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<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>