Cited by 105Mitochondrial Function and PathologyNF-κB Signaling PathwaysCell death mechanisms and regulation

NF-κB pathway controls mitochondrial dynamics

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Laforge, M, Rodrigues, V, Silvestre, R, Gautier, C, Weil, R, Corti, O, Estaquier, J·2016·Cell Death & Differentiation

Abstract

The Optic atrophy 1 protein (OPA1) is a key element in the dynamics and morphology of mitochondria. We demonstrated that the absence of IκB 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-κB essential modulator (NEMO) or IκB kinase-β, both of which are essential for the canonical NF-κB 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 PARK2 overexpression did not modify the expression of OPA1. PARK2 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-κB pathway in the regulation of mitochondrial dynamics and OPA1 expression.

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References 31 · Cited by 105

Authors
Laforge, M., Rodrigues, V, Silvestre, R., Gautier, C., Weil, R., Corti, O., & Estaquier, J.
Affiliations
  • Centre National de la Recherche Scientifique (FR)
  • University of Minho (PT)
Corresponding author
Estaquier, J
Venue
Cell Death & Differentiation
Published
2015-05-29
Volume
23
Issue
1
Pages
89-98
ISSN
  • 1350-9047 (ISSN-L)
  • 1476-5403
OpenAlex
W423113600
Cited by
105
References
31
Citations by year
2026: 9 · 2025: 9 · 2024: 18 · 2023: 11 · 2022: 12 · 2021: 11 · 2020: 11 · 2019: 10 · 2018: 6 · 2017: 2 · 2016: 6
FWCI
2.03
Type
journal article
Language
en
Open access
Locations
  • Cell Death and Differentiation (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • HAL (submittedVersion, cc-by-nc-nd)
  • HAL (submittedVersion)
  • Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion, other-oa)
Funders
  • Styrelsen för Internationellt Utvecklingssamarbete
  • Association pour la Recherche sur le Cancer
  • Agence Nationale de la Recherche (ANR-10-IAIHU06, 10-IAIHU-06, ANR-10, ANR-10-IAHU-0006)
  • Fondation pour la Recherche Médicale (ANR-10-IAIHU-06)
  • Agence Nationale de Recherches sur le Sida et les Hépatites Virales
  • Ligue Contre le Cancer
  • Fundação para a Ciência e a Tecnologia (SFRH/BD/64064/2009, /2009)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
NF-κB signaling, mitochondrial dynamics, OPA1, IkappaB kinase alpha, NEMO, IκB kinase β, Parkin, Bax, Bak, mitochondrial morphology, stress-induced cell death, mouse embryonic fibroblasts
MeSH terms
Animals, Cell Line, Fibroblasts, Mitochondria, Signal Transduction, NF-kappa B, Apoptosis, Gene Expression Regulation, Developmental, GTP Phosphohydrolases, Ubiquitin-Protein Ligases, Intracellular Signaling Peptides and Proteins, bcl-2-Associated X Protein, Mice, I-kappa B Kinase

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