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Here we show that lamin A/C plays a vital role in embryonic stem cell formation, safeguarding nau00efve pluripotency and ensuring appropriate cell fate choices during cardiogenesis. Gata4 is triggered by lamin A/C loss, and Gata4 silencing or haploinsufficiency restores the irregular cardiovascular cell fate choices triggered by lamin A/C deficiency. We note in particular, that lamin A/C in nafve pluripotent stem cells and cardiomyocytes has divergent functions, which is consistent with patient with LMNA-associated cardiomyopathy. Ratemia inhibitory factor was measured for ATAC-seq, Conrol, Lmna H222P Homo, Lmna G609G Het, and Lmna G609G Tg mESCs on mitomycin treated mouse embryo embryonic fibroblasts with 15% fetal bovine serum, 2 mM L-glutamine, 0. 1 mM non-essential amino acids, 0. 1 mM sodium pyrut ml leukemia inhibitory factor, mo ml mo mna t mna Tg mna hemo hemna hemo t mna phosphate, 2 se, 1 se, tamine, mna tamine, mna mna, hetamine, mna, mna hemo mna.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/867576
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