Publikation:

Protein Kinase C Inhibitors Arrest the C6 Glioma Cell Cycle at a Mid-G1 Phase Restriction Point : Implications for the Antiproliferative Action of Valproate

Lade...
Vorschaubild

Dateien

OBrien_1998.pdf
OBrien_1998.pdfGröße: 490.75 KBDownloads: 522

Datum

1997

Autor:innen

O'Brien, Evelyn
Regan, Ciaran M.

Herausgeber:innen

Kontakt

ISSN der Zeitschrift

Electronic ISSN

ISBN

Bibliografische Daten

Verlag

Schriftenreihe

Auflagebezeichnung

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

Toxicology in vitro. 1997, 12(1), pp. 9-14. ISSN 0887-2333. Available under: doi: 10.1016/S0887-2333(97)00103-3

Zusammenfassung

The teratogenic mechanism(s) of valproate (VPA) have been suggested to arise through inhibition of proliferation coupled with differentiation at a mid-G1 phase restriction point in the cell cycle. As protein kinase C (PKC) plays a pivotal role in cell proliferation and differentiation, the effect of inhibitors specific for the catalytic and regulatory domains on transit through the G1 phase of the cell cycle was determined. Calphostin C and bisindolylmaleimide GF 109203X produced a dose-dependent decrease in proliferation of C6 glioma with approximate 50% inhibitory concentration values of 10 nImage and 1 μImage, respectively. Flow cytometric analysis indicated proliferative arrest to be in the G1 phase with the expected concomitant decrease of cells in the G2/M and S phases. Following release from drug-induced proliferative arrest, cells exhibited a synchronous entry into S phase as evidenced by an increase in [3H]thymidine incorporation after approximately 6-8 hr, indicating the restriction point to be in the mid-G1 phase. Using mitotically synchronized cells continuously exposed to valproate (2 mImage), PKC activity was found to be significantly reduced in the mid-G1 phase (5.5 hr) but not at an earlier (2.5 hr) time point, implying VPA to exert its effect at a site upstream to the point of proliferative arrest at 5-6 hr into the G1 phase which as yet, remains to be defined.

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 690O'BRIEN, Evelyn, Ciaran M. REGAN, 1997. Protein Kinase C Inhibitors Arrest the C6 Glioma Cell Cycle at a Mid-G1 Phase Restriction Point : Implications for the Antiproliferative Action of Valproate. In: Toxicology in vitro. 1997, 12(1), pp. 9-14. ISSN 0887-2333. Available under: doi: 10.1016/S0887-2333(97)00103-3
BibTex
@article{OBrien1997Prote-8333,
  year={1997},
  doi={10.1016/S0887-2333(97)00103-3},
  title={Protein Kinase C Inhibitors Arrest the C6 Glioma Cell Cycle at a Mid-G1 Phase Restriction Point : Implications for the Antiproliferative Action of Valproate},
  number={1},
  volume={12},
  issn={0887-2333},
  journal={Toxicology in vitro},
  pages={9--14},
  author={O'Brien, Evelyn and Regan, Ciaran M.}
}
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/123456789/8333">
    <dc:contributor>Regan, Ciaran M.</dc:contributor>
    <dc:rights>Attribution-NonCommercial-NoDerivs 2.0 Generic</dc:rights>
    <foaf:homepage rdf:resource="http://localhost:8080/"/>
    <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:42:45Z</dcterms:available>
    <dc:format>application/pdf</dc:format>
    <dc:creator>O'Brien, Evelyn</dc:creator>
    <dcterms:bibliographicCitation>First publ. in: Toxicology in vitro 12 (1998), 1, pp. 9-14</dcterms:bibliographicCitation>
    <dc:language>eng</dc:language>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:42:45Z</dc:date>
    <dcterms:abstract xml:lang="eng">The teratogenic mechanism(s) of valproate (VPA) have been suggested to arise through inhibition of proliferation coupled with differentiation at a mid-G1 phase restriction point in the cell cycle. As protein kinase C (PKC) plays a pivotal role in cell proliferation and differentiation, the effect of inhibitors specific for the catalytic and regulatory domains on transit through the G1 phase of the cell cycle was determined. Calphostin C and bisindolylmaleimide GF 109203X produced a dose-dependent decrease in proliferation of C6 glioma with approximate 50% inhibitory concentration values of 10 nImage and 1 μImage, respectively. Flow cytometric analysis indicated proliferative arrest to be in the G1 phase with the expected concomitant decrease of cells in the G2/M and S phases. Following release from drug-induced proliferative arrest, cells exhibited a synchronous entry into S phase as evidenced by an increase in [3H]thymidine incorporation after approximately 6-8 hr, indicating the restriction point to be in the mid-G1 phase. Using mitotically synchronized cells continuously exposed to valproate (2 mImage), PKC activity was found to be significantly reduced in the mid-G1 phase (5.5 hr) but not at an earlier (2.5 hr) time point, implying VPA to exert its effect at a site upstream to the point of proliferative arrest at 5-6 hr into the G1 phase which as yet, remains to be defined.</dcterms:abstract>
    <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/8333"/>
    <dc:contributor>O'Brien, Evelyn</dc:contributor>
    <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/>
    <dspace:hasBitstream rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/8333/1/OBrien_1998.pdf"/>
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dcterms:title>Protein Kinase C Inhibitors Arrest the C6 Glioma Cell Cycle at a Mid-G1 Phase Restriction Point : Implications for the Antiproliferative Action of Valproate</dcterms:title>
    <dc:creator>Regan, Ciaran M.</dc:creator>
    <dcterms:hasPart rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/8333/1/OBrien_1998.pdf"/>
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dcterms:issued>1997</dcterms:issued>
    <dcterms:rights rdf:resource="http://creativecommons.org/licenses/by-nc-nd/2.0/"/>
  </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
Begutachtet
Diese Publikation teilen