Increased excitation and decreased inhibition associated with abnormal neuronal morphology, aberrant ion channel properties, and synaptic dysfunction contribute to hyperexcitability in Alzheimer’s disease hiPSC-derived neuronal cultures and cerebral organoids.

Autism-associated iPSC-derived neurons mutant in CNTN5 or EHMT2 are hyperactive.

Evolutionarily conserved hypoxic stress response genes are depleted for association with expression quantitative trait loci.

During reprogramming of human fibroblasts to naïve iPSCs there is transient reactivation of transcripts with the characteristics of 8-cell-stage-embryos.

A panel of chimpanzee induced pluripotent stem cells (iPSCs) will help realise the potential of iPSCs in primate studies, and in combination with genomic technologies, transform studies of comparative evolution.

Genetic variants that modulate transcriptomic response to doxorubicin in human iPSC-derived cardiomyocytes are predictive of cardiac damage and in vivo sensitivity to anthracycline cardiotoxicity.

Jumu is required for the proper differentiation of prohemocytes and the proliferation and location of PSC cells.

Neural crest cells differentiated from patient-derived cells with mutations in the chromatin remodeler CHD7 show defective delamination, migration and motility in vitro, and defective migration in chick embryos.

Mutations causing proinsulin misfolding trigger unfolded protein response and lead to impaired proliferation and reduced mTORC1 signalling of developing beta-cells in a patient-derived induced pluripotent stem cell disease model.

Correction of the DNA methyltransferase 3B gene in ICF1 syndrome fails to rescue the abnormal DNA hypomethylation at subtelomeric regions due to accompanied epigenetic abnormalities in these regions.