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Perturb-seq uncovers pathological obstacles to direct cardiac reprogramming in vivo

GSE305453 Mus musculus Expression profiling by high throughput sequencing 15 samples Submitted 2026/03/21 Platform 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
Published in
Perturb-seq uncovers pathological obstacles to direct cardiac reprogramming in vivo
Cai Y, Yang Y, Yang J et al. · Cell stem cell 2026 · PMID 41916284 · doi:10.1016/j.stem.2026.03.006
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Direct links to NCBI, no account and no request form: the whole study as GSE305453_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 15 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1306002 and SRA study SRP608910. Searching any of these in the dataset finder brings you back here.

Study design
5 conditions, mostly in triplicate
MICF_0w ×3 shCalr_1w ×3 shCalr_2w ×3 shNT_1w ×3 shNT_2w ×3

Supports a between-group comparison across 15 samples.

5 replicated groups read from 15 sample titles; they account for 15 of them. Check it against the sample list below before relying on it.

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