NF-κB pathway controls mitochondrial dynamics
Identifieur interne : 000577 ( Main/Merge ); précédent : 000576; suivant : 000578NF-κB pathway controls mitochondrial dynamics
Auteurs : M. Laforge [France] ; V. Rodrigues [France, Portugal] ; R. Silvestre [Portugal] ; C. Gautier [France] ; R. Weil [France] ; O. Corti [France] ; J. Estaquier [France, Canada]Source :
- Cell Death and Differentiation [ 1350-9047 ] ; 2015.
Abstract
The Optic atrophy 1 protein (OPA1) is a key element in the dynamics and morphology of mitochondria. We demonstrated that the absence of I
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DOI: 10.1038/cdd.2015.42
PubMed: 26024391
PubMed Central: 4815975
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Laforge</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>CNRS FR 3636, Université Paris Descartes</institution>, Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Rodrigues, V" sort="Rodrigues, V" uniqKey="Rodrigues V" first="V" last="Rodrigues">V. Rodrigues</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>CNRS FR 3636, Université Paris Descartes</institution>, Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Parasite Disease Group, Instituto de Biologia Molecular e Celular, Universidade do Porto</institution>, Porto,<country>Portugal</country></nlm:aff><country xml:lang="fr">Portugal</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Silvestre, R" sort="Silvestre, R" uniqKey="Silvestre R" first="R" last="Silvestre">R. Silvestre</name><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho; ICVS/3B's-PT Government Associate Laboratory</institution>, Braga/Guimarães,<country>Portugal</country></nlm:aff><country xml:lang="fr">Portugal</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Gautier, C" sort="Gautier, C" uniqKey="Gautier C" first="C" last="Gautier">C. 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Weil</name><affiliation wicri:level="1"><nlm:aff id="aff7"><institution>Unité de Signalisation Moléculaire et Activation Cellulaire, Institut Pasteur, Unité CNRS URA 2582</institution>, Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Corti, O" sort="Corti, O" uniqKey="Corti O" first="O" last="Corti">O. Corti</name><affiliation wicri:level="1"><nlm:aff id="aff4"><institution>Inserm, U 1127</institution>, F-75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff5"><institution>CNRS, UMR 7225</institution>, F-75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff6"><institution>Sorbonne Universités, UPMC Univ Paris 06, UMR S 1127</institution>, F-75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Estaquier, J" sort="Estaquier, J" uniqKey="Estaquier J" first="J" last="Estaquier">J. Estaquier</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>CNRS FR 3636, Université Paris Descartes</institution>, Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff8"><institution>Centre de Recherche en Infectiologie, Université Laval</institution>, Québec,<country>Canada</country></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Cell Death and Differentiation</title><idno type="ISSN">1350-9047</idno><idno type="eISSN">1476-5403</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The Optic atrophy 1 protein (OPA1) is a key element in the dynamics and morphology of mitochondria. We demonstrated that the absence of I<italic>κ</italic>B kinase-α, which is a key element of the nonclassical NF-κB pathway, has an impact on the mitochondrial network morphology and OPA1 expression. In contrast, the absence of NF-<italic>κ</italic>B essential modulator (NEMO) or I<italic>κ</italic>B kinase-β, both of which are essential for the canonical NF-<italic>κ</italic>B pathway, has no impact on mitochondrial dynamics. Whereas Parkin has been reported to positively regulate the expression of OPA1 through NEMO, herein we found that <italic>PARK2</italic> overexpression did not modify the expression of OPA1. <italic>PARK2</italic> expression reduced the levels of Bax, and it prevented stress-induced cell death only in Bak-deficient mouse embryonic fibroblast cells. Collectively, our results point out a role of the nonclassical NF-<italic>κ</italic>B pathway in the regulation of mitochondrial dynamics and OPA1 expression.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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