Ablation of SOCS3 in Cardiomyocytes Exacerbates Cardiac hypertrophy and Dysfunction by Increasing GRP78-medieated ER Stress after pressure overload

ABSTRACT: To explore the mechanisms for SOCS3 in cardiomyocytes to regulate cardiac hypertrophic remodeling after pressure overload, we therefore performed proteomic analysis to identify novel protein targets or pathways in left ventricular samples from SOCS3 knockout (SOCS3cko) mice and their WT littermates.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Shuang Liu  

LAB HEAD: Huihua Li

PROVIDER: PXD014946 | Pride | 2021-09-08

REPOSITORIES: Pride