Taking the message to the nucleus: MAD protein as a mediator of bone morphogenetic protein signaling

in European Journal of Endocrinology
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The cell largely depends upon the actions of autocrine and paracrine peptide growth factors. After binding to, and activating, their respective serin/threonine or tyrosine kinase receptors, a diverse network of local growth factors orchestrates cellular proliferation and differentiation. Members of the transforming growth factor β (TGF-β) superfamily, usually disulfide-linked homodimers, play a crucial role in embryogenesis and growth as well as in reproductive and immune functions. These members (TGF-β, activin, bone morphogenetic proteins) exclusively bind to extracellularly located serin/threonine kinase receptors. Bone morphogenetic proteins (BMPs), originally identified by, and named after, their osteoinductive ability, constitute a major subgroup of the TGF-β superfamily (1, 2). Members of the BMPs have been implicated recently in early embryogenesis (3) and in shifting bone marrow stroma-residing pluripotent osteoprogenitor cells from the adipocyte to the osteoblast differentiation pathway (4). Although there is a steadily growing literature in bone cell biology on the cellular phenomena induced,

 

     European Society of Endocrinology

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