ArticleProceedings of the National Academy of Sciences of the United States of America2013
Rescue of a primary myelofibrosis model by retinoid-antagonist therapy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- SMRT regulation of nuclear receptors orchestrates bile acid homeostasis.Experimental & molecular medicine · 2026Article
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- Targeting nuclear receptor corepressors for reversible male contraception.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Review
- All-trans retinoic acid enhances, and a pan-RAR antagonist counteracts, the stem cell promoting activity of EVI1 in acute myeloid leukemia.Cell death & disease · 2019Article
- Bones in human CYP26B1 deficiency and rats with hypervitaminosis A phenocopyBone reports · 2018Article
- Genomic characterization of spleens in patients with myelofibrosis.Haematologica · 2018Article
- A retinoic acid-dependent stroma-leukemia crosstalk promotes chronic lymphocytic leukemia progression.Nature communications · 2018Article
- Efficacy of ALK5 inhibition in myelofibrosis.JCI insight · 2017Article
- Imaging Fibrosis and Separating Collagens using Second Harmonic Generation and Phasor Approach to Fluorescence Lifetime Imaging.Scientific reports · 2015Article
- Short linear motif acquisition, exon formation and alternative splicing determine a pathway to diversity for NCoR-family co-repressors.Open biology · 2015Article
- NCoR1 and SMRT play unique roles in thyroid hormone action in vivo.Molecular and cellular biology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Molecular targeting of the two receptor interaction domains of the epigenetic repressor silencing mediator of retinoid and thyroid hormone receptors (SMRT(mRID)) produced a transplantable skeletal syndrome that reduced radial bone growth, increased numbers of bone-resorbing periosteal osteoclasts, and increased bone fracture risk. Furthermore, SMRT(mRID) mice develop spontaneous primary myelofibrosis, a chronic, usually idiopathic disorder characterized by progressive bone marrow fibrosis. Frequently linked to polycythemia vera and chronic myeloid leukemia, myelofibrosis displays high patient morbidity and mortality, and current treatment is mostly palliative. To decipher the etiology of this disease, we identified the thrombopoietin (Tpo) gene as a target of the SMRT-retinoic acid receptor signaling pathway in bone marrow stromal cells. Chronic induction of Tpo in SMRT(mRID) mice results in up-regulation of TGF-β and PDGF in megakaryocytes, uncontrolled proliferation of bone marrow reticular cells, and fibrosis of the marrow compartment. Of therapeutic relevance, we show that this syndrome can be rescued by retinoid antagonists, demonstrating that the physical interface between SMRT and retinoic acid receptor can be a potential therapeutic target to block primary myelofibrosis disease progression.
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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.