Author

J. Jalife

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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Cell Biology· 2

Signature Assays, Organisms & Methods

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Research Focus:cell signaling & trafficking· 2 Assay:electrophysiology· 2 Approach:experimental assay· 2 Research Focus:cell type annotation· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1

Frequent Co-Authors

A. Macias· 2 shared F. M. Cruz· 2 shared M. L. Vera-Pedrosa· 2 shared A. Gonzalez-Guerra· 1 shared A. I. Moreno-Manuel· 1 shared A. J. Cuttita· 1 shared A. Monteiro da Rocha· 1 shared D. E. Michele· 1 shared

Activity by Year

2021-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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2 shared papersCell Biology

A. Macias

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

SNTA1 GeneRescues Ion Channel Function in Cardiomyocytes Derived from Induced Pluripotent Stem Cells Reprogrammed from Muscular Dystrophy Patients with Arrhythmias

J. Jalife, E. N. Jimenez-Vazquez, M. Arad, A. Macias, M. L. Vera-Pedrosa, F. M. Cruz, A. J. Cuttita, A. Monteiro da Rocha, T. J. Herron, D. Ponce-Balbuena, G. Guerrero-Serna, O. Binah, D. E. Michele

This study shows that iPSC-CMs from DMD patients with arrhythmias have NaV1.5-Kir2.1 channelosome dysfunction, which can be rescued by 1-syntrophin.

bioRxiv · Jan 25, 2022 · PreprintCell Biology

Dual Dysfunction of Kir2.1 Underlies Conduction and Excitation-Contraction Coupling Defects Promoting Arrhythmias in a Mouse Model of Andersen-Tawil Syndrome Type 1

A. Macias, A. Gonzalez-Guerra, A. I. Moreno-Manuel, F. M. Cruz, N. Garcia-Quintans, L. K. Gutierrez, M. Roche-Molina, F. J. Bermudez-Jimenez, V. Andres, M. L. Vera-Pedrosa, I. Martinez-Carrascoso, J. A. Bernal, J. Jalife

This study identifies a dual dysfunction of Kir2.1 in a mouse model of ATS1, linking it to conduction and excitation-contraction coupling defects that promote arrhythmias.

bioRxiv · Jun 17, 2021 · PreprintCell Biology