ArticleNature communications2012
A crucial role for bone morphogenetic protein-Smad1 signalling in the DNA damage response.
Article in Nature communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- Post-translational modification crosstalk in pulmonary arterial hypertension: mechanisms and therapeutic implications.Molecular biology reports · 2026Review
- Human Placental Genomic Instability Predicts Adverse Pregnancy Outcomes.Research square · 2025Article
- BMP signaling promotes zebrafish heart regeneration via alleviation of replication stress.Nature communications · 2025Article
- Smad1 Promotes Tumorigenicity and Chemoresistance of Glioblastoma by Sequestering p300 From p53.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- BRCC3 Regulation of ALK2 in Vascular Smooth Muscle Cells: Implication in Pulmonary Hypertension.Circulation · 2024Article
- Article
- BMP4 enhances anoikis resistance and chemoresistance of breast cancer cells through canonical BMP signaling.Journal of cell communication and signaling · 2022Article
- The transcriptional cofactor Jab1/Cops5 is crucial for BMP-mediated mouse chondrocyte differentiation by repressing p53 activity.Journal of cellular physiology · 2021Article
- Isoforms of the p53 Family and Gastric Cancer: A Ménage à Trois for an Unfinished Affair.Cancers · 2021Review
- DNA damage response manages cell cycle restriction of senile multipotent mesenchymal stromal cells.Molecular biology reports · 2020Review
- TGF-β Family Signaling in Mesenchymal Differentiation.Cold Spring Harbor perspectives in biology · 2018Review
- The Dual Role of Bone Morphogenetic Proteins in Cancer.Molecular therapy oncolytics · 2018Review
- p53 inhibits SP7/Osterix activity in the transcriptional program of osteoblast differentiation.Cell death and differentiation · 2017Article
- c-Abl inhibits breast cancer tumorigenesis through reactivation of p53-mediated p21 expression.Oncotarget · 2016Article
- A potential role for protein palmitoylation and zDHHC16 in DNA damage response.BMC molecular biology · 2016Article
- The dynamic behavior of Ect2 in response to DNA damage.Scientific reports · 2016Article
- p57Kip2 is an unrecognized DNA damage response effector molecule that functions in tumor suppression and chemoresistance.Oncogene · 2015Article
- miR-181c associates with tumor relapse of high grade osteosarcoma.Oncotarget · 2015Article
- Augmented BMP signaling in the neural crest inhibits nasal cartilage morphogenesis by inducing p53-mediated apoptosis.Development (Cambridge, England) · 2015Article
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Corrections and comments
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Authors and funding
20 authors at 9 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA damage and the elicited cellular response underlie the etiology of tumorigenesis and ageing. Yet, how this response integrates inputs from cells' environmental cues remains underexplored. Here we report that the BMP-Smad1 pathway, which is essential for embryonic development and tissue homeostasis, has an important role in the DNA damage response and oncogenesis. On genotoxic stress, Atm phosphorylates BMPs-activated Smad1 in the nucleus on S239, which disrupts Smad1 interaction with protein phosphatase PPM1A, leading to enhanced activation and upregulation of Smad1. Smad1 then interacts with p53 and inhibits Mdm2-mediated p53 ubiquitination and degradation to regulate cell proliferation and survival. Enhanced Smad1 S239 phosphorylation, and Smad1 mutations causing S239 substitution were detected in oesophageal and gastric cancer samples, respectively. These findings suggest that BMP-Smad1 signalling participates in the DNA damage response via the Atm-p53 pathway, thus providing a molecular mechanism whereby BMP-Smad1 loss-of-function leads to tumorigenesis, for example, juvenile polyposis and Cowden syndromes.
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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.