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  • Signal Transduction  (28)
  • American Association for the Advancement of Science (AAAS)  (28)
  • American Chemical Society
  • Cambridge University Press
  • 2000-2004  (28)
  • 2003  (28)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (28)
  • American Chemical Society
  • Cambridge University Press
Years
  • 2000-2004  (28)
Year
  • 1
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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
    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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    Hematopoietic cell regulation by Rac1 and Rac2 guanosine triphosphatases (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: The Rho guanosine triphosphatases (GTPases) Rac1 and Rac2 are critical signaling regulators in mammalian cells. The deletion of both Rac1 and Rac2 murine alleles leads to a massive egress of hematopoietic stem/progenitor cells (HSC/Ps) into the blood from the marrow, whereas Rac1-/- but not Rac2-/- HSC/Ps fail to engraft in the bone marrow of irradiated recipient mice. In contrast, Rac2, but not Rac1, regulates superoxide production and directed migration in neutrophils, and in each cell type, the two GTPases play distinct roles in actin organization, cell survival, and proliferation. Thus, Rac1 and Rac2 regulate unique aspects of hematopoietic development and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, Yi -- Filippi, Marie-Dominique -- Cancelas, Jose A -- Siefring, Jamie E -- Williams, Emily P -- Jasti, Aparna C -- Harris, Chad E -- Lee, Andrew W -- Prabhakar, Rethinasamy -- Atkinson, Simon J -- Kwiatkowski, David J -- Williams, David A -- DK62757/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):445-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Experimental Hematology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564009" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Apoptosis ; Bone Marrow Transplantation ; Cell Adhesion ; Cell Cycle ; Cell Movement ; Cell Size ; Colony-Forming Units Assay ; Cyclin D1/metabolism ; Fibronectins/metabolism ; Hematopoiesis ; Hematopoietic Stem Cell Mobilization ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*physiology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mitogen-Activated Protein Kinases/metabolism ; Neutrophils/*physiology ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Recombination, Genetic ; Signal Transduction ; Stem Cell Factor/pharmacology ; Superoxides/metabolism ; rac GTP-Binding Proteins/genetics/*metabolism ; rac1 GTP-Binding Protein/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    PDGFRA activating mutations in gastrointestinal stromal tumors (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-11
    Description: Most gastrointestinal stromal tumors (GISTs) have activating mutations in the KIT receptor tyrosine kinase, and most patients with GISTs respond well to Gleevec, which inhibits KIT kinase activity. Here we show that approximately 35% (14 of 40) of GISTs lacking KIT mutations have intragenic activation mutations in the related receptor tyrosine kinase, platelet-derived growth factor receptor alpha (PDGFRA). Tumors expressing KIT or PDGFRA oncoproteins were indistinguishable with respect to activation of downstream signaling intermediates and cytogenetic changes associated with tumor progression. Thus, KIT and PDGFRA mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heinrich, Michael C -- Corless, Christopher L -- Duensing, Anette -- McGreevey, Laura -- Chen, Chang-Jie -- Joseph, Nora -- Singer, Samuel -- Griffith, Diana J -- Haley, Andrea -- Town, Ajia -- Demetri, George D -- Fletcher, Christopher D M -- Fletcher, Jonathan A -- New York, N.Y. -- Science. 2003 Jan 31;299(5607):708-10. Epub 2003 Jan 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Department of Pathology, Oregon Health & Science University Cancer Institute and Portland VA Medical Center, Portland, OR 97201, USA. heinrich@ohsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12522257" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; Chromosome Aberrations ; Cricetinae ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; Exons ; Gastrointestinal Neoplasms/*genetics/metabolism ; Humans ; Karyotyping ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Oncogenes ; Phosphorylation ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-kit/*genetics/metabolism ; Receptor, Platelet-Derived Growth Factor alpha/*genetics/metabolism ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; Signal Transduction ; Trans-Activators/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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    Melanopsin is required for non-image-forming photic responses in blind mice (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-28
    Description: Although mice lacking rod and cone photoreceptors are blind, they retain many eye-mediated responses to light, possibly through photosensitive retinal ganglion cells. These cells express melanopsin, a photopigment that confers this photosensitivity. Mice lacking melanopsin still retain nonvisual photoreception, suggesting that rods and cones could operate in this capacity. We observed that mice with both outer-retinal degeneration and a deficiency in melanopsin exhibited complete loss of photoentrainment of the circadian oscillator, pupillary light responses, photic suppression of arylalkylamine-N-acetyltransferase transcript, and acute suppression of locomotor activity by light. This indicates the importance of both nonvisual and classical visual photoreceptor systems for nonvisual photic responses in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Panda, Satchidananda -- Provencio, Ignacio -- Tu, Daniel C -- Pires, Susana S -- Rollag, Mark D -- Castrucci, Ana Maria -- Pletcher, Mathew T -- Sato, Trey K -- Wiltshire, Tim -- Andahazy, Mary -- Kay, Steve A -- Van Gelder, Russell N -- Hogenesch, John B -- K08-EY00403/EY/NEI NIH HHS/ -- MH 62405/MH/NIMH NIH HHS/ -- MH51573/MH/NIMH NIH HHS/ -- R01-EY14988/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):525-7. Epub 2003 Jun 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomics Institute of the Novartis Research Foundation, 10675 John J. Hopkins Drive, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12829787" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arylamine N-Acetyltransferase/genetics/metabolism ; Blindness/genetics/*physiopathology ; Circadian Rhythm ; *Light ; *Light Signal Transduction ; Mice ; Mice, Inbred C3H ; Motor Activity ; Photoreceptor Cells, Vertebrate/*physiology ; Reflex, Pupillary ; Retinal Degeneration/genetics/physiopathology ; Retinal Ganglion Cells/physiology ; Rod Opsins/deficiency/genetics/*physiology ; Signal Transduction ; Suprachiasmatic Nucleus/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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  • 5
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    Cell corpse engulfment mediated by C. elegans phosphatidylserine receptor through CED-5 and CED-12 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-04
    Description: During apoptosis, phosphatidylserine, which is normally restricted to the inner leaflet of the plasma membrane, is exposed on the surface of apoptotic cells and has been suggested to act as an "eat-me" signal to trigger phagocytosis. It is unclear how phagocytes recognize phosphatidylserine. Recently, a putative phosphatidylserine receptor (PSR) was identified and proposed to mediate recognition of phosphatidylserine and phagocytosis. We report that psr-1, the Caenorhabditis elegans homolog of PSR, is important for cell corpse engulfment. In vitro PSR-1 binds preferentially phosphatidylserine or cells with exposed phosphatidylserine. In C. elegans, PSR-1 acts in the same cell corpse engulfment pathway mediated by intracellular signaling molecules CED-2 (homologous to the human CrkII protein), CED-5 (DOCK180), CED-10 (Rac GTPase), and CED-12 (ELMO), possibly through direct interaction with CED-5 and CED-12. Our findings suggest that PSR-1 is likely an upstream receptor for the signaling pathway containing CED-2, CED-5, CED-10, and CED-12 proteins and plays an important role in recognizing phosphatidylserine during phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Xiaochen -- Wu, Yi-Chun -- Fadok, Valerie A -- Lee, Ming-Chia -- Gengyo-Ando, Keiko -- Cheng, Li-Chun -- Ledwich, Duncan -- Hsu, Pei-Ken -- Chen, Jia-Yun -- Chou, Bin-Kuan -- Henson, Peter -- Mitani, Shohei -- Xue, Ding -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1563-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645848" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; *Apoptosis ; Caenorhabditis elegans/cytology/embryology/metabolism/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Carrier Proteins/genetics/*metabolism ; *Cytoskeletal Proteins ; Embryo, Nonmammalian/cytology/metabolism ; Embryonic Development ; Humans ; Jumonji Domain-Containing Histone Demethylases ; Membrane Proteins/genetics/*metabolism ; Molecular Sequence Data ; Mutation ; *Phagocytosis ; Phosphatidylserines/metabolism ; Protein Binding ; Receptors, Cell Surface/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; rac GTP-Binding Proteins/genetics/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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  • 6
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    Keeping G proteins at bay: a complex between G protein-coupled receptor kinase 2 and Gbetagamma (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-24
    Description: The phosphorylation of heptahelical receptors by heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptor kinases (GRKs) is a universal regulatory mechanism that leads to desensitization of G protein signaling and to the activation of alternative signaling pathways. We determined the crystallographic structure of bovine GRK2 in complex with G protein beta1gamma2 subunits. Our results show how the three domains of GRK2-the RGS (regulator of G protein signaling) homology, protein kinase, and pleckstrin homology domains-integrate their respective activities and recruit the enzyme to the cell membrane in an orientation that not only facilitates receptor phosphorylation, but also allows for the simultaneous inhibition of signaling by Galpha and Gbetagamma subunits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lodowski, David T -- Pitcher, Julie A -- Capel, W Darrell -- Lefkowitz, Robert J -- Tesmer, John J G -- HL16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 May 23;300(5623):1256-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cellular and Molecular Biology, Department of Chemistry and Biochemistry, University of Texas at Austin, Austin, TX 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12764189" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cattle ; Cell Membrane/metabolism ; Crystallography, X-Ray ; Cyclic AMP-Dependent Protein Kinases/*chemistry/*metabolism ; *GTP-Binding Protein beta Subunits ; *GTP-Binding Protein gamma Subunits ; Heterotrimeric GTP-Binding Proteins/*chemistry/*metabolism ; Hydrophobic and Hydrophilic Interactions ; Models, Molecular ; Molecular Sequence Data ; Phosphorylation ; Protein Binding ; Protein Conformation ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Signal Transduction ; beta-Adrenergic Receptor Kinases
    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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  • 7
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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
    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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    Stem cells. Setting standards for human embryonic stem cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brivanlou, Ali H -- Gage, Fred H -- Jaenisch, Rudolf -- Jessell, Thomas -- Melton, Douglas -- Rossant, Janet -- New York, N.Y. -- Science. 2003 May 9;300(5621):913-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York, NY 10021, USA. brvnlou@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12738841" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Specimen Banks ; Cell Culture Techniques/methods ; Cell Differentiation ; Cell Division ; *Cell Line ; Culture Media ; Culture Media, Conditioned ; Databases, Factual ; *Embryo Research ; Embryo, Mammalian/*cytology ; Humans ; Quality Control ; Registries ; Research/standards ; Signal Transduction ; Stem Cell Transplantation ; *Stem Cells/cytology/physiology ; 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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  • 9
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    Virology. Forced entry--or does HTLV-I have the key? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Derse, David -- Heidecker, Gisela -- New York, N.Y. -- Science. 2003 Mar 14;299(5613):1670-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basic Research Laboratory, National Cancer Institute, Frederick, MD 21702, USA. derse@ncifcrf.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12637723" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Adhesion Molecules/metabolism ; Cell Communication ; Cell Polarity ; Dendritic Cells/virology ; Extracellular Space/virology ; Gene Products, env/metabolism ; Gene Products, tax/physiology ; HTLV-I Infections/virology ; Human T-lymphotropic virus 1/genetics/*physiology ; Humans ; Intercellular Junctions/*physiology/ultrastructure/virology ; Microtubule-Organizing Center/*physiology/ultrastructure ; Receptors, Virus/metabolism ; Signal Transduction ; T-Lymphocytes/*ultrastructure/*virology ; Talin/metabolism ; Virion/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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  • 10
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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
    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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