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  • 1
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    Role of heteromer formation in GABAB receptor function (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Recently, GBR1, a seven-transmembrane domain protein with high affinity for gamma-aminobutyric acid (GABA)B receptor antagonists, was identified. Here, a GBR1-related protein, GBR2, was shown to be coexpressed with GBR1 in many brain regions and to interact with it through a short domain in the carboxyl-terminal cytoplasmic tail. Heterologously expressed GBR2 mediated inhibition of adenylyl cyclase; however, inwardly rectifying potassium channels were activated by GABAB receptor agonists only upon coexpression with GBR1 and GBR2. Thus, the interaction of these receptors appears to be crucial for important physiological effects of GABA and provides a mechanism in receptor signaling pathways that involve a heterotrimeric GTP-binding protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuner, R -- Kohr, G -- Grunewald, S -- Eisenhardt, G -- Bach, A -- Kornau, H C -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):74-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BASF-LYNX Bioscience AG, Department of Neuroscience, Im Neuenheimer Feld 515, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872744" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Amino Acid Sequence ; Animals ; Brain/*metabolism ; Cell Line ; Cyclic AMP/metabolism ; Dimerization ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GABA-B Receptor Agonists ; Humans ; In Situ Hybridization ; Molecular Sequence Data ; Neurons/metabolism ; Potassium/metabolism ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; RNA, Messenger/genetics/metabolism ; Rats ; Receptors, GABA/*chemistry/*metabolism ; Receptors, GABA-B/*chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Sequence Alignment
    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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    Phosphatidic acid-mediated mitogenic activation of mTOR signaling (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-12-01
    Description: The mammalian target of rapamycin (mTOR) governs cell growth and proliferation by mediating the mitogen- and nutrient-dependent signal transduction that regulates messenger RNA translation. We identified phosphatidic acid (PA) as a critical component of mTOR signaling. In our study, mitogenic stimulation of mammalian cells led to a phospholipase D-dependent accumulation of cellular PA, which was required for activation of mTOR downstream effectors. PA directly interacted with the domain in mTOR that is targeted by rapamycin, and this interaction was positively correlated with mTOR's ability to activate downstream effectors. The involvement of PA in mTOR signaling reveals an important function of this lipid in signal transduction and protein synthesis, as well as a direct link between mTOR and mitogens. Furthermore, these studies suggest a potential mechanism for the in vivo actions of the immunosuppressant rapamycin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fang, Y -- Vilella-Bach, M -- Bachmann, R -- Flanigan, A -- Chen, J -- GM58064/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2001 Nov 30;294(5548):1942-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Structural Biology, University of Illinois at Urbana-Champaign, 601 South Goodwin Avenue, B107, Urbana, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11729323" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Butanols/pharmacology ; Carrier Proteins/metabolism ; Cell Line ; Culture Media, Serum-Free ; Enzyme Activation/drug effects ; Humans ; Immunosuppressive Agents/pharmacology ; Mitogens/*pharmacology ; Phosphatidic Acids/*metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phospholipase D/metabolism ; Phosphoproteins/metabolism ; Phosphorylation/drug effects ; Protein Binding ; Protein Kinases/chemistry/*metabolism ; Protein Structure, Tertiary ; Ribosomal Protein S6 Kinases/metabolism ; Signal Transduction/*drug effects ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases ; Time Factors
    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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    The tetrameric structure of a glutamate receptor channel (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: The subunit stoichiometry of several ligand-gated ion channel receptors is still unknown. A counting method was developed to determine the number of subunits in one family of brain glutamate receptors. Successful application of this method in an HEK cell line provides evidence that ionotropic glutamate receptors share a tetrameric structure with the voltage-gated potassium channels. The average conductance of these channels depends on how many subunits are occupied by an agonist.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenmund, C -- Stern-Bach, Y -- Stevens, C F -- NS 12961/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Workgroup Cellular Neurobiology, Max-Planck-Institute for Biophysical Chemistry, Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616121" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cell Line ; Electric Conductivity ; Excitatory Amino Acid Agonists/metabolism ; Excitatory Amino Acid Antagonists/metabolism ; Humans ; Ligands ; Macromolecular Substances ; Models, Biological ; Patch-Clamp Techniques ; Quinoxalines/metabolism ; Quisqualic Acid/metabolism ; Receptors, AMPA/agonists/antagonists & inhibitors/*chemistry/*metabolism ; Receptors, Glutamate/chemistry/metabolism ; Receptors, Kainic Acid/agonists/antagonists & inhibitors/*chemistry/metabolism ; Recombinant Fusion Proteins/chemistry/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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    Resistance to ddI and sensitivity to AZT induced by a mutation in HIV-1 reverse transcriptase (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-27
    Description: Serial human immunodeficiency virus type-1 (HIV-1) isolates were obtained from five individuals with acquired immunodeficiency syndrome (AIDS) who changed therapy to 2',3'-dideoxyinosine (ddI) after at least 12 months of treatment with 3'-azido-3'-deoxythymidine (zidovudine, AZT). The in vitro sensitivity to ddI decreased during the 12 months following ddI initiation, whereas AZT sensitivity increased. Analysis of the reverse transcriptase coding region revealed a mutation associated with reduced sensitivity to ddI. When this mutation was present in the same genome as a mutation known to confer AZT resistance, the isolates showed increased sensitivity to AZT. Analysis of HIV-1 variants confirmed that the ddI resistance mutation alone conferred ddI and 2',3'-dideoxycytidine resistance, and suppressed the effect of the AZT resistance mutation. The use of combination therapy for HIV-1 disease may prevent drug-resistant isolates from emerging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉St Clair, M H -- Martin, J L -- Tudor-Williams, G -- Bach, M C -- Vavro, C L -- King, D M -- Kellam, P -- Kemp, S D -- Larder, B A -- New York, N.Y. -- Science. 1991 Sep 27;253(5027):1557-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Virology, Burroughs Wellcome Co., Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1716788" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*drug therapy/microbiology ; Base Sequence ; DNA, Viral/*genetics ; Didanosine/*pharmacology/*therapeutic use ; Drug Resistance, Microbial ; Genotype ; HIV-1/*drug effects/enzymology/isolation & purification ; Humans ; Molecular Sequence Data ; *Mutation ; Oligodeoxyribonucleotides ; RNA-Directed DNA Polymerase/*genetics/metabolism ; Zidovudine/pharmacology/*therapeutic use
    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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    Chronic lymphocytic leukaemia is driven by antigen-independent cell-autonomous signalling (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-08-14
    Description: B-cell antigen receptor (BCR) expression is an important feature of chronic lymphocytic leukaemia (CLL), one of the most prevalent B-cell neoplasias in Western countries. The presence of stereotyped and quasi-identical BCRs in different CLL patients suggests that recognition of specific antigens might drive CLL pathogenesis. Here we show that, in contrast to other B-cell neoplasias, CLL-derived BCRs induce antigen-independent cell-autonomous signalling, which is dependent on the heavy-chain complementarity-determining region (HCDR3) and an internal epitope of the BCR. Indeed, transferring the HCDR3 of a CLL-derived BCR provides autonomous signalling capacity to a non-autonomously active BCR, whereas mutations in the internal epitope abolish this capacity. Because BCR expression was required for the binding of secreted CLL-derived BCRs to target cells, and mutations in the internal epitope reduced this binding, our results indicate a new model for CLL pathogenesis, with cell-autonomous antigen-independent signalling as a crucial pathogenic mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duhren-von Minden, Marcus -- Ubelhart, Rudolf -- Schneider, Dunja -- Wossning, Thomas -- Bach, Martina P -- Buchner, Maike -- Hofmann, Daniel -- Surova, Elena -- Follo, Marie -- Kohler, Fabian -- Wardemann, Hedda -- Zirlik, Katja -- Veelken, Hendrik -- Jumaa, Hassan -- England -- Nature. 2012 Sep 13;489(7415):309-12. doi: 10.1038/nature11309.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Biological Signaling Studies (BIOSS), Albert-Ludwigs Universitat Freiburg, 79104 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22885698" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Autoantigens/immunology/metabolism ; Calcium Signaling ; Complementarity Determining Regions/immunology/metabolism ; Epitopes, B-Lymphocyte/immunology/metabolism ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/immunology/*metabolism/*pathology ; Receptors, Antigen, B-Cell/immunology/*metabolism ; *Signal Transduction
    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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  • 6
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    Psychopharmacologic drugs: mechanisms of action (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bach-y-Rita, P -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):642-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171313" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*drug effects ; Fluoxetine/*pharmacology ; Humans ; Psychotropic Drugs/*pharmacology ; Synaptic Transmission/*drug effects
    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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    The human immune response to the OKT3 monoclonal antibody is oligoclonal (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-06-13
    Description: The availability of highly specific and homogeneous antibodies to human T cells by the hybridoma technique has elicited new interest in the clinical use of antibodies to lymphocytes as immunosuppressive agents. OKT3 is the murine monoclonal antibody that has been the most widely used in clinical transplantation to induce immunosuppression. This antibody recognizes a membrane molecular complex, exclusively present on mature human T lymphocytes, which is tightly linked to the T-cell antigen receptor. The long-term therapeutic use of murine monoclonal antibodies in vivo is hampered by the intense antibody response that occurs in most human patients. Thus, when administered alone, OKT3 manifests its immunosuppressive activity only during the 10 to 15 days that precede the onset of sensitization. The results presented here show, by use of isoelectrofocusing, that the antibody response to OKT3, already reported to be restricted in its specificity (only anti-isotypic and anti-idiotypic antibodies are produced), is in addition oligoclonal. This restriction of the anti-monoclonal response may suggest that an efficient way to circumvent the sensitization problem would be to administer consecutively different monoclonal antibodies presenting the same specificity but distinct idiotypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chatenoud, L -- Jonker, M -- Villemain, F -- Goldstein, G -- Bach, J F -- New York, N.Y. -- Science. 1986 Jun 13;232(4756):1406-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3086976" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal/*immunology/therapeutic use ; Antibody Formation ; Antibody Specificity ; Antigens, Differentiation, T-Lymphocyte ; Antigens, Surface/immunology ; Clone Cells/immunology ; Humans ; Immunoglobulin Idiotypes/immunology ; Immunosuppressive Agents ; T-Lymphocytes/*immunology
    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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