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  • 1
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    Two-amino acid molecular switch in an epithelial morphogen that regulates binding to two distinct receptors (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-20
    Description: Ectodysplasin, a member of the tumor necrosis factor family, is encoded by the anhidrotic ectodermal dysplasia (EDA) gene. Mutations in EDA give rise to a clinical syndrome characterized by loss of hair, sweat glands, and teeth. EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that differ only by an insertion of two amino acids. This insertion functions to determine receptor binding specificity, such that EDA-A1 binds only the receptor EDAR, whereas EDA-A2 binds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR). In situ binding and organ culture studies indicate that EDA-A1 and EDA-A2 are differentially expressed and play a role in epidermal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, M -- Wang, L C -- Hymowitz, S G -- Schilbach, S -- Lee, J -- Goddard, A -- de Vos, A M -- Gao, W Q -- Dixit, V M -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):523-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, 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/11039935" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Binding Sites ; Cell Line ; DNA-Binding Proteins/metabolism ; Ectodermal Dysplasia/genetics ; Ectodysplasins ; Epidermis/embryology/*metabolism ; Humans ; *I-kappa B Proteins ; In Situ Hybridization ; Ligands ; Membrane Proteins/*chemistry/*metabolism ; Mice ; Models, Molecular ; Molecular Sequence Data ; Morphogenesis ; NF-kappa B/metabolism ; Phosphorylation ; Point Mutation ; Protein Conformation ; Proteins/metabolism ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 6 ; Transfection
    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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    Regulation of interferon regulatory factor-3 by the hepatitis C virus serine protease (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-19
    Description: Persistent infections with hepatitis C virus (HCV) are likely to depend on viral inhibition of host defenses. We show that the HCV NS3/4A serine protease blocks the phosphorylation and effector action of interferon regulatory factor-3 (IRF-3), a key cellular antiviral signaling molecule. Disruption of NS3/4A protease function by mutation or a ketoamide peptidomimetic inhibitor relieved this blockade and restored IRF-3 phosphorylation after cellular challenge with an unrelated virus. Furthermore, dominant-negative or constitutively active IRF-3 mutants, respectively, enhanced or suppressed HCV RNA replication in hepatoma cells. Thus, the NS3/4A protease represents a dual therapeutic target, the inhibition of which may both block viral replication and restore IRF-3 control of HCV infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Foy, Eileen -- Li, Kui -- Wang, Chunfu -- Sumpter, Rhea Jr -- Ikeda, Masanori -- Lemon, Stanley M -- Gale, Michael Jr -- U01-AI48235/AI/NIAID NIH HHS/ -- U19-AI40035/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2003 May 16;300(5622):1145-8. Epub 2003 Apr 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9048, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702807" target="_blank"〉PubMed〈/a〉
    Keywords: DNA-Binding Proteins/*antagonists & inhibitors/metabolism ; Gene Expression Regulation ; Gene Expression Regulation, Viral ; Hepacivirus/enzymology/immunology/*physiology ; Hepatitis C/therapy/virology ; Humans ; Interferon Regulatory Factor-3 ; Interferons/biosynthesis/genetics ; Mutation ; Phosphorylation ; Protease Inhibitors/pharmacology ; RNA, Viral/metabolism ; RNA-Binding Proteins/genetics/metabolism ; Serine Endopeptidases/*metabolism ; Transcription Factors/*antagonists & inhibitors/metabolism ; Tumor Cells, Cultured ; Viral Nonstructural Proteins/antagonists & inhibitors/*metabolism ; Virus Replication
    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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  • 3
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    Gastric cancer originating from bone marrow-derived cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-30
    Description: Epithelial cancers are believed to originate from transformation of tissue stem cells. However, bone marrow-derived cells (BMDCs), which are frequently recruited to sites of tissue injury and inflammation, might also represent a potential source of malignancy. We show that although acute injury, acute inflammation, or transient parietal cell loss within the stomach do not lead to BMDC recruitment, chronic infection of C57BL/6 mice with Helicobacter, a known carcinogen, induces repopulation of the stomach with BMDCs. Subsequently, these cells progress through metaplasia and dysplasia to intraepithelial cancer. These findings suggest that epithelial cancers can originate from marrow-derived sources and thus have broad implications for the multistep model of cancer progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Houghton, Jeanmarie -- Stoicov, Calin -- Nomura, Sachiyo -- Rogers, Arlin B -- Carlson, Jane -- Li, Hanchen -- Cai, Xun -- Fox, James G -- Goldenring, James R -- Wang, Timothy C -- CA95103/CA/NCI NIH HHS/ -- K22 CA90518/CA/NCI NIH HHS/ -- R01 CA87958/CA/NCI NIH HHS/ -- R01 DK58/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2004 Nov 26;306(5701):1568-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA. jeanmarie.houghton@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15567866" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Bone Marrow Cells/*cytology ; Bone Marrow Transplantation ; Carcinoma in Situ/pathology ; Cell Differentiation ; Cell Fusion ; Disease Progression ; Female ; Gastric Mucosa/chemistry/pathology ; Gastritis/*pathology ; Helicobacter Infections/*pathology ; *Helicobacter felis ; Keratins/analysis ; Male ; Mesenchymal Stromal Cells/physiology ; Metaplasia ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mucins/analysis ; Muscle Proteins/analysis ; Parietal Cells, Gastric/physiology ; Peptides/analysis ; Phenotype ; Stem Cells/*physiology ; Stomach Neoplasms/*pathology
    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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