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• W2149887568 abstract "Although the physiological basis of canonical or classical IκB kinase β (IKKβ)-nuclear factor κB (NF-κB) signaling pathway is well established, how alternative NF-κB signaling functions beyond its role in lymphoid development remains unclear. In particular, alternative NF-κB signaling has been linked with cellular metabolism, but this relationship is poorly understood. In this study, we show that mice deleted for the alternative NF-κB components IKKα or RelB have reduced mitochondrial content and function. Conversely, expressing alternative, but not classical, NF-κB pathway components in skeletal muscle stimulates mitochondrial biogenesis and specifies slow twitch fibers, suggesting that oxidative metabolism in muscle is selectively controlled by the alternative pathway. The alternative NF-κB pathway mediates this specificity by direct transcriptional activation of the mitochondrial regulator PPAR-γ coactivator 1β (PGC-1β) but not PGC-1α. Regulation of PGC-1β by IKKα/RelB also is mammalian target of rapamycin (mTOR) dependent, highlighting a cross talk between mTOR and NF-κB in muscle metabolism. Together, these data provide insight on PGC-1β regulation during skeletal myogenesis and reveal a unique function of alternative NF-κB signaling in promoting an oxidative metabolic phenotype." @default.
• W2149887568 created "2016-06-24" @default.
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• W2149887568 date "2012-02-20" @default.
• W2149887568 modified "2023-10-14" @default.
• W2149887568 title "IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism" @default.
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• W2149887568 doi "https://doi.org/10.1083/jcb.201108118" @default.
• W2149887568 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3284000" @default.
• W2149887568 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22351927" @default.
• W2149887568 hasPublicationYear "2012" @default.
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