180 results found
    1. Chromosomes and Gene Expression
    2. Genetics and Genomics

    Two locus inheritance of non-syndromic midline craniosynostosis via rare SMAD6 and common BMP2 alleles

    Andrew T Timberlake et al.
    Epistatic interactions of rare loss of function mutations in SMAD6 and a common variant modifier near BMP2 are the most common cause of midline craniosynostosis in humans.
    1. Chromosomes and Gene Expression

    Distinct modes of SMAD2 chromatin binding and remodeling shape the transcriptional response to NODAL/Activin signaling

    Davide M Coda et al.
    NODAL/Activin-induced SMAD2 binding directly drives remodeling of both open and closed chromatin and does not directly correlate with temporal patterns of gene expression upon prolonged signaling.
    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.
    1. Stem Cells and Regenerative Medicine

    Smad4 restricts differentiation to promote expansion of satellite cell derived progenitors during skeletal muscle regeneration

    Nicole D Paris et al.
    Ablation of canonical TGFβ signaling in muscle stem cells at any age is detrimental, and not beneficial, to effective skeletal muscle regeneration due to the promotion of premature fate commitment at the expense of progenitor amplification.
    1. Developmental Biology
    2. Stem Cells and Regenerative Medicine

    WNT signaling memory is required for ACTIVIN to function as a morphogen in human gastruloids

    Anna Yoney et al.
    The requirement for WNT signaling in mesendoderm differentiation is temporally separate from that of ACTIVIN signaling and acts to switch the output of ACTIVIN/SMAD2 from pluripotency maintenance to mesendoderm patterning.
    1. Chromosomes and Gene Expression

    Tissue damage drives co-localization of NF-κB, Smad3, and Nrf2 to direct Rev-erb sensitive wound repair in mouse macrophages

    Dawn Z Eichenfield et al.
    Combinatorial signaling leads to transcription factor co-localization at Rev-erb sensitive enhancers, enabling a diversified cellular response to complex stimuli.
    1. Developmental Biology

    Dullard-mediated Smad1/5/8 inhibition controls mouse cardiac neural crest cells condensation and outflow tract septation

    Jean-François Darrigrand et al.
    New views on the relevance of bone morphogenetic protein signalling fine tuning in the cardiac neural crest cells for the heart outflow tract septation and the formation of the great arteries.
    1. Stem Cells and Regenerative Medicine

    Tgfb3 collaborates with PP2A and notch signaling pathways to inhibit retina regeneration

    Mi-Sun Lee et al.
    Tgfb3 inhibits Muller glial cell reprogramming and drives Muller cell quiescence in the injured zebrafish retina, thereby inhibiting retina regeneration.
    1. Developmental Biology

    Hippo signaling determines the number of venous pole cells that originate from the anterior lateral plate mesoderm in zebrafish

    Hajime Fukui et al.
    The Hippo signaling restricts the number of SHF cardiomyocytes in the venous pole by negatively regulating Bmp-Smad signaling in the cells of lateral plate mesoderm.
    1. Developmental Biology

    Osteocalcin expressing cells from tendon sheaths in mice contribute to tendon repair by activating Hedgehog signaling

    Yi Wang et al.
    Cells in tendon sheaths, considered to be extrinsic tissues of tendon, possess stem or progenitor cell properties that are involved in tendon repair by activating the Hh-TGFb/Smad3 axis.

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