ArticleStem cell research2019
Receptor interacting protein kinase 3 (RIP3) regulates iPSCs generation through modulating cell cycle progression genes.
Article in Stem cell research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- RIPK3 signaling and its role in regulated cell death and diseases.Cell death discovery · 2024Review
- Pervasive loss of regulated necrotic cell death genes in elephants, hyraxes, and sea cows (bioRxiv : the preprint server for biology · 2024Article
- RIPK necrotic cell death pathway in both donor photoreceptor and host immune cells synergize to affect photoreceptor graft survival.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Roles of RIPK3 in necroptosis, cell signaling, and disease.Experimental & molecular medicine · 2022Review
- RIPK3 signaling and its role in the pathogenesis of cancers.Cellular and molecular life sciences : CMLS · 2021Review
- Leaky Gut Driven by Dysbiosis Augments Activation and Accumulation of Liver MacrophagesFrontiers in immunology · 2021Article
- Apoptosis, the only cell death pathway that can be measured in human diploid dermal fibroblasts following lethal UVB irradiation.Scientific reports · 2020Article
- Acadesine suppresses TNF-α induced complement component 3 (C3), in retinal pigment epithelial (RPE) cells.PloS one · 2020Article
- RIP1 kinase mediates angiogenesis by modulating macrophages in experimental neovascularization.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The molecular mechanisms involved in induced pluripotent stem cells (iPSCs) generation are poorly understood. The cell death machinery of apoptosis-inducing caspases have been shown to facilitate the process of iPSCs reprogramming. However, the effect of other cell death processes, such as programmed necrosis (necroptosis), on iPSCs induction has not been studied. In this study, we investigated the role of receptor-interacting protein kinase 3 (RIP3), an essential regulator of necroptosis, in reprogramming mouse embryonic fibroblast cells (MEFs) into iPSCs. RIP3 was found to be upregulated in iPSCs compared to MEFs. Deletion of RIP3 dramatically suppressed the reprogramming of iPSCs (~82%). RNA-seq analysis and qRT-PCR showed that RIP3 KO MEFs expressed lower levels of genes that control cell cycle progression and cell division and higher levels of extracellular matrix-regulating genes. The growth rate of RIP3 KO MEFs was significantly slower than WT MEFs. These findings can partially explain the inhibitory effects of RIP3 deletion on iPSCs generation and show for the first time that the necroptosis kinase RIP3 plays an important role in iPSC reprogramming. In contrast to RIP3, the kinase and scaffolding functions of RIPK1 appeared to have distinct effects on reprogramming.
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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.