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  • Cells, Cultured  (85)
  • American Association for the Advancement of Science (AAAS)  (85)
  • 2000-2004  (85)
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  • American Association for the Advancement of Science (AAAS)  (85)
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  • 1
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    A natural product that lowers cholesterol as an antagonist ligand for FXR (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-04
    Description: Extracts of the resin of the guggul tree (Commiphora mukul) lower LDL (low-density lipoprotein) cholesterol levels in humans. The plant sterol guggulsterone [4,17(20)-pregnadiene-3,16-dione] is the active agent in this extract. We show that guggulsterone is a highly efficacious antagonist of the farnesoid X receptor (FXR), a nuclear hormone receptor that is activated by bile acids. Guggulsterone treatment decreases hepatic cholesterol in wild-type mice fed a high-cholesterol diet but is not effective in FXR-null mice. Thus, we propose that inhibition of FXR activation is the basis for the cholesterol-lowering activity of guggulsterone. Other natural products with specific biologic effects may modulate the activity of FXR or other relatively promiscuous nuclear hormone receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Urizar, Nancy L -- Liverman, Amy B -- Dodds, D'Nette T -- Silva, Frank Valentin -- Ordentlich, Peter -- Yan, Yingzhuo -- Gonzalez, Frank J -- Heyman, Richard A -- Mangelsdorf, David J -- Moore, David D -- New York, N.Y. -- Science. 2002 May 31;296(5573):1703-6. Epub 2002 May 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Caco-2 Cells ; Carrier Proteins/genetics/metabolism ; Cells, Cultured ; Chenodeoxycholic Acid/pharmacology ; Cholesterol/*metabolism ; Cholesterol, Dietary/administration & dosage ; DNA/metabolism ; DNA-Binding Proteins/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Hepatocytes/metabolism ; Histone Acetyltransferases ; Humans ; *Hydroxysteroid Dehydrogenases ; Hypolipidemic Agents/metabolism/*pharmacology ; Ligands ; Liver/metabolism ; *Membrane Glycoproteins ; Mice ; Nuclear Receptor Coactivator 1 ; Pregnenediones/metabolism/*pharmacology ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors/genetics/metabolism ; Receptors, Steroid/antagonists & inhibitors/metabolism ; Transcription Factors/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Transcriptional Activation/drug effects ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    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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    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
    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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    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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  • 4
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    Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-05-08
    Description: The c-Jun NH2-terminal kinase (JNK) is activated when cells are exposed to ultraviolet (UV) radiation. However, the functional consequence of JNK activation in UV-irradiated cells has not been established. It is shown here that JNK is required for UV-induced apoptosis in primary murine embryonic fibroblasts. Fibroblasts with simultaneous targeted disruptions of all the functional Jnk genes were protected against UV-stimulated apoptosis. The absence of JNK caused a defect in the mitochondrial death signaling pathway, including the failure to release cytochrome c. These data indicate that mitochondria are influenced by proapoptotic signal transduction through the JNK pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tournier, C -- Hess, P -- Yang, D D -- Xu, J -- Turner, T K -- Nimnual, A -- Bar-Sagi, D -- Jones, S N -- Flavell, R A -- Davis, R J -- New York, N.Y. -- Science. 2000 May 5;288(5467):870-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Program in Molecular Medicine, Department of Biochemistry & Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10797012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspase 3 ; Caspase 9 ; Caspases/metabolism ; Cell Count ; Cell Division ; Cells, Cultured ; Cytochrome c Group/*metabolism ; DNA Fragmentation ; Enzyme Activation ; Fibroblasts ; Gene Targeting ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Signaling System ; Methyl Methanesulfonate/pharmacology ; Mice ; Mitochondria/metabolism ; Mitogen-Activated Protein Kinases/genetics/*metabolism ; NF-kappa B/metabolism ; *Protein-Serine-Threonine Kinases ; Proteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Tumor Suppressor Protein p53/metabolism ; Ultraviolet Rays
    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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    Defective lymphotoxin-beta receptor-induced NF-kappaB transcriptional activity in NIK-deficient mice (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-17
    Description: The role of NF-kappaB-inducing kinase (NIK) in cytokine signaling remains controversial. To identify the physiologic functions of NIK, we disrupted the NIK locus by gene targeting. Although NIK-/- mice displayed abnormalities in both lymphoid tissue development and antibody responses, NIK-/- cells manifested normal NF-kappaB DNA binding activity when treated with a variety of cytokines, including tumor necrosis factor (TNF), interleukin-1 (IL-1), and lymphotoxin-beta (LTbeta). However, NIK was selectively required for gene transcription induced through ligation of LTbeta receptor but not TNF receptors. These results reveal that NIK regulates the transcriptional activity of NF-kappaB in a receptor-restricted manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yin, L -- Wu, L -- Wesche, H -- Arthur, C D -- White, J M -- Goeddel, D V -- Schreiber, R D -- New York, N.Y. -- Science. 2001 Mar 16;291(5511):2162-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology, Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11251123" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; B-Lymphocytes/metabolism ; Cells, Cultured ; DNA/metabolism ; Fibroblasts/metabolism ; Gene Targeting ; Genes, Reporter ; Interleukin-1/metabolism/pharmacology ; Ligands ; Lymphoid Tissue/abnormalities ; Lymphotoxin beta Receptor ; Mice ; Mice, Inbred C57BL ; NF-kappa B/genetics/*metabolism ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Receptors, Tumor Necrosis Factor/immunology/*metabolism ; Signal Transduction ; *Transcription, Genetic ; Tumor Necrosis Factor-alpha/metabolism/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Potential regulatory function of human dendritic cells expressing indoleamine 2,3-dioxygenase (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-14
    Description: Antigen-presenting cells (APCs) can induce tolerance or immunity. We describe a subset of human APCs that express indoleamine 2,3-dioxygenase (IDO) and inhibit T cell proliferation in vitro. IDO-positive APCs constituted a discrete subset identified by coexpression of the cell-surface markers CD123 and CCR6. In the dendritic cell (DC) lineage, IDO-mediated suppressor activity was present in fully mature as well as immature CD123+ DCs. IDO+ DCs could also be readily detected in vivo, which suggests that these cells may represent a regulatory subset of APCs in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Munn, David H -- Sharma, Madhav D -- Lee, Jeffrey R -- Jhaver, Kanchan G -- Johnson, Theodore S -- Keskin, Derin B -- Marshall, Brendan -- Chandler, Phillip -- Antonia, Scott J -- Burgess, Russell -- Slingluff, Craig L Jr -- Mellor, Andrew L -- AI44219/AI/NIAID NIH HHS/ -- AI44759/AI/NIAID NIH HHS/ -- HL60137/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2002 Sep 13;297(5588):1867-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, GA 30912, USA. dmunn@mail.mcg.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12228717" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen-Presenting Cells/enzymology/immunology ; Antigens, CD/analysis ; Cell Adhesion ; Cell Lineage ; Cells, Cultured ; Dendritic Cells/*enzymology/*immunology ; Down-Regulation ; Enzyme Inhibitors/pharmacology ; Humans ; Indoleamine-Pyrrole 2,3,-Dioxygenase ; Interferon-gamma/pharmacology ; Interleukin-10/pharmacology ; Interleukin-3 Receptor alpha Subunit ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Lymphoid Tissue/cytology/enzymology ; Macrophages/enzymology ; Receptors, CCR6 ; Receptors, Chemokine/analysis ; Receptors, Interleukin-3/analysis ; T-Lymphocytes/*immunology ; Tryptophan/*analogs & derivatives/pharmacology ; Tryptophan Oxygenase/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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  • 7
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    An anti-apoptotic role for the p53 family member, p73, during developmental neuron death (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-15
    Description: p53 plays an essential pro-apoptotic role, a function thought to be shared with its family members p73 and p63. Here, we show that p73 is primarily present in developing neurons as a truncated isoform whose levels are dramatically decreased when sympathetic neurons apoptose after nerve growth factor (NGF) withdrawal. Increased expression of truncated p73 rescues these neurons from apoptosis induced by NGF withdrawal or p53 overexpression. In p73-/- mice, all isoforms of p73 are deleted and the apoptosis of developing sympathetic neurons is greatly enhanced. Thus, truncated p73 is an essential anti-apoptotic protein in neurons, serving to counteract the pro-apoptotic function of p53.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pozniak, C D -- Radinovic, S -- Yang, A -- McKeon, F -- Kaplan, D R -- Miller, F D -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):304-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neuronal Survival, Brain Tumor Research Center, Montreal Neurological Institute, McGill University, Montreal, Canada H3A 2B4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894779" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Apoptosis/*physiology ; Cells, Cultured ; DNA-Binding Proteins/biosynthesis/chemistry/*physiology ; Escherichia coli ; Genes, Tumor Suppressor ; Humans ; Mice ; Mice, Inbred BALB C ; Nerve Growth Factor/pharmacology ; Neurons/*physiology ; Nuclear Proteins/biosynthesis/chemistry/*physiology ; Protein Isoforms/biosynthesis/chemistry/physiology ; Recombinant Proteins ; Sympathetic Nervous System/cytology/*physiology ; Tumor Suppressor Protein p53/antagonists & inhibitors/*physiology ; Tumor Suppressor 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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  • 8
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    Operant reward learning in Aplysia: neuronal correlates and mechanisms (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-06-01
    Description: Operant conditioning is a form of associative learning through which an animal learns about the consequences of its behavior. Here, we report an appetitive operant conditioning procedure in Aplysia that induces long-term memory. Biophysical changes that accompanied the memory were found in an identified neuron (cell B51) that is considered critical for the expression of behavior that was rewarded. Similar cellular changes in B51 were produced by contingent reinforcement of B51 with dopamine in a single-cell analog of the operant procedure. These findings allow for the detailed analysis of the cellular and molecular processes underlying operant conditioning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brembs, Bjorn -- Lorenzetti, Fred D -- Reyes, Fredy D -- Baxter, Douglas A -- Byrne, John H -- MH 58321/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2002 May 31;296(5573):1706-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Anatomy, W. M. Keck Center for the Neurobiology of Learning and Memory, The University of Texas-Houston Medical School, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12040200" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aplysia/*physiology ; Cells, Cultured ; *Conditioning, Operant ; Dopamine/pharmacology/physiology ; Eating ; Electric Stimulation ; Electrophysiology ; Esophagus/innervation ; Feeding Behavior ; Food ; Ganglia, Invertebrate/physiology ; Iontophoresis ; Membrane Potentials ; *Memory ; Nerve Net/physiology ; Neuronal Plasticity ; Neurons/*physiology ; Patch-Clamp Techniques ; Reinforcement (Psychology) ; *Reward
    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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    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
    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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    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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