Intronic polyadenylation of PDGFRα in resident stem cells attenuates muscle fibrosis
Alisa A. Mueller,
Cindy T. van Velthoven,
Kathryn D. Fukumoto,
Tom H. Cheung and
Thomas A. Rando ()
Additional contact information
Alisa A. Mueller: Paul F. Glenn Center for the Biology of Aging, Stanford University School of Medicine
Cindy T. van Velthoven: Paul F. Glenn Center for the Biology of Aging, Stanford University School of Medicine
Kathryn D. Fukumoto: Paul F. Glenn Center for the Biology of Aging, Stanford University School of Medicine
Tom H. Cheung: Paul F. Glenn Center for the Biology of Aging, Stanford University School of Medicine
Thomas A. Rando: Paul F. Glenn Center for the Biology of Aging, Stanford University School of Medicine
Nature, 2016, vol. 540, issue 7632, 276-279
Abstract:
Changes in intronic polyadenylation of the Pdgfra in fibro/adipogenic progenitors lead to increased expression of a shorter variant with a truncated kinase domain, which modulates pro-fibrotic pathways to reduce tissue fibrosis in muscle.
Date: 2016
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DOI: 10.1038/nature20160
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