GEO series
Perturb-seq uncovers pathological obstacles to direct cardiac reprogramming in vivo
GSE305453
Mus musculus
Expression profiling by high throughput sequencing
15 samples
2026/03/21
GPL24247
Summary
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
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Paper (PMID 41916284) ↗
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