Author

M. R. Pricolo

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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Physiology· 2 Biophysics· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:host-pathogen & immune response· 3 Organism:human· 2 Organism:mouse· 2 Research Focus:cell signaling & trafficking· 1 Assay:imaging· 1 Approach:microscopy & imaging analysis· 1 Assay:protein sequence· 1

Frequent Co-Authors

C. Suay-Corredera· 2 shared D. Velazquez-Carreras· 2 shared E. Calvo· 2 shared E. Herrero-Galan· 2 shared F. Dominguez· 2 shared J. Alegre-Cebollada· 2 shared J. Vazquez· 2 shared L. Carrier· 2 shared

Activity by Year

2020-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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2 shared papersBiophysics

C. Suay-Corredera

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Author profile →

4 papers

Recent·Most cited

Broad therapeutic benefit of myosin inhibition in hypertrophic cardiomyopathy

L. Sen Martin, A. Fernandez Trasancos, M. A. Lopez Unzu, D. Pathak, A. Ferrarini, V. Labrador Cantarero, D. Sanchez Ortiz, M. R. Pricolo, N. Vicente, D. Velazquez Carreras, L. Sanchez Garcia, J. A. Nicolas Avila, M. Sanchez Diaz, S. Schlossarek, L. Cusso, , J. Alegre Cebollada

This study shows that myosin inhibition with mavacamten is effective in treating HCM caused by both truncating and missense variants in MYBPC3, despite different pathomechanisms.

bioRxiv · Mar 22, 2024Physiology

Imaging of existing and newly translated proteins elucidates mechanisms of sarcomere turnover

G. Douvdevany, I. Erlich, L. Haimovich-Caspi, T. Mashiah, M. Prondzynski, M. R. Pricolo, J. Alegre-Cebollada, W. A. Linke, L. Carrier, I. Kehat

The paper uses imaging to show that sarcomere proteins are replaced by newly translated ones, disproving the existing protein pool model and revealing a unidirectional replacement mechanism.

bioRxiv · Aug 31, 2023Cell Biology

Nanomechanical phenotypes in cMyBP-C mutants that cause hypertrophic cardiomyopathy

C. Suay-Corredera, M. R. Pricolo, D. Velazquez-Carreras, C. Pimenta-Lopes, D. Sanchez-Ortiz, I. Urrutia-Irazabal, S. Vilches, F. Dominguez, G. Frisso, L. Monserrat, P. Garcia-Pavia, E. Herrero-Galan, J. Alegre-Cebollada

This study investigates nanomechanical changes in cMyBP-C mutants linked to hypertrophic cardiomyopathy, finding that pathogenic mutations alter mechanical properties compared to non-pathogenic variants.

bioRxiv · Sep 19, 2020 · PreprintBiophysics

Conserved cysteines in titin sustain the mechanical function of cardiomyocytes

E. Herrero-Galan, F. Dominguez, I. Martinez-Martin, C. Sanchez-Gonzalez, N. Vicente, L. Lalaguna, E. Bonzon-Kulichenko, E. Calvo, E. Gonzalez-Lopez, M. Cobo-Marcos, B. Bornstein, A. Briceno, J. P. Ochoa, J. M. Garcia-Aznar, C. Suay-Corredera, , Aleg

The paper identifies that mutations in conserved titin cysteines disrupt mechanoredox control, leading to dilated cardiomyopathy in humans.

bioRxiv · Sep 5, 2020Physiology