Publikation:

9-cis retinoic acid inhibition of activation-induced apoptosis is mediated via regulation of Fas ligand and requires retinoic acid receptor and retinoic X receptor activation

Lade...
Vorschaubild

Dateien

1995_brunner_9-cis retinoic .pdf
1995_brunner_9-cis retinoic .pdfGröße: 1.69 MBDownloads: 442

Datum

1995

Autor:innen

Bissonnette, Reid P.
Lazarchik, Steven B.
Yoo, Nam Jin
Boehm, Marcus F.
Green, Douglas R.
Heyman, Richard D.

Herausgeber:innen

Kontakt

ISSN der Zeitschrift

Electronic ISSN

ISBN

Bibliografische Daten

Verlag

Schriftenreihe

Auflagebezeichnung

DOI (zitierfähiger Link)
ArXiv-ID

Internationale Patentnummer

Angaben zur Forschungsförderung

Projekt

Open Access-Veröffentlichung
Open Access Green
Core Facility der Universität Konstanz

Gesperrt bis

Titel in einer weiteren Sprache

Publikationstyp
Zeitschriftenartikel
Publikationsstatus
Published

Erschienen in

Molecular and Cellular Biology. 1995, 15(10), pp. 5576-5585

Zusammenfassung

T-cell hybridomas, thymocytes, and T cells can be induced to undergo apoptotic cell death by activation through the T-cell receptor. This process requires macromolecular synthesis and thus gene expression, and it has been shown to be influenced by factors regulating transcription. Recently, activation, T-cell hybridomas rapidly express the Fas/CD95 receptor and its ligand, Fas ligand (FasL), which interact to transduce the death signal in the activated cell. Retinoids, the active metabolites of vitamin A, modulate expression of specific target genes by binding to two classes of intracellular receptors, retinoic acid receptors (RARs) and retinoid X receptors (RXRs). They are potent modulators of apoptosis in a number of experimental models, and they have been shown to inhibit activation-induced apoptosis in T-cell hybridomas and thymocytes. Particularly effective is the prototypic pan- agonist 9-cis retinoic acid (9-cis RA), which has high affinity for both RARs and RXRs. We report here that 9-cis RA inhibits T-cell receptor-mediated apoptosis in T-cell hybridomas by blocking the expression of Fas ligand following activation. This inhibition appears to be at the level of FasL mRNA, with the subsequent failure to express cell surface FasL. RAR-selective (TTNPB) or RXR-selective (LG100268) ligands alone were considerably less potent than RAR-RXR pan-agonists. However, the addition of both RAR- and RXR-selective ligands was as effective as the addition of 9-cis RA alone. The demonstrates that the inhibitory effect requires the ligand-mediated activation of both retinoid receptor signaling pathways.

Zusammenfassung in einer weiteren Sprache

Fachgebiet (DDC)
570 Biowissenschaften, Biologie

Schlagwörter

Konferenz

Rezension
undefined / . - undefined, undefined

Forschungsvorhaben

Organisationseinheiten

Zeitschriftenheft

Zugehörige Datensätze in KOPS

Zitieren

ISO 690BISSONNETTE, Reid P., Thomas BRUNNER, Steven B. LAZARCHIK, Nam Jin YOO, Marcus F. BOEHM, Douglas R. GREEN, Richard D. HEYMAN, 1995. 9-cis retinoic acid inhibition of activation-induced apoptosis is mediated via regulation of Fas ligand and requires retinoic acid receptor and retinoic X receptor activation. In: Molecular and Cellular Biology. 1995, 15(10), pp. 5576-5585
BibTex
@article{Bissonnette1995retin-14319,
  year={1995},
  title={9-cis retinoic acid inhibition of activation-induced apoptosis is mediated via regulation of Fas ligand and requires retinoic acid receptor and retinoic X receptor activation},
  number={10},
  volume={15},
  journal={Molecular and Cellular Biology},
  pages={5576--5585},
  author={Bissonnette, Reid P. and Brunner, Thomas and Lazarchik, Steven B. and Yoo, Nam Jin and Boehm, Marcus F. and Green, Douglas R. and Heyman, Richard D.}
}
RDF
<rdf:RDF
    xmlns:dcterms="http://purl.org/dc/terms/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
    xmlns:bibo="http://purl.org/ontology/bibo/"
    xmlns:dspace="http://digital-repositories.org/ontologies/dspace/0.1.0#"
    xmlns:foaf="http://xmlns.com/foaf/0.1/"
    xmlns:void="http://rdfs.org/ns/void#"
    xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > 
  <rdf:Description rdf:about="https://kops.uni-konstanz.de/server/rdf/resource/123456789/14319">
    <foaf:homepage rdf:resource="http://localhost:8080/"/>
    <dcterms:abstract xml:lang="eng">T-cell hybridomas, thymocytes, and T cells can be induced to undergo apoptotic cell death by activation through the T-cell receptor. This process requires macromolecular synthesis and thus gene expression, and it has been shown to be influenced by factors regulating transcription. Recently, activation, T-cell hybridomas rapidly express the Fas/CD95 receptor and its ligand, Fas ligand (FasL), which interact to transduce the death signal in the activated cell. Retinoids, the active metabolites of vitamin A, modulate expression of specific target genes by binding to two classes of intracellular receptors, retinoic acid receptors (RARs) and retinoid X receptors (RXRs). They are potent modulators of apoptosis in a number of experimental models, and they have been shown to inhibit activation-induced apoptosis in T-cell hybridomas and thymocytes. Particularly effective is the prototypic pan- agonist 9-cis retinoic acid (9-cis RA), which has high affinity for both RARs and RXRs. We report here that 9-cis RA inhibits T-cell receptor-mediated apoptosis in T-cell hybridomas by blocking the expression of Fas ligand following activation. This inhibition appears to be at the level of FasL mRNA, with the subsequent failure to express cell surface FasL. RAR-selective (TTNPB) or RXR-selective (LG100268) ligands alone were considerably less potent than RAR-RXR pan-agonists. However, the addition of both RAR- and RXR-selective ligands was as effective as the addition of 9-cis RA alone. The demonstrates that the inhibitory effect requires the ligand-mediated activation of both retinoid receptor signaling pathways.</dcterms:abstract>
    <dcterms:title>9-cis retinoic acid inhibition of activation-induced apoptosis is mediated via regulation of Fas ligand and requires retinoic acid receptor and retinoic X receptor activation</dcterms:title>
    <dc:contributor>Bissonnette, Reid P.</dc:contributor>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-07-29T09:24:36Z</dc:date>
    <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/>
    <dspace:hasBitstream rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/14319/2/1995_brunner_9-cis%20retinoic%20.pdf"/>
    <dcterms:bibliographicCitation>First publ. in: Molecular and Cellular Biology ; 15 (1995), 10. - pp. 5576-5585</dcterms:bibliographicCitation>
    <dc:contributor>Yoo, Nam Jin</dc:contributor>
    <dc:contributor>Green, Douglas R.</dc:contributor>
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:creator>Yoo, Nam Jin</dc:creator>
    <dc:contributor>Brunner, Thomas</dc:contributor>
    <dc:creator>Green, Douglas R.</dc:creator>
    <dc:creator>Heyman, Richard D.</dc:creator>
    <dc:contributor>Heyman, Richard D.</dc:contributor>
    <dc:creator>Brunner, Thomas</dc:creator>
    <dc:creator>Bissonnette, Reid P.</dc:creator>
    <dc:rights>terms-of-use</dc:rights>
    <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-07-29T09:24:36Z</dcterms:available>
    <dc:language>eng</dc:language>
    <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/14319"/>
    <dc:contributor>Boehm, Marcus F.</dc:contributor>
    <dcterms:hasPart rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/14319/2/1995_brunner_9-cis%20retinoic%20.pdf"/>
    <dc:contributor>Lazarchik, Steven B.</dc:contributor>
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:creator>Lazarchik, Steven B.</dc:creator>
    <dcterms:issued>1995</dcterms:issued>
    <dc:creator>Boehm, Marcus F.</dc:creator>
    <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/>
  </rdf:Description>
</rdf:RDF>

Interner Vermerk

xmlui.Submission.submit.DescribeStep.inputForms.label.kops_note_fromSubmitter

Kontakt
URL der Originalveröffentl.

Prüfdatum der URL

Prüfungsdatum der Dissertation

Finanzierungsart

Kommentar zur Publikation

Allianzlizenz
Corresponding Authors der Uni Konstanz vorhanden
Internationale Co-Autor:innen
Universitätsbibliographie
Nein
Begutachtet
Diese Publikation teilen