In vivo Perturb-seq uncovers key obstacles to heart repair and regeneration through direct reprogramming
Ontology highlight
ABSTRACT: We investigated the mechanism underlying Calr suppression-enhanced cardiac reprogramming. As CALR functions as an ER-resident chaperone and Ca2+-binding protein, with Ca2+ acting as a second messenger in fate-determining pathways, particularly cardiogenesis we performed RNA-seq on MGTMyoS-induced MICFs transduced with shCalr or shNT at days 7 and 14 in vitro
ORGANISM(S): Mus musculus
PROVIDER: GSE305453 | GEO | 2026/03/21
REPOSITORIES: GEO
ACCESS DATA