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Mitochondrial dysfunction reactivates α-fetoprotein expression that drives copper-dependent immunosuppression in mitochondrial disease models.
Jett KA, Baker ZN, Hossain A, Boulet A, Cobine PA, Ghosh S, Ng P, Yilmaz O, Barreto K, DeCoteau J, Mochoruk K, Ioannou GN, Savard C, Yuan S, Abdalla OH, Lowden C, Kim BE, Cheng HM, Battersby BJ, Gohil VM, Leary SC. Jett KA, et al. Among authors: boulet a. J Clin Invest. 2023 Jan 3;133(1):e154684. doi: 10.1172/JCI154684. J Clin Invest. 2023. PMID: 36301669 Free PMC article.
Elesclomol restores mitochondrial function in genetic models of copper deficiency.
Soma S, Latimer AJ, Chun H, Vicary AC, Timbalia SA, Boulet A, Rahn JJ, Chan SSL, Leary SC, Kim BE, Gitlin JD, Gohil VM. Soma S, et al. Among authors: boulet a. Proc Natl Acad Sci U S A. 2018 Aug 7;115(32):8161-8166. doi: 10.1073/pnas.1806296115. Epub 2018 Jul 23. Proc Natl Acad Sci U S A. 2018. PMID: 30038027 Free PMC article.
The Mitochondrial Metallochaperone SCO1 Is Required to Sustain Expression of the High-Affinity Copper Transporter CTR1 and Preserve Copper Homeostasis.
Hlynialuk CJ, Ling B, Baker ZN, Cobine PA, Yu LD, Boulet A, Wai T, Hossain A, El Zawily AM, McFie PJ, Stone SJ, Diaz F, Moraes CT, Viswanathan D, Petris MJ, Leary SC. Hlynialuk CJ, et al. Among authors: boulet a. Cell Rep. 2015 Feb 17;10(6):933-943. doi: 10.1016/j.celrep.2015.01.019. Epub 2015 Feb 13. Cell Rep. 2015. PMID: 25683716 Free article.