Integrated Quantitative Phosphoproteomics and Cell-based Functional Screening Reveals Specific Pathological Cardiac Hypertrophy-related Phosphorylation Sites

ABSTRACT: 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.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

DISEASE(S): Cardiovascular System Disease

SUBMITTER: Hye-Kyeong Kwon  

LAB HEAD: Zee-Yong Park

PROVIDER: PXD011421 | Pride | 2021-09-08

REPOSITORIES: Pride