Signaling Receptors for TGF-β Family Members

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This review describes how TGF-β family members signal through heterotetrameric receptor complexes regulated by posttranslational modifications and protein interactions, activating Smad-dependent and non-Smad pathways.

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Abstract

Transforming growth factor β (TGF-β) family members signal via heterotetrameric complexes of type I and type II dual specificity kinase receptors. The activation and stability of the receptors are controlled by posttranslational modifications, such as phosphorylation, ubiquitylation, sumoylation, and neddylation, as well as by interaction with other proteins at the cell surface and in the cytoplasm. Activation of TGF-β receptors induces signaling via formation of Smad complexes that are translocated to the nucleus where they act as transcription factors, as well as via non-Smad pathways, including the Erk1/2, JNK and p38 MAP kinase pathways, and the Src tyrosine kinase, phosphatidylinositol 3'-kinase, and Rho GTPases.

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MeSH descriptors

Receptors, Transforming Growth Factor beta Signal Transduction Transforming Growth Factor beta Cell Nucleus Cell Nucleus Cytoplasm Cytoplasm Endocytosis Humans Membrane Proteins Membrane Proteins MicroRNAs MicroRNAs Phosphorylation Protein Transport Receptors, Transforming Growth Factor beta Sumoylation Transforming Growth Factor beta Up-Regulation

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europepmc
last seen: 2026-10-18T09:30:06.152893+00:00
pubmed
last seen: 2026-10-08T21:18:17.876363+00:00
unpaywall
last seen: 2026-10-19T06:34:38.229974+00:00