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Article

BMP-SMAD-ID promotes reprogramming to pluripotency by inhibiting p16/INK4A-dependent senescence.

Proceedings of the National Academy of Sciences of the United States of America - 15 Nov 2016

Hayashi Yohei, Hsiao Edward C, Sami Salma, Lancero Mariselle, Schlieve Christopher R, Nguyen Trieu, Yano Koyori, Nagahashi Ayako, Ikeya Makoto, Matsumoto Yoshihisa, Nishimura Ken, Fukuda Aya, Hisatake Koji, Tomoda Kiichiro, Asaka Isao, Toguchida Junya, Conklin Bruce R, Yamanaka Shinya

Abstract excerpt

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...

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Share to Activin Receptors, Type I
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cellular Reprogramming

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Share to Cyclin-Dependent Kinase Inhibitor p16

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Source

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Identifiers

PMID: 27794120
DOI: 10.1073/pnas.1603668113
PMCID: PMC5135304

Genes

ACVR1
BMP4
SMAD1
SMAD6
SMAD7

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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