Kate L. Weeks

β-Adrenergic Stimulation Induces Histone Deacetylase 5 (HDAC5) Nuclear Accumulation in Cardiomyocytes by B55α-PP2A-Mediated Dephosphorylation.

Phosphoinositide 3-kinase (p110α) gene delivery limits diabetes-induced cardiac NADPH oxidase and cardiomyopathy in a mouse model with established diastolic dysfunction.

The IGF1-PI3K-Akt Signaling Pathway in Mediating Exercise-Induced Cardiac Hypertrophy and Protection.

Understanding Key Mechanisms of Exercise-Induced Cardiac Protection to Mitigate Disease: Current Knowledge and Emerging Concepts.

Gene delivery of medium chain acyl-coenzyme A dehydrogenase induces physiological cardiac hypertrophy and protects against pathological remodelling.

Divergent Effects of PKC (Protein Kinase C) α in the Human and Animal Heart? Therapeutic Implications for PKC Inhibitors in Cardiac Patients.

Adeno-Associated Virus Gene Therapy: Translational Progress and Future Prospects in the Treatment of Heart Failure.

Nucleocytoplasmic shuttling: The ins and outs of quantitative imaging.

Role of type 2A phosphatase regulatory subunit B56α in regulating cardiac responses to β-adrenergic stimulation in vivo.

HDAC inhibitors and cardioprotection: Homing in on a mechanism of action.

Histone deacetylases in cardiovascular and metabolic diseases.

CORP: Practical tools for improving experimental design and reporting of laboratory studies of cardiovascular physiology and metabolism.

Gene therapy targeting cardiac phosphoinositide 3-kinase (p110α) attenuates cardiac remodeling in type 2 diabetes.

FoxO1 is required for physiological cardiac hypertrophy induced by exercise but not by constitutively active PI3K.

A protocol for rapid and parallel isolation of myocytes and non-myocytes from multiple mouse hearts.