Author

R. Acin-Perez

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Biochemistry· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:metabolism & bioenergetics· 2 Assay:metabolomics· 2 Approach:biophysical modeling· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

A. Petcherski· 2 shared O. S. Shirihai· 2 shared A. Bogdanova· 1 shared A. Cogolludo· 1 shared A. Cortes· 1 shared A. E. Jones· 1 shared A. Emili· 1 shared A. Hamvas· 1 shared

Activity by Year

2019-2020 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

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2 shared papersCell Biology

A. Petcherski

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Patient-specific iPSCs carrying an SFTPC mutation reveal the intrinsic alveolar epithelial dysfunction at the inception of interstitial lung disease

K.-D. Alysandratos, S. J. Russo, A. Petcherski, E. P. Taddeo, R. Acin-Perez, C. Villacorta-Martin, J.-C. Jean, S. Mulugeta, B. C. Blum, R. M. Hekman, M. Vedaie, S. Kook, J. A. Wambach, F. S. Cole, A. Hamvas, , D. N. Kotton

This study uses patient-derived iPSCs with an SFTPC mutation to model early alveolar epithelial dysfunction in interstitial lung disease, revealing proteostasis, metabolic, and inflammatory changes.

bioRxiv · Nov 13, 2020Cell Biology

Blocking mitochondrial pyruvate import causes energy wasting via futile lipid cycling in brown fat

M. Veliova, C. Mendes Ferreira, I. Y. Benador, A. E. Jones, B. R. Desousa, K. Mahdaviani, R. Acin-Perez, A. Petcherski, A. S. Divakaruni, M. Prentki, B. E. Corkey, M. Liesa, M. F. Oliveira, O. S. Shirihai

The paper shows that blocking mitochondrial pyruvate import increases ATP synthesis via futile lipid cycling in brown adipocytes, enhancing energy expenditure without adrenergic stimulation.

bioRxiv · Nov 15, 2019 · PreprintBiochemistry

Mitochondrial Na+ controls oxidative phosphorylation and hypoxic redox signalling

P. Hernansanz-Agustin, C. Choya-Foces, S. Carregal-Romero, E. Ramos, T. Oliva, T. Villa-Pina, L. Moreno, A. Izquierdo-Alvarez, J. D. Cabrera-Garcia, A. Cortes, A. V. Lechuga-Vieco, P. Jadiya, E. Navarro, E. Parada, A. Palomino-Antolin, , A. Martinez-Ruiz

This study shows that mitochondrial Na+ acts as a second messenger regulating OXPHOS and ROS production through interactions with phospholipids during hypoxia.

bioRxiv · Oct 31, 2019Biochemistry