Abstract 2535 Mitochondrial matrix Cu transport is required for cytoplasmic signaling and metabolic reprogramming
The transition metal copper (Cu) is an essential catalytic cofactor in the active sites of Cu-dependent enzymes responsible for a diverse range of biological functions including mitochondrial respiration and cellular proliferation. In the case of mitochondria, Cu import is facilitated by the dual Cu and phosphate carrier, SLC25A3, whose knockout causes loss in activity of Cu-dependent enzymes like the cytochrome c oxidase (COX) complex. Given that Cu homeostasis is integral to normal cell survival as evidenced by Menkes disease, surprisingly little is known about Cu-sensing mechanisms and their interaction with key signaling molecules that translates copper abundance to distinct cellular functions.
Authors
- Pedro Costa‐Pinheiro (ORCID: https://orcid.org/0000-0002-2049-6889)
- Donita C. Brady (ORCID: https://orcid.org/0000-0002-2786-2802)
- Scot C. Leary (ORCID: https://orcid.org/0000-0001-8488-7822)
- Paul A. Cobine (ORCID: https://orcid.org/0000-0001-6012-0985)
- Santanu Ghosh (ORCID: https://orcid.org/0000-0001-7201-2498)
- Gina M. DeNicola (ORCID: https://orcid.org/0000-0001-6611-6696)
- Yumi Kim (ORCID: https://orcid.org/0000-0001-8815-3121)
- Kathryn E. Wellen (ORCID: https://orcid.org/0000-0002-2281-0042)
Institutions
- California University of Pennsylvania (US)
Publication Details
- Journal
- Journal of Biological Chemistry
- Published
- 2025-05-01
- DOI
- https://doi.org/10.1016/j.jbc.2025.109534
- Primary Topic
- Metabolism and Genetic Disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00