Probing the CaV1.2 interactome in heart failure identifies a positive modulator of inotropy and lusitropy

ABSTRACT: Maladaptive changes in the function, expression and localization of proteins involved in calcium-handling worsen the impaired contractility of systolic heart failure (HF). Standard proteomics techniques require cell lysis and so are unable to characterize changes specific to the critical sub-cellular domain bounded by the T-tubule and the sarcoplasmic reticulum, known as the cardiac dyad. Traditional approaches are also less likely to capture low-affinity protein-protein interactions on lipid membranes. To improve our understanding of heart failure pathophysiology, we applied proximity proteomics to cardiac dyads of mice with ischemic cardiomyopathy.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart, Cardiac Muscle Myoblast

DISEASE(S): Heart Failure

SUBMITTER: Marian Kalocsay  

LAB HEAD: Jared Kushner

PROVIDER: PXD063582 | Pride | 2026-04-15

REPOSITORIES: Pride