Understanding the Cell Biology of Heart Arrhythmias

The Shaw Lab studies how cardiac ion channels are formed and delivered to their specific subdomains of the heart muscle cell membrane — and how that delivery changes in the failing heart — to develop novel diagnostics and therapeutics for heart failure.

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The Targeted Delivery Paradigm

The Shaw Laboratory defined the paradigm of Targeted Delivery, which describes how the cytoskeleton delivers membrane proteins directly to their functional membrane subdomain — and why there is less delivery in the failing heart. Our models explore Connexin43 gap junction trafficking to the cardiomyocyte intercalated disc and L-type calcium channel trafficking to cardiomyocyte T-tubules.

About Shaw Lab

Our Research

The Shaw Lab focuses on the cell biology of heart arrhythmias and heart failure progression — spanning RNA translation, cytoskeleton-based delivery of ion channels, heart failure mechanisms, and clinical studies of patients with heart failure.

Targeted Delivery — How the cytoskeleton delivers ion channels directly to their functional membrane subdomains, and why delivery is reduced in the failing heart.

GJA1-20k and Alternative Translation — Cx43 mRNA is alternatively translated to generate truncated isoforms; the most abundant, GJA1-20k, is essential for Connexin43 forward trafficking to the intercalated disc.

GJA1-20k and Mitochondrial Function — GJA1-20k organizes the actin cytoskeleton to regulate mitochondrial organization, transport, and function, including mitochondrial protection and ischemic preconditioning.

cBIN1 Biomarker and Therapeutics — Cardiac BIN1 folds T-tubule membrane and controls ion flux; blood-based cBIN1 forms the cBIN1 Score, a biomarker of cardiac muscle health, and cBIN1 gene therapy is being developed for heart failure.

Featured Publications

Recent publications highlight groundbreaking findings on the genetic mechanisms of heart disease, novel therapeutic approaches for heart failure, and innovative strategies for improving cardiovascular health outcomes.

Baum R, et al. A truncated isoform of Connexin43 caps actin to organize forward delivery of full-length Connexin43. Journal of Cell Biology. 2025.

Xiao S, et al. Auxiliary trafficking subunit GJA1-20k protects Connexin43 from degradation and limits ventricular arrhythmias. Journal of Clinical Investigation. 2020.

Hong T, et al. Cardiac BIN1 folds T-tubule membrane, controlling ion flux and limiting arrhythmia. Nature Medicine. 2014.

Palatinus JA, et al. GJA1-20k rescues Cx43 localization and arrhythmias in arrhythmogenic cardiomyopathy. Circulation Research. 2023.

Mentorship and Training

The Shaw Lab trains graduate students, postdoctoral fellows, medical students, and undergraduate researchers in the cell biology of heart arrhythmias and heart failure. Lab alumni have gone on to faculty and research positions at the University of Utah, Stanford, UCSF, Virginia Tech, and Cedars-Sinai.

Meet the Team

Faculty

Robin M. Shaw, MD, PhD

Nora Eccles Harrison Presidential Endowed Chair; Professor of Medicine; Director, Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI)

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