binding Protein 2 ; Mice ; Mutation ; Nervous System/embryology ; Neurons/metabolism ; Phosphorylation ; Potassium Chloride/pharmacology ; Promoter Regions, Genetic ; Rats ; *Repressor Proteins ; Rett Syndrome/genetics ; Transcription, Genetic ; Xenopus Proteins/genetics/metabolism ; Xenopus laevis
    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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  • 84
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    Modulation of heterochromatin protein 1 dynamics in primary Mammalian cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-01
    Description: Heterochromatin protein 1 (HP1beta), a key component of condensed DNA, is strongly implicated in gene silencing and centromeric cohesion. Heterochromatin has been considered a static structure, stabilizing crucial aspects of nuclear organization and prohibiting access to transcription factors. We demonstrate here, by fluorescence recovery after photobleaching, that a green fluorescent protein-HP1beta fusion protein is highly mobile within both the euchromatin and heterochromatin of ex vivo resting murine T cells. Moreover, T cell activation greatly increased this mobility, indicating that such a process may facilitate (hetero)chromatin remodeling and permit access of epigenetic modifiers and transcription factors to the many genes that are consequently derepressed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Festenstein, Richard -- Pagakis, Stamatis N -- Hiragami, Kyoko -- Lyon, Debbie -- Verreault, Alain -- Sekkali, Belaid -- Kioussis, Dimitris -- New York, N.Y. -- Science. 2003 Jan 31;299(5607):719-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CSC Gene Control Mechanisms and Disease Group, Division of Medicine, Imperial College School of Medicine, Hammersmith Campus, Du Cane Road, London W12 ONN, UK. r.festenstein@ic.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12560554" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cells, Cultured ; Chromosomal Proteins, Non-Histone/*metabolism ; Dimerization ; Euchromatin/*metabolism ; Fluorescence ; Fluorescence Recovery After Photobleaching ; Heterochromatin/*metabolism ; Histones/metabolism ; Kinetics ; Lymphocyte Activation ; Methylation ; Mice ; Microscopy, Confocal ; T-Lymphocytes/*metabolism
    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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  • 85
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    Activation of lysosomal function during dendritic cell maturation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: In response to a variety of stimuli, dendritic cells (DCs) transform from immature cells specialized for antigen capture into mature cells specialized for T cell stimulation. During maturation, the DCs acquire an enhanced capacity to form and accumulate peptide-MHC (major histocompatibility complex) class II complexes. Here we show that a key mechanism responsible for this alteration was the generalized activation of lysosomal function. In immature DCs, internalized antigens were slowly degraded and inefficiently used for peptide loading. Maturation induced activation of the vacuolar proton pump that enhanced lysosomal acidification and antigen proteolysis, facilitating efficient formation of peptide-MHC class II complexes. Lysosomal function in DCs thus appears to be specialized for the developmentally regulated processing of internalized antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trombetta, E Sergio -- Ebersold, Melanie -- Garrett, Wendy -- Pypaert, Marc -- Mellman, Ira -- R37-AI34098/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1400-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Department of Immunobiology, Ludwig Institute for Cancer Research, Yale University School of Medicine, 333 Cedar Street, Post Office Box 208002, New Haven, CT 06520-8002, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Cathepsins/metabolism ; Cells, Cultured ; Cysteine Endopeptidases/metabolism ; Dendritic Cells/*immunology/*metabolism ; Enzyme Activation ; Fluorescein-5-isothiocyanate/*analogs & derivatives/metabolism ; Histocompatibility Antigens Class II/immunology/metabolism ; Horseradish Peroxidase/immunology/metabolism ; Hydrogen-Ion Concentration ; Lipopolysaccharides/immunology ; Lysosomes/enzymology/*metabolism ; Mice ; Muramidase/immunology/metabolism ; Ovalbumin/metabolism ; Protein Subunits ; Serum Albumin, Bovine/immunology/metabolism ; Tetanus Toxoid/metabolism ; Vacuolar Proton-Translocating ATPases/metabolism
    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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  • 86
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    DNA methylation-related chromatin remodeling in activity-dependent BDNF gene regulation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-01
    Description: In conjunction with histone modifications, DNA methylation plays critical roles in gene silencing through chromatin remodeling. Changes in DNA methylation perturb neuronal function, and mutations in a methyl-CpG-binding protein, MeCP2, are associated with Rett syndrome. We report that increased synthesis of brain-derived neurotrophic factor (BDNF) in neurons after depolarization correlates with a decrease in CpG methylation within the regulatory region of the Bdnf gene. Moreover, increased Bdnf transcription involves dissociation of the MeCP2-histone deacetylase-mSin3A repression complex from its promoter. Our findings suggest that DNA methylation-related chromatin remodeling is important for activity-dependent gene regulation that may be critical for neural plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinowich, Keri -- Hattori, Daisuke -- Wu, Hao -- Fouse, Shaun -- He, Fei -- Hu, Yan -- Fan, Guoping -- Sun, Yi E -- NS44405/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):890-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Interdepartmental Program, UCLA School of Medicine, 760 Westwood Plaza, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593184" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/biosynthesis/*genetics ; Cells, Cultured ; Chromatin/*metabolism ; *Chromosomal Proteins, Non-Histone ; CpG Islands/*physiology ; Cyclic AMP Response Element-Binding Protein/metabolism ; *DNA Methylation ; DNA-Binding Proteins/metabolism ; *Gene Expression Regulation ; Gene Silencing ; Histone Deacetylases/metabolism ; Methyl-CpG-Binding Protein 2 ; Mice ; Mice, Inbred BALB C ; Models, Genetic ; Neuronal Plasticity ; Neurons/*metabolism/physiology ; Potassium Chloride/pharmacology ; Promoter Regions, Genetic ; Repressor Proteins/metabolism ; Response Elements ; Transcription Factors/metabolism ; Transcription, Genetic ; 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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  • 87
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    Trophoblast L-selectin-mediated adhesion at the maternal-fetal interface (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: Trophoblast adhesion to the uterine wall is the requisite first step of implantation and, subsequently, placentation. At the maternal-fetal interface, we investigated the expression of selectin adhesion systems that enable leukocyte capture from the bloodstream. On the maternal side, human uterine epithelial cells up-regulated selectin oligosaccharide-based ligands during the window of receptivity. On the fetal side, human trophoblasts expressed L-selectin. This ligand-receptor system was functional, because beads coated with the selectin ligand 6-sulfo sLe(x) bound to trophoblasts, and trophoblasts bound to ligand-expressing uterine luminal epithelium in tissue sections. These results suggest that trophoblast L-selectin mediates interactions with the uterus and that this adhesion mechanism may be critical to establishing human pregnancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Genbacev, Olga D -- Prakobphol, Akraporn -- Foulk, Russell A -- Krtolica, Ana R -- Ilic, Dusko -- Singer, Mark S -- Yang, Zhi-Qiang -- Kiessling, Laura L -- Rosen, Steven D -- Fisher, Susan J -- DE 07244/DE/NIDCR NIH HHS/ -- HL 64597/HL/NHLBI NIH HHS/ -- R37GM23547/GM/NIGMS NIH HHS/ -- U01 HD 42283/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):405-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Stomatology, Anatomy, and Pharmaceutical Chemistry, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532021" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Blastocyst/physiology ; Cell Adhesion ; Cells, Cultured ; *Embryo Implantation ; Endometrium/cytology/metabolism/*physiology ; Epithelial Cells/metabolism ; Female ; Follicular Phase ; Humans ; Immunoblotting ; Jurkat Cells ; L-Selectin/immunology/*metabolism ; Ligands ; Luteal Phase ; Mice ; Microspheres ; Oligosaccharides/*metabolism ; Organ Culture Techniques ; Pregnancy ; Trophoblasts/metabolism/*physiology ; Up-Regulation
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 88
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    Angiogenesis-independent endothelial protection of liver: role of VEGFR-1 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-08
    Description: The vascular endothelium was once thought to function primarily in nutrient and oxygen delivery, but recent evidence suggests that it may play a broader role in tissue homeostasis. To explore the role of sinusoidal endothelial cells (LSECs) in the adult liver, we studied the effects of vascular endothelial growth factor (VEGF) receptor activation on mouse hepatocyte growth. Delivery of VEGF-A increased liver mass in mice but did not stimulate growth of hepatocytes in vitro, unless LSECs were also present in the culture. Hepatocyte growth factor (HGF) was identified as one of the LSEC-derived paracrine mediators promoting hepatocyte growth. Selective activation of VEGF receptor-1 (VEGFR-1) stimulated hepatocyte but not endothelial proliferation in vivo and reduced liver damage in mice exposed to a hepatotoxin. Thus, VEGFR-1 agonists may have therapeutic potential for preservation of organ function in certain liver disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LeCouter, Jennifer -- Moritz, Dirk R -- Li, Bing -- Phillips, Gail Lewis -- Liang, Xiao Huan -- Gerber, Hans-Peter -- Hillan, Kenneth J -- Ferrara, Napoleone -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):890-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Molecular Oncology, Protein Engineering, and Pathology, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574630" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; Carbon Tetrachloride/toxicity ; Cell Division ; Cells, Cultured ; Coculture Techniques ; Cricetinae ; DNA Replication ; Drug-Induced Liver Injury ; Endothelial Growth Factors/genetics/*metabolism/pharmacology ; Endothelium, Vascular/*cytology/physiology ; Gene Expression Regulation ; Growth Substances/genetics/metabolism ; Hepatocyte Growth Factor/genetics/metabolism/pharmacology ; Hepatocytes/cytology/pathology/*physiology ; Humans ; Intercellular Signaling Peptides and Proteins/genetics/*metabolism/pharmacology ; Liver/blood supply/*cytology/pathology/*physiology ; Liver Diseases/metabolism/pathology/prevention & control ; Liver Regeneration ; Lymphokines/genetics/*metabolism/pharmacology ; Mice ; Mice, Nude ; Mitosis ; Mutation ; Necrosis ; Neovascularization, Physiologic ; Paracrine Communication ; RNA, Messenger/genetics/metabolism ; Signal Transduction ; Up-Regulation ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor Receptor-1/*metabolism ; Vascular Endothelial Growth Factor Receptor-2/metabolism ; Vascular Endothelial Growth Factors
    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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  • 89
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    Development. Smelling the roses? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Babcock, Donner F -- New York, N.Y. -- Science. 2003 Mar 28;299(5615):1993-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Washington, Seattle, WA 98195, USA. donner@u.washington.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12663902" target="_blank"〉PubMed〈/a〉
    Keywords: Aldehydes/chemistry/metabolism/pharmacology ; Animals ; Calcium/metabolism ; Calcium Signaling ; Cells, Cultured ; Chemotactic Factors/chemistry/metabolism/*pharmacology ; *Chemotaxis ; Female ; Fertilization ; Humans ; Invertebrates/physiology ; Male ; Metabolism ; Odors ; Receptors, Odorant/genetics/*physiology ; Recombinant Fusion Proteins/metabolism ; Seminal Plasma Proteins/genetics/*physiology ; *Sperm Motility ; Sperm Tail/physiology ; Spermatozoa/metabolism/*physiology ; Testis/*metabolism
    Print ISSN: 0036-8075
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  • 90
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    Targeted protein degradation and synapse remodeling by an inducible protein kinase (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-25
    Description: Synaptic plasticity involves the reorganization of synapses at the protein and the morphological levels. Here, we report activity-dependent remodeling of synapses by serum-inducible kinase (SNK). SNK was induced in hippocampal neurons by synaptic activity and was targeted to dendritic spines. SNK bound to and phosphorylated spine-associated Rap guanosine triphosphatase activating protein (SPAR), a postsynaptic actin regulatory protein, leading to degradation of SPAR. Induction of SNK in hippocampal neurons eliminated SPAR protein, depleted postsynaptic density-95 and Bassoon clusters, and caused loss of mature dendritic spines. These results implicate SNK as a mediator of activity-dependent change in the molecular composition and morphology of synapses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pak, Daniel T S -- Sheng, Morgan -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1368-73. Epub 2003 Oct 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Picower Center for Learning and Memory, RIKEN Massachusetts Institute of Technology (MIT) Neuroscience Research Center, Howard Hughes Medical Institute, MIT, Cambridge, MA 02139, USA. dtp6@georgetown.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576440" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; COS Cells ; Cells, Cultured ; Cysteine Endopeptidases/metabolism ; Dendrites/chemistry/*physiology/ultrastructure ; Enzyme Induction ; Fluorescent Antibody Technique ; GTPase-Activating Proteins/analysis/*metabolism ; Hippocampus/cytology ; Immunohistochemistry ; Multienzyme Complexes/metabolism ; Nerve Tissue Proteins/metabolism ; *Neuronal Plasticity ; Phosphorylation ; Proteasome Endopeptidase Complex ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases ; Pseudopodia/ultrastructure ; Rats ; Recombinant Fusion Proteins/metabolism ; Synapses/*physiology/ultrastructure ; Transfection ; Two-Hybrid System Techniques ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/metabolism
    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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  • 91
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    Society for Neuroscience meeting. Neurons get connected via glia (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1323.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631017" target="_blank"〉PubMed〈/a〉
    Keywords: Astrocytes/metabolism/*physiology ; Brain/growth & development/metabolism ; Cells, Cultured ; Culture Media ; Neurons/*physiology ; Synapses/*physiology ; Thrombospondins/metabolism/*physiology
    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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  • 92
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    Immune control of tuberculosis by IFN-gamma-inducible LRG-47 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-25
    Description: Interferon-gamma (IFN-gamma) provides an essential component of immunity to tuberculosis by activating infected host macrophages to directly inhibit the replication of Mycobacterium tuberculosis (Mtb). IFN-gamma-inducible nitric oxide synthase 2 (NOS2) is considered a principal effector mechanism, although other pathways may also exist. Here, we identify one member of a newly emerging 47-kilodalton (p47) guanosine triphosphatase family, LRG-47, that acts independently of NOS2 to protect against disease. Mice lacking LRG-47 failed to control Mtb replication, unlike those missing the related p47 guanosine triphosphatases IRG-47 or IGTP. Defective bacterial killing in IFN-gamma-activated LRG-47-/- macrophages was associated with impaired maturation of Mtb-containing phagosomes, vesicles that otherwise recruited LRG-47 in wild-type cells. Thus, LRG-47 may serve as a critical vacuolar trafficking component used to dispose of intracellular pathogens like Mtb.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacMicking, John D -- Taylor, Gregory A -- McKinney, John D -- R01 A1051702/PHS HHS/ -- New York, N.Y. -- Science. 2003 Oct 24;302(5645):654-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Infection Biology, Rockefeller University, 1230 York Avenue, New York, NY 10021, USA. macmicj@mail.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Computational Biology ; Disease Susceptibility ; Female ; GTP Phosphohydrolases/genetics/physiology ; GTP-Binding Proteins/genetics/*physiology ; Hydrogen-Ion Concentration ; Immunity, Innate ; Interferon-gamma/*immunology ; Macrophage Activation ; Macrophages/immunology/metabolism ; Macrophages, Alveolar/immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Mycobacterium tuberculosis/*growth & development ; Nitric Oxide Synthase/genetics/metabolism ; Nitric Oxide Synthase Type II ; Oligonucleotide Array Sequence Analysis ; Phagosomes/microbiology/physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Tuberculosis/*immunology/microbiology
    Print ISSN: 0036-8075
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    Generation of fertile cloned rats by regulating oocyte activation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Qi -- Renard, Jean-Paul -- Le Friec, Gaelle -- Brochard, Vincent -- Beaujean, Nathalie -- Cherifi, Yacine -- Fraichard, Alexandre -- Cozzi, Jean -- New York, N.Y. -- Science. 2003 Nov 14;302(5648):1179. Epub 2003 Sep 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Biology and Reproduction Unit, INRA, Jouy en Josas, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512506" target="_blank"〉PubMed〈/a〉
    Keywords: 4-Butyrolactone/*analogs & derivatives/pharmacology ; Animals ; Cells, Cultured ; *Cloning, Organism ; Embryo Transfer ; Enzyme Inhibitors/pharmacology ; Female ; Fertility ; Leupeptins/pharmacology ; Male ; Meiosis ; Microsatellite Repeats ; Mitosis ; Nuclear Transfer Techniques ; Oocytes/*physiology ; Rats ; Rats, Sprague-Dawley/*genetics/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 94
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    Control of synaptic strength by glial TNFalpha (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-03-23
    Description: Activity-dependent modulation of synaptic efficacy in the brain contributes to neural circuit development and experience-dependent plasticity. Although glia are affected by activity and ensheathe synapses, their influence on synaptic strength has largely been ignored. Here, we show that a protein produced by glia, tumor necrosis factor alpha (TNFalpha), enhances synaptic efficacy by increasing surface expression of AMPA receptors. Preventing the actions of endogenous TNFalpha has the opposite effects. Thus, the continual presence of TNFalpha is required for preservation of synaptic strength at excitatory synapses. Through its effects on AMPA receptor trafficking, TNFalpha may play roles in synaptic plasticity and modulating responses to neural injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beattie, Eric C -- Stellwagen, David -- Morishita, Wade -- Bresnahan, Jacqueline C -- Ha, Byeong Keun -- Von Zastrow, Mark -- Beattie, Michael S -- Malenka, Robert C -- DA00439/DA/NIDA NIH HHS/ -- MH063394/MH/NIMH NIH HHS/ -- NS 31193/NS/NINDS NIH HHS/ -- NS38079/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2002 Mar 22;295(5563):2282-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94304, USA. beattie.2@osu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11910117" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/pharmacology ; Astrocytes/*metabolism ; Cells, Cultured ; Culture Media, Conditioned/pharmacology ; Gene Expression Regulation/drug effects ; Hippocampus/cytology/metabolism ; Neuronal Plasticity/drug effects ; Neurons/drug effects/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/metabolism ; Receptors, Tumor Necrosis Factor ; Receptors, Tumor Necrosis Factor, Type I ; Synapses/drug effects/*metabolism ; Synaptic Transmission/drug effects ; Tumor Necrosis Factor-alpha/antagonists & inhibitors/*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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  • 95
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    Genomic instability in mice lacking histone H2AX (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-06
    Description: Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage. Double-strand breaks (DSBs) induce histone H2AX phosphorylation, which is associated with the recruitment of repair factors to damaged DNA. To help clarify the physiological role of H2AX, we targeted H2AX in mice. Although H2AX is not essential for irradiation-induced cell-cycle checkpoints, H2AX-/- mice were radiation sensitive, growth retarded, and immune deficient, and mutant males were infertile. These pleiotropic phenotypes were associated with chromosomal instability, repair defects, and impaired recruitment of Nbs1, 53bp1, and Brca1, but not Rad51, to irradiation-induced foci. Thus, H2AX is critical for facilitating the assembly of specific DNA-repair complexes on damaged DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721576/" 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/PMC4721576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Celeste, Arkady -- Petersen, Simone -- Romanienko, Peter J -- Fernandez-Capetillo, Oscar -- Chen, Hua Tang -- Sedelnikova, Olga A -- Reina-San-Martin, Bernardo -- Coppola, Vincenzo -- Meffre, Eric -- Difilippantonio, Michael J -- Redon, Christophe -- Pilch, Duane R -- Olaru, Alexandru -- Eckhaus, Michael -- Camerini-Otero, R Daniel -- Tessarollo, Lino -- Livak, Ferenc -- Manova, Katia -- Bonner, William M -- Nussenzweig, Michel C -- Nussenzweig, Andre -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2002 May 3;296(5569):922-7. Epub 2002 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11934988" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology/physiology ; Base Sequence ; Cell Aging ; Cell Cycle ; Cells, Cultured ; *Chromosome Aberrations ; DNA Damage ; *DNA Repair ; Female ; Gene Targeting ; Histones/chemistry/*genetics/*physiology ; Immunoglobulin Class Switching ; Infertility, Male/genetics/physiopathology ; Lymphocyte Count ; Male ; Meiosis ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; Phosphorylation ; *Recombination, Genetic ; Spermatocytes/physiology ; T-Lymphocytes/immunology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    Signal transduction. History matters (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-08-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ingolia, Nicholas T -- Murray, Andrew W -- New York, N.Y. -- Science. 2002 Aug 9;297(5583):948-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology and Bauer Center for Genomics Research, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12169717" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Biological Evolution ; *Cell Cycle Proteins ; Cells, Cultured ; Dual Specificity Phosphatase 1 ; *Feedback, Physiological ; Immediate-Early Proteins/*metabolism ; *MAP Kinase Signaling System ; Mitogen-Activated Protein Kinases/*metabolism ; Models, Biological ; *Phosphoprotein Phosphatases ; Platelet-Derived Growth Factor/metabolism/pharmacology ; Protein Phosphatase 1 ; Protein Tyrosine Phosphatases/*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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  • 97
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    Historical essay. The early years of HIV/AIDS (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-12-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallo, Robert C -- New York, N.Y. -- Science. 2002 Nov 29;298(5599):1728-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Human Virology and Department of Microbiology and Immunology, University of Maryland, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12459576" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Serodiagnosis/history ; Acquired Immunodeficiency Syndrome/diagnosis/*history/immunology/virology ; CD4-Positive T-Lymphocytes/virology ; Cell Line ; Cells, Cultured ; France ; *HIV/classification/isolation & purification/physiology ; History, 20th Century ; Human T-lymphotropic virus 1/isolation & purification/physiology ; Human T-lymphotropic virus 2/isolation & purification/physiology ; Humans ; Interleukin-2/history/isolation & purification/physiology ; Patents as Topic/history ; RNA-Directed DNA Polymerase/history/isolation & purification/metabolism ; United States ; Virus Cultivation
    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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  • 98
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    Discrete microdomains with high concentration of cAMP in stimulated rat neonatal cardiac myocytes (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-03-02
    Description: The second messenger cyclic adenosine monophosphate (cAMP) is the most important modulator of sympathetic control over cardiac contractility. In cardiac myocytes and many other cell types, however, cAMP transduces the signal generated upon stimulation of various receptors and activates different cellular functions, raising the issue of how specificity can be achieved. In the general field of signal transduction, the view is emerging that specificity is guaranteed by tight localization of signaling events. Here, we show that in neonatal rat cardiac myocytes, beta-adrenergic stimulation generates multiple microdomains with increased concentration of cAMP in correspondence with the region of the transverse tubule/junctional sarcoplasmic reticulum membrane. The restricted pools of cAMP show a range of action as small as approximately 1 micrometer, and free diffusion of the second messenger is limited by the activity of phosphodiesterases. Furthermore, we demonstrate that such gradients of cAMP specifically activate a subset of protein kinase A molecules anchored in proximity to the T tubule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zaccolo, Manuela -- Pozzan, Tullio -- TCP00089/Telethon/Italy -- New York, N.Y. -- Science. 2002 Mar 1;295(5560):1711-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Sciences and Venetian Institute for Molecular Medicine, University of Padua, Via Orus 2, 35129 Padua, Italy. manuela.zaccolo@unipd.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11872839" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; A Kinase Anchor Proteins ; Adaptor Proteins, Signal Transducing ; Animals ; Animals, Newborn ; Cells, Cultured ; Colforsin/pharmacology ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Fluorescence ; Green Fluorescent Proteins ; Intracellular Membranes/metabolism ; Kinetics ; Luminescent Proteins ; Myocardium/*cytology/*metabolism/ultrastructure ; Norepinephrine/pharmacology ; Phosphodiesterase Inhibitors/pharmacology ; Proto-Oncogene Proteins/pharmacology ; Rats ; Receptors, Adrenergic, beta/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sarcoplasmic Reticulum/*metabolism ; Second Messenger Systems ; Transfection
    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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  • 99
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    Contribution of human alpha-defensin 1, 2, and 3 to the anti-HIV-1 activity of CD8 antiviral factor (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-28
    Description: It has been known since 1986 that CD8 T lymphocytes from certain HIV-1-infected individuals who are immunologically stable secrete a soluble factor, termed CAF, that suppresses HIV-1 replication. However, the identity of CAF remained elusive despite an extensive search. By means of a protein-chip technology, we identified a cluster of proteins that were secreted when CD8 T cells from long-term nonprogressors with HIV-1 infection were stimulated. These proteins were identified as alpha-defensin 1, 2, and 3 on the basis of specific antibody recognition and amino acid sequencing. CAF activity was eliminated or neutralized by an antibody specific for human alpha-defensins. Synthetic and purified preparations of alpha-defensins also inhibited the replication of HIV-1 isolates in vitro. Taken together, our results indicate that alpha-defensin 1, 2, and 3 collectively account for much of the anti-HIV-1 activity of CAF that is not attributable to beta-chemokines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Linqi -- Yu, Wenjie -- He, Tian -- Yu, Jian -- Caffrey, Rebecca E -- Dalmasso, Enrique A -- Fu, Siyu -- Pham, Thang -- Mei, Jianfeng -- Ho, Jaclyn J -- Zhang, Wenyong -- Lopez, Peter -- Ho, David D -- AI-42848/AI/NIAID NIH HHS/ -- M01-RR00102/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2002 Nov 1;298(5595):995-1000. Epub 2002 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aaron Diamond AIDS Research Center, The Rockefeller University, 455 First Avenue, New York, NY 10016, USA. lzhang@adarc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12351674" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antibodies, Monoclonal ; Antiviral Agents/chemistry/isolation & purification/*pharmacology ; CD8-Positive T-Lymphocytes/chemistry/*immunology ; Cells, Cultured ; Chemokines, CC/immunology/physiology ; HIV Infections/*immunology/virology ; HIV Long-Term Survivors ; HIV-1/drug effects/*physiology ; Humans ; Mass Spectrometry ; Molecular Sequence Data ; Neutrophils/chemistry/immunology ; Protein Array Analysis ; Virus Replication ; alpha-Defensins/chemistry/isolation & purification/pharmacology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    A heat-sensitive TRP channel expressed in keratinocytes (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-23
    Description: Mechanical and thermal cues stimulate a specialized group of sensory neurons that terminate in the skin. Three members of the transient receptor potential (TRP) family of channels are expressed in subsets of these neurons and are activated at distinct physiological temperatures. Here, we describe the cloning and characterization of a novel thermosensitive TRP channel. TRPV3 has a unique threshold: It is activated at innocuous (warm) temperatures and shows an increased response at noxious temperatures. TRPV3 is specifically expressed in keratinocytes; hence, skin cells are capable of detecting heat via molecules similar to those in heat-sensing neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peier, Andrea M -- Reeve, Alison J -- Andersson, David A -- Moqrich, Aziz -- Earley, Taryn J -- Hergarden, Anne C -- Story, Gina M -- Colley, Sian -- Hogenesch, John B -- McIntyre, Peter -- Bevan, Stuart -- Patapoutian, Ardem -- New York, N.Y. -- Science. 2002 Jun 14;296(5575):2046-9. Epub 2002 May 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomics Institute of the Novartis Research Foundation, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12016205" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Newborn ; Blotting, Northern ; CHO Cells ; Capsaicin/*analogs & derivatives/pharmacology ; *Cation Transport Proteins ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; Cricetinae ; Epidermis/cytology/innervation/metabolism ; Ganglia, Spinal/metabolism ; *Hot Temperature ; Humans ; In Situ Hybridization ; Ion Channels/chemistry/genetics/*metabolism ; Keratinocytes/*metabolism ; Membrane Potentials ; Mice ; Molecular Sequence Data ; Nerve Endings/physiology ; Neurons/physiology ; Patch-Clamp Techniques ; RNA, Messenger/genetics/metabolism ; Ruthenium Red/pharmacology ; Signal Transduction ; Spinal Cord/metabolism ; TRPV Cation Channels ; Temperature
    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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