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dc.contributor.authorGonzález, José M.-
dc.contributor.authorNavarro, Ana-
dc.contributor.authorCasar, Berta-
dc.contributor.authorCrespo, Piero-
dc.contributor.authorAndrés, Vicente-
dc.identifier.citationJournal of Cell Biology 183(4): 653-66 (2008)en_US
dc.descriptionThis article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication.en_US
dc.description.abstractSequestration of c-Fos at the nuclear envelope (NE) through interaction with A-type lamins suppresses AP-1-dependent transcription. We show here that c-Fos accumulation within the extraction-resistant nuclear fraction (ERNF) and its interaction with lamin A are reduced and enhanced by gain-of and loss-of ERK1/2 activity, respectively. Moreover, hindering ERK1/2-dependent phosphorylation of c-Fos attenuates its release from the ERNF induced by serum and promotes its interaction with lamin A. Accordingly, serum stimulation rapidly releases preexisting c-Fos from the NE via ERK1/2-dependent phosphorylation, leading to a fast activation of AP-1 before de novo c-Fos synthesis. Moreover, lamin A-null cells exhibit increased AP-1 activity and reduced levels of c-Fos phosphorylation. We also find that active ERK1/2 interacts with lamin A and colocalizes with c-Fos and A-type lamins at the NE. Thus, NE-bound ERK1/2 functions as a molecular switch for rapid mitogen-dependent AP-1 activation through phosphorylation-induced release of preexisting c-Fos from its inhibitory interaction with lamin A/C.en_US
dc.description.sponsorshipThis work was supported by grants SAF2004-03057 and SAF2007-6211 (Spanish Ministry of Science and Innovation–MICINN, and European Regional Development Fund -FEDER), and RD06/0014/0021 (Red Temática de Investigación Cooperativa en Enfermedades Cardiovasculares, Instituto de Salud Carlos III –ISCIII). P. Crespo’s laboratory is supported by grants BFU2005-00777 and GEN2003-20239-C06-03 (MICINN), the EU Sixth Framework Program under the GROWTHSTOP (LSHC CT-2006-037731) and SIMAP (IST-2004-027265) projects, and RD06/0020/0105 (Red Temática de Investigación Cooperativa en Cáncer, ISCIII). JMG received salary support from ISCIII and a research grant from Generalitat Valenciana (GVPRE/2008/163).en_US
dc.format.extent3870787 bytes-
dc.publisherRockefeller University Pressen_US
dc.subjectA-type laminsen_US
dc.subjectNuclear envelopeen_US
dc.titleFast regulation of AP-1 activity through interaction of lamin A/C, ERK1/2, and c-Fos at the nuclear envelopeen_US
dc.description.peerreviewedPeer revieweden_US
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