Updated project metadata. Ventricle arrhythmias and atrial fibrillation resulting from alternation of intracellular Ca2+ handling capacity leads to pathological cardiac hypertrophy. Junctate-1 TG mouse model is considered as a genetic model of clinical relevant atrial fibrillation. Phosphorylation is one of the most important signaling cascade for cardiac hypertrophy. To further investigate the phosphoproteome changes during abnormal Ca2+ release in junctate-1, we carried out label-free LC-MS/MS coupled with IMAC phosphopeptide enrichment.