ArticleCellular and molecular life sciences : CMLS2021
AP-1 activity is a major barrier of human somatic cell reprogramming.
Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Systemic epigenetic dysregulation as a driver of ageing and a therapeutic target.Nature reviews. Molecular cell biology · 2026Review
- Genome-wide investigation of transcription factor footprints and dynamics using cFOOT-seq.Protein & cell · 2025Article
- Reconstitution of pluripotency from mouse fibroblast through Sall4 overexpression.Nature communications · 2024Article
- Characterization of human pluripotent stem cell differentiation by single-cell dual-omics analyses.Stem cell reports · 2023Article
- The NuRD complex cooperates with SALL4 to orchestrate reprogramming.Nature communications · 2023Article
- Integration of ATAC-Seq and RNA-Seq reveals FOSL2 drives human liver progenitor-like cell aging by regulating inflammatory factors.BMC genomics · 2023Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Human induced pluripotent stem cells (iPSCs) technology has been widely applied to cell regeneration and disease modeling. However, most mechanism of somatic reprogramming is studied on mouse system, which is not always generic in human. Consequently, the generation of human iPSCs remains inefficient. Here, we map the chromatin accessibility dynamics during the induction of human iPSCs from urine cells. Comparing to the mouse system, we found that the closing of somatic loci is much slower in human. Moreover, a conserved AP-1 motif is highly enriched among the closed loci. The introduction of AP-1 repressor, JDP2, enhances human reprogramming and facilitates the reactivation of pluripotent genes. However, ESRRB, KDM2B and SALL4, several known pluripotent factors promoting mouse somatic reprogramming fail to enhance human iPSC generation. Mechanistically, we reveal that JDP2 promotes the closing of somatic loci enriching AP-1 motifs to enhance human reprogramming. Furthermore, JDP2 can rescue reprogramming deficiency without MYC or KLF4. These results indicate AP-1 activity is a major barrier to prevent chromatin remodeling during somatic cell reprogramming.
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Registered trials
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