ArticleProceedings of the National Academy of Sciences of the United States of America2016
BMP-SMAD-ID promotes reprogramming to pluripotency by inhibiting p16/INK4A-dependent senescence.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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Who cites it
68 citing papers in PubMed, 115 citations in OpenAlex.
- Micropatterned neural induction with heat-inactivated extracellular matrix protein by on-demand high-speed laser.Regenerative therapy · 2026Article
- BMP4 cocktail promotes utricular progenitor reprogramming and vestibular functional recovery in adult mice.Journal of advanced research · 2026Article
- Biochemical principles of SMAD signaling across the animal kingdom.The Biochemical journal · 2026Review
- Human BMP4 mRNA Encapsulated in Lipid Nanoparticle for Bone and Articular Cartilage Repair in Aged Mice.Journal of functional biomaterials · 2026Article
- Reprogramming of Human Limbal Niche Progenitors.International journal of medical sciences · 2026Review
- Generation of human induced pluripotent stem cell lines derived from Wolf-Hirschhorn syndrome patients with chromosomal 4p deletion.Human cell · 2025Article
- Article
- Nanohybrid Hydrogel with Dual Functions: Controlled Low-Temperature Photothermal Antibacterial Activity and Promoted Regeneration for Treating MRSA-Infected Bone Defects.Advanced healthcare materials · 2025Article
- Reprogramming of skin fibroblasts by 3D spheroid culture promotes peripheral nerve regeneration via the ID3/semaphorin7a pathway.Stem cells translational medicine · 2025Article
- Generation of human induced pluripotent stem cell lines derived from patients of cystic biliary atresia.Human cell · 2024Article
- Article
- Timing and Graded BMP Signalling Determines Fate of Neural Crest and Ectodermal Placode Derivatives from Pluripotent Stem Cells.Biomedicines · 2024Review
- Cellular senescence by loss of Men1 in osteoblasts is critical for age-related osteoporosis.Aging cell · 2024Article
- An engineered human cardiac tissue model reveals contributions of systemic lupus erythematosus autoantibodies to myocardial injury.Nature cardiovascular research · 2024Article
- Cell fate decision by a morphogen-transcription factor-chromatin modifier axis.Nature communications · 2024Article
- PRDM6 promotes medulloblastoma by repressing chromatin accessibility and altering gene expression.Scientific reports · 2024Article
- Tracking single hiPSC-derived cardiomyocyte contractile function using CONTRAX an efficient pipeline for traction force measurement.Nature communications · 2024Article
- The NRF2/ID2 Axis in Vascular Smooth Muscle Cells: Novel Insights into the Interplay between Vascular Calcification and Aging.Aging and disease · 2024Article
- Cell Senescence in Heterotopic Ossification.Biomolecules · 2024Review
- Glycogen synthase kinase 3 signaling in neural regeneration in vivo.Journal of molecular cell biology · 2024Review
8 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
Fibrodysplasia ossificans progressiva (FOP) patients carry a missense mutation in ACVR1 [617G > A (R206H)] that leads to hyperactivation of BMP-SMAD signaling. Contrary to a previous study, here we show that FOP fibroblasts showed an increased efficiency of induced pluripotent stem cell (iPSC) generation. This positive effect was attenuated by inhibitors of BMP-SMAD signaling (Dorsomorphin or LDN1931890) or transducing inhibitory SMADs (SMAD6 or SMAD7). In normal fibroblasts, the efficiency of iPSC generation was enhanced by transducing mutant ACVR1 (617G > A) or SMAD1 or adding BMP4 protein at early times during the reprogramming. In contrast, adding BMP4 at later times decreased iPSC generation. ID genes, transcriptional targets of BMP-SMAD signaling, were critical for iPSC generation. The BMP-SMAD-ID signaling axis suppressed p16/INK4A-mediated cell senescence, a major barrier to reprogramming. These results using patient cells carrying the ACVR1 R206H mutation reveal how cellular signaling and gene expression change during the reprogramming processes.
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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.