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  • 1
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    Metabolic regulation of brain Abeta by neprilysin (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-05-26
    Description: Amyloid beta peptide (Abeta), the pathogenic agent of Alzheimer's disease (AD), is a physiological metabolite in the brain. We examined the role of neprilysin, a candidate Abeta-degrading peptidase, in the metabolism using neprilysin gene-disrupted mice. Neprilysin deficiency resulted in defects both in the degradation of exogenously administered Abeta and in the metabolic suppression of the endogenous Abeta levels in a gene dose-dependent manner. The regional levels of Abeta in the neprilysin-deficient mouse brain were in the distinct order of hippocampus, cortex, thalamus/striatum, and cerebellum, where hippocampus has the highest level and cerebellum the lowest, correlating with the vulnerability to Abeta deposition in brains of humans with AD. Our observations suggest that even partial down-regulation of neprilysin activity, which could be caused by aging, can contribute to AD development by promoting Abeta accumulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwata, N -- Tsubuki, S -- Takaki, Y -- Shirotani, K -- Lu, B -- Gerard, N P -- Gerard, C -- Hama, E -- Lee, H J -- Saido, T C -- New York, N.Y. -- Science. 2001 May 25;292(5521):1550-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako-shi 351-0198 Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11375493" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/metabolism ; Alzheimer Disease/etiology/genetics/metabolism ; Amyloid beta-Peptides/*metabolism ; Animals ; Brain/enzymology/*metabolism ; Chromatography, High Pressure Liquid ; Down-Regulation ; Enhancer Elements, Genetic ; Enzyme-Linked Immunosorbent Assay ; Gene Dosage ; Hippocampus/enzymology/metabolism ; Humans ; Membrane Proteins/genetics/metabolism ; Mice ; Mice, Knockout ; Mutation ; Neprilysin/genetics/*metabolism ; Neurons/enzymology ; Peptide Fragments/metabolism ; Presenilin-1 ; Response Elements ; Up-Regulation
    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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  • 2
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    CD8(+) T lymphocyte mobilization to virus-infected tissue requires CD4(+) T-cell help (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-11-10
    Description: CD4(+) T helper cells are well known for their role in providing critical signals during priming of cytotoxic CD8(+) T lymphocyte (CTL) responses in vivo. T-cell help is required for the generation of primary CTL responses as well as in promoting protective CD8(+) memory T-cell development. However, the role of CD4 help in the control of CTL responses at the effector stage is unknown. Here we show that fully helped effector CTLs are themselves not self-sufficient for entry into the infected tissue, but rely on the CD4(+) T cells to provide the necessary cue. CD4(+) T helper cells control the migration of CTL indirectly through the secretion of IFN-gamma and induction of local chemokine secretion in the infected tissue. Our results reveal a previously unappreciated role of CD4 help in mobilizing effector CTL to the peripheral sites of infection where they help to eliminate infected cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789415/" 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/PMC2789415/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakanishi, Yusuke -- Lu, Bao -- Gerard, Craig -- Iwasaki, Akiko -- AI054359/AI/NIAID NIH HHS/ -- AI062428/AI/NIAID NIH HHS/ -- AI39759/AI/NIAID NIH HHS/ -- HL51366/HL/NHLBI NIH HHS/ -- R01 AI054359/AI/NIAID NIH HHS/ -- R01 AI054359-06A2/AI/NIAID NIH HHS/ -- R01 AI062428/AI/NIAID NIH HHS/ -- R01 AI062428-05/AI/NIAID NIH HHS/ -- England -- Nature. 2009 Nov 26;462(7272):510-3. doi: 10.1038/nature08511. Epub 2009 Nov 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19898495" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Chemokines/immunology/secretion ; *Chemotaxis ; Female ; Herpes Simplex/immunology/virology ; Herpesvirus 2, Human/*immunology ; Immunity, Mucosal/immunology ; Interferon-gamma/antagonists & inhibitors/immunology/secretion ; Mice ; Mice, Inbred C57BL ; Models, Immunological ; Mucous Membrane/immunology/virology ; Receptors, CXCR3/metabolism ; T-Lymphocytes, Cytotoxic/*cytology/*immunology ; T-Lymphocytes, Helper-Inducer/*immunology/secretion ; Vagina/*immunology/*virology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Molecular cloning of the thyrotropin receptor (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-12-22
    Description: The pituitary hormone thyrotropin, or thyroid-stimulating hormone (TSH), is the main physiological agent that regulates the thyroid gland. The thyrotropin receptor (TSHR) was cloned by selective amplification with the polymerase chain reaction of DNA segments presenting sequence similarity with genes for G protein-coupled receptors. Out of 11 new putative receptor clones obtained from genomic DNA, one had sequence characteristics different from all the others. Although this clone did not hybridize to thyroid transcripts, screening of a dog thyroid complementary DNA (cDNA) library at moderate stringency identified a cDNA encoding a 4.9-kilobase thyroid-specific transcript. The polypeptide encoded by this thyroid-specific transcript consisted of a 398-amino acid residue amino-terminal segment, constituting a putative extracellular domain, connected to a 346-residue carboxyl-terminal domain that contained seven putative transmembrane segments. Expression of the cDNA conferred TSH responsiveness to Xenopus oocytes and Y1 cells and a TSH binding phenotype to COS cells. The TSHR and the receptor for luteinizing hormone-choriogonadotropin constitute a subfamily of G protein-coupled receptors with distinct sequence characteristics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parmentier, M -- Libert, F -- Maenhaut, C -- Lefort, A -- Gerard, C -- Perret, J -- Van Sande, J -- Dumont, J E -- Vassart, G -- R01-DK21732/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1620-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Recherche Interdisciplinaire, Faculte de Medecine, Universite Libre de Bruxelles, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2556796" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Cell Line ; *Cloning, Molecular ; Cyclic AMP ; Dogs ; Female ; *Genes ; Molecular Sequence Data ; Oocytes/drug effects/metabolism ; Organ Specificity ; Polymerase Chain Reaction/methods ; RNA, Messenger/genetics ; Receptors, Thyrotropin/*genetics ; Thyrotropin/pharmacology ; Transcription, Genetic ; Xenopus
    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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  • 4
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    CD4-independent binding of SIV gp120 to rhesus CCR5 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: CCR5 and CD4 are coreceptors for immunodeficiency virus entry into target cells. The gp120 envelope glycoprotein from human immunodeficiency virus strain HIV-1(YU2) bound human CCR5 (CCR5hu) or rhesus macaque CCR5 (CCR5rh) only in the presence of CD4. The gp120 from simian immunodeficiency virus strain SIVmac239 bound CCR5rh without CD4, but CCR5hu remained CD4-dependent. The CD4-independent binding of SIVmac239 gp120 depended on a single amino acid, Asp13, in the CCR5rh amino-terminus. Thus, CCR5-binding moieties on the immunodeficiency virus envelope glycoprotein can be generated by interaction with CD4 or by direct interaction with the CCR5 amino-terminus. These results may have implications for the evolution of receptor use among lentiviruses as well as utility in the development of effective intervention.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, K A -- Wyatt, R -- Farzan, M -- Choe, H -- Marcon, L -- Desjardins, E -- Robinson, J -- Sodroski, J -- Gerard, C -- Gerard, N P -- AI41581/AI/NIAID NIH HHS/ -- HL36162/HL/NHLBI NIH HHS/ -- HL51366/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Nov 21;278(5342):1470-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Perlmutter Laboratory, Children's Hospital, Department of 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/9367961" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal ; Antigens, CD4/*physiology ; Cell Line ; HIV Antibodies/immunology ; HIV Envelope Protein gp120/chemistry/*metabolism ; HIV-2/immunology ; Humans ; Macaca mulatta ; Macrophages/virology ; *Membrane Glycoproteins ; Mutation ; Receptors, CCR5/chemistry/*metabolism ; Simian Immunodeficiency Virus/*metabolism ; Transfection ; *Viral Envelope Proteins
    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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  • 5
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    A critical role for eosinophils in allergic airways remodeling (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-18
    Description: Features of chronic asthma include airway hyperresponsiveness, inflammatory infiltrates, and structural changes in the airways, termed remodeling. The contribution of eosinophils, cells associated with asthma and allergy, remains to be established. We show that in mice with a total ablation of the eosinophil lineage, increases in airway hyperresponsiveness and mucus secretion were similar to those observed in wild-type mice, but eosinophil-deficient mice were significantly protected from peribronchiolar collagen deposition and increases in airway smooth muscle. These data suggest that eosinophils contribute substantially to airway remodeling but are not obligatory for allergen-induced lung dysfunction, and support an important role for eosinophil-targeted therapies in chronic asthma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Humbles, Alison A -- Lloyd, Clare M -- McMillan, Sarah J -- Friend, Daniel S -- Xanthou, Georgina -- McKenna, Erin E -- Ghiran, Sorina -- Gerard, Norma P -- Yu, Channing -- Orkin, Stuart H -- Gerard, Craig -- 087618/Wellcome Trust/United Kingdom -- AI39759/AI/NIAID NIH HHS/ -- HL10463/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Sep 17;305(5691):1776-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. alison.humbles@childrens.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15375268" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asthma/immunology/*pathology/physiopathology ; Bronchi/pathology ; Cell Division ; Collagen/analysis ; Eosinophils/*physiology ; Interleukins/analysis ; Leukocyte Count ; Lung/immunology/*pathology/physiopathology ; Mice ; Mice, Inbred BALB C ; Mucus/secretion ; Muscle, Smooth/pathology ; Respiratory Function Tests ; Respiratory Hypersensitivity/immunology/pathology/physiopathology ; Th2 Cells/immunology ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta1
    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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    Biomedicine. Asthmatics breathe easier when it's SNO-ing (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-06-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerard, Craig -- New York, N.Y. -- Science. 2005 Jun 10;308(5728):1560-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Hospital, Harvard Medical School, Children's Hospital and Harvard Medical School, Boston, MA 02115 USA. craig.gerard@childrens.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15947161" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/pharmacology ; Alcohol Dehydrogenase ; Animals ; Asthma/drug therapy/*physiopathology ; Bronchi/physiology/physiopathology ; Bronchial Hyperreactivity/physiopathology ; Glutathione Reductase/antagonists & inhibitors/genetics/*metabolism ; Humans ; Isoproterenol/pharmacology ; Lung/metabolism/*physiopathology ; Mice ; Mice, Knockout ; Muscle, Smooth/physiology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/metabolism ; Nitric Oxide Synthase Type II ; Receptors, G-Protein-Coupled/metabolism ; S-Nitrosoglutathione/metabolism ; S-Nitrosothiols/*metabolism ; Signal Transduction
    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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  • 7
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    Neurogenic amplification of immune complex inflammation (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-09-20
    Description: The formation of intrapulmonary immune complexes in mice generates a vigorous inflammatory response characterized by microvascular permeability and polymorphonuclear neutrophil influx. Gene-targeted disruption of the substance P receptor (NK-1R) protected the lung from immune complex injury, as did disruption of the C5a anaphylatoxin receptor. Immunoreactive substance P was measurable in fluids lining the lung at time points before neutrophil influx and may thus be involved in an early step in the inflammatory response to immune complexes in the lung.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bozic, C R -- Lu, B -- Hopken, U E -- Gerard, C -- Gerard, N P -- HL36162/HL/NHLBI NIH HHS/ -- HL51366/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Sep 20;273(5282):1722-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Perlmutter Laboratory, Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8781237" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Complex/*immunology ; Antigens, CD/genetics/physiology ; Bronchoalveolar Lavage Fluid/chemistry ; Capillary Permeability ; Complement C5a/*physiology ; Female ; Gene Targeting ; Immune Complex Diseases/immunology/*metabolism/pathology ; Inflammation/immunology/metabolism/pathology ; Lung/chemistry/pathology ; Lung Diseases/immunology/*metabolism/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Neutrophils ; Receptor, Anaphylatoxin C5a ; Receptors, Complement/genetics/physiology ; Receptors, Neurokinin-1/genetics/physiology ; Substance P/analysis/*physiology ; Tumor Necrosis Factor-alpha/analysis
    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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