ArticlePloS one2016
PI3K/AKT Signaling Pathway Is Essential for Survival of Induced Pluripotent Stem Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Natural compounds as multitarget agents in Alzheimer's diseases: evidence fromFrontiers in pharmacology · 2026Pooled it
- Cholesteatoma: An Updated Review of Molecular Pathogenesis and Potential Therapeutic Directions.Current medicinal chemistry · 2026Review
- Topical medium-length PDRN enhances dermal extracellular matrix repair in photodamaged skin via PI3K-Akt/TGF-β-regulated pathways.PloS one · 2026Article
- Phytosterols from Rosaceae Species as Dual Modulators of Neuroinflammation and Induced Pluripotency.Journal of molecular neuroscience : MN · 2025Article
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- MAPK, PI3K/Akt Pathways, and GSK-3β Activity in Severe Acute Heart Failure in Intensive Care Patients: An Updated Review.Journal of cardiovascular development and disease · 2025Review
- MiR-3664-3p through suppressingHeliyon · 2025Article
- Metformin and the PI3K/AKT signaling pathway: implications for cancer, cardiovascular, and central nervous system diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Triazole-Estradiol Analogs Induce Apoptosis and Inhibit EGFR and Its Downstream Pathways in Triple Negative Breast Cancer.Molecules (Basel, Switzerland) · 2025Article
- Efficacy of Chlorogenic Acid in Treating Tripterygium Glycoside-Induced Asthenozoospermia in Rats and Its Possible Mechanisms.Veterinary sciences · 2025Article
- Mechanical scratch injury on differentiated motor neuron of NSC-34 cells as an in vitro model for evaluation of neuroregeneration potential of NeuroAiD II (MLC901).In vitro models · 2024Article
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- Article
- Article
- Review
- Advances in Genetic Reprogramming: Prospects from Developmental Biology to Regenerative Medicine.Current medicinal chemistry · 2024Review
- Improved Cryopreservation of Human Induced Pluripotent Stem Cell (iPSC) and iPSC-derived Neurons Using Ice-Recrystallization Inhibitors.Stem cells (Dayton, Ohio) · 2023Article
- An Alzheimer's disease risk variant in TTC3 modifies the actin cytoskeleton organization and the PI3K-Akt signaling pathway in iPSC-derived forebrain neurons.Neurobiology of aging · 2023Article
- Mechanisms Underlying Cognitive Impairment Induced by Prenatal Alcohol Exposure.Brain sciences · 2022Review
- Laminin-511 Activates the Human Induced Pluripotent Stem Cell Survival via α6β1 Integrin-Fyn-RhoA-ROCK Signaling.Stem cells and development · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis is a highly conserved biochemical mechanism which is tightly controlled in cells. It contributes to maintenance of tissue homeostasis and normally eliminates highly proliferative cells with malignant properties. Induced pluripotent stem cells (iPSCs) have recently been described with significant functional and morphological similarities to embryonic stem cells. Human iPSCs are of great hope for regenerative medicine due to their broad potential to differentiate into specialized cell types in culture. They may be useful for exploring disease mechanisms and may provide the basis for future cell-based replacement therapies. However, there is only poor insight into iPSCs cell signaling as the regulation of apoptosis. In this study, we focused our attention on the apoptotic response of Alzheimer fibroblast-derived iPSCs and two other Alzheimer free iPSCs to five biologically relevant kinase inhibitors as well as to the death ligand TRAIL. To our knowledge, we are the first to report that the relatively high basal apoptotic rate of iPSCs is strongly suppressed by the pancaspase inhibitor QVD-Oph, thus underlining the dependency on proapoptotic caspase cascades. Furthermore, wortmannin, an inhibitor of phosphoinositid-3 kinase / Akt signaling (PI3K-AKT), dramatically and rapidly induced apoptosis in iPSCs. In contrast, parental fibroblasts as well as iPSC-derived neuronal cells were not responsive. The resulting condensation and fragmentation of DNA and decrease of the membrane potential are typical features of apoptosis. Comparable effects were observed with an AKT inhibitor (MK-2206). Wortmannin resulted in disappearance of phosphorylated AKT and activation of the main effector caspase-3 in iPSCs. These results clearly demonstrate for the first time that PI3K-AKT represents a highly essential survival signaling pathway in iPSCs. The findings provide improved understanding on the underlying mechanisms of apoptosis regulation in iPSCs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.