untitled
<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd>
<responseDate>2018-01-15T18:39:50Z</responseDate>
<request identifier=oai:HAL:hal-00702089v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request>
<GetRecord>
<record>
<header>
<identifier>oai:HAL:hal-00702089v1</identifier>
<datestamp>2017-12-21</datestamp>
<setSpec>type:ART</setSpec>
<setSpec>subject:sdv</setSpec>
<setSpec>collection:IFR140</setSpec>
<setSpec>collection:UNIV-AG</setSpec>
<setSpec>collection:IRSET</setSpec>
<setSpec>collection:UNIV-RENNES1</setSpec>
<setSpec>collection:IRSET-SMLF</setSpec>
<setSpec>collection:BIOSIT</setSpec>
<setSpec>collection:UR1-UFR-SVE</setSpec>
<setSpec>collection:STATS-UR1</setSpec>
<setSpec>collection:UR1-HAL</setSpec>
<setSpec>collection:EHESP</setSpec>
<setSpec>collection:USPC</setSpec>
<setSpec>collection:UR1-SDV</setSpec>
<setSpec>collection:IRSET-5</setSpec>
<setSpec>collection:UNIV-ANGERS</setSpec>
</header>
<metadata><dc>
<publisher>HAL CCSD</publisher>
<title lang=en>An MLCK-dependent window in late G1 controls S phase entry of proliferating rodent hepatocytes via ERK-p70S6K pathway.</title>
<creator>Bessard, Anne</creator>
<creator>Coutant, Alexandre</creator>
<creator>Rescan, Claude</creator>
<creator>Ezan, Frédéric</creator>
<creator>Frémin, Christophe</creator>
<creator>Courselaud, Brice</creator>
<creator>Ilyin, Gennady</creator>
<creator>Baffet, Georges</creator>
<contributor>Signalisation et Réponses aux Agents Infectieux et Chimiques (SeRAIC) ; Université de Rennes 1 (UR1) - IFR140</contributor>
<contributor>Régulations des équilibres fonctionnels du foie normal et pathologique ; Université de Rennes 1 (UR1) - IFR140 - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>Department of Developmental Biology ; Hagedorn Research Institute</contributor>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<description>International audience</description>
<source>ISSN: 0270-9139</source>
<source>EISSN: 1527-3350</source>
<source>Hepatology</source>
<publisher>Wiley-Blackwell</publisher>
<identifier>hal-00702089</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00702089</identifier>
<source>https://hal.archives-ouvertes.fr/hal-00702089</source>
<source>Hepatology, Wiley-Blackwell, 2006, 44 (1), pp.152-63. 〈10.1002/hep.21222〉</source>
<identifier>DOI : 10.1002/hep.21222</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1002/hep.21222</relation>
<identifier>PUBMED : 16799973</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/16799973</relation>
<language>en</language>
<subject>[SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>We show that MLCK (myosin light chain kinase) plays a key role in cell cycle progression of hepatocytes: either chemical inhibitor ML7 or RNA interference led to blockade of cyclin D1 expression and DNA replication, providing evidence that MLCK regulated S phase entry. Conversely, inhibition of RhoK by specific inhibitor Y27632 or RhoK dominant-negative vector did not influence progression in late G1 and S phase entry. Inhibition of either MLCK or RhoK did not block ERK1/2 phosphorylation, whereas MLCK regulated ERK2-dependent p70S6K activation. In addition, DNA synthesis was reduced in hepatocytes treated with p70S6K siRNA, demonstrating the key role played by the kinase in S phase entry. Interestingly, after the G1/S transition, DNA replication in S phase was no longer dependent on MLCK activity. We strengthened this result by ex vivo experiments and evidenced an MLCK-dependent window in late G1 phase of regenerating liver after two-thirds partial hepatectomy. In conclusion, our results underline an MLCK-dependent restriction point in G1/S transition, occurring downstream of ERK2 through the regulation of p70S6K activation, and highlighting a new signaling pathway critical for hepatocyte proliferation.</description>
<date>2006-07</date>
</dc>
</metadata>
</record>
</GetRecord>
</OAI-PMH>