6 results found
    1. Developmental Biology

    Fibrodysplasia ossificans progressiva mutant ACVR1 signals by multiple modalities in the developing zebrafish

    Robyn S Allen et al.
    The human Fibrodysplasia-Ossificans-Progressiva BMP-receptor mutant signals in zebrafish in the absence of ligand-binding, displays BMP ligand-responsive hyperactivity, neither requiring other type-I-BMP receptors, unlike wild-type, challenging views of the pathological mechanism.
    1. Biochemistry and Chemical Biology
    2. Cell Biology

    Activin A forms a non-signaling complex with ACVR1 and type II Activin/BMP receptors via its finger 2 tip loop

    Senem Aykul et al.
    The non-signaling complex formed by Activin A and ACVR1 is operant in vivo and is required to temper the degree of heterotopic ossification in the genetic disorder fibrodysplasia ossificans progressiva.
    1. Stem Cells and Regenerative Medicine

    Response to comment on 'Palovarotene reduces heterotopic ossification in juvenile FOP mice but exhibits pronounced skeletal toxicity'

    David J Goldhamer, John B Lees-Shepard
    We respond to concerns expressed by Pacifici and Shore (2019) about our recent paper (Lees-Shepard et al., 2018a).
    1. Stem Cells and Regenerative Medicine

    Comment on 'Palovarotene reduces heterotopic ossification in juvenile FOP mice but exhibits pronounced skeletal toxicity'

    Maurizio Pacifici, Eileen M Shore
    We are writing to communicate our concerns regarding the recently published study by Lees-Shepard et al. (2018).
    1. Stem Cells and Regenerative Medicine

    Palovarotene reduces heterotopic ossification in juvenile FOP mice but exhibits pronounced skeletal toxicity

    John B Lees-Shepard et al.
    Daily palovarotene treatment reduces pathogenic expansion of fibro/adipogenic progenitors but results in long bone growth plate loss and overgrowths of synovial cartilage in juvenile mice.
    1. Biochemistry and Chemical Biology
    2. Cell Biology

    TGF-β uses a novel mode of receptor activation to phosphorylate SMAD1/5 and induce epithelial-to-mesenchymal transition

    Anassuya Ramachandran et al.
    SMAD1/5 signaling is essential for the full transforming growth factor β (TGF-β)-induced transcriptional program and physiological responses and is induced via a novel receptor activation mechanism, involving two distinct type I receptors.

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