Non-Smad pathways in TGF-beta signaling.
Transforming growth factor-beta utilizes a multitude of intracellular signaling pathways in addition to Smads to regulate a wide array of cellular functions. These non-canonical, non-Smad pathways are activated directly by ligand-occupied receptors to reinforce, attenuate, or otherwise modulate downstream cellular responses. These non-Smad pathways include various branches of MAP kinase pathways, Rho-like GTPase signaling pathways, and phosphatidylinositol-3-kinase/AKT pathways. This review focuses on recent advances in the understanding of the molecular and biochemical mechanisms of non-Smad pathways. In addition, functions of these non-Smad pathways are also discussed.
Zhang
Ying E
YE
Laboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. yingz@helix.nih.gov
D000818:Animals; D020935:MAP Kinase Signaling System; D051058:Oncogene Protein v-akt / Q000502:physiology; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D018125:Receptors, Transforming Growth Factor beta / Q000502:physiology*; D015398:Signal Transduction; D016212:Transforming Growth Factor beta / Q000502:physiology*; D020741:rho GTP-Binding Proteins / Q000502:physiology
D018125:Receptors, Transforming Growth Factor beta; D016212:Transforming Growth Factor beta; D019869:Phosphatidylinositol 3-Kinases; D051058:Oncogene Protein v-akt; D020741:rho GTP-Binding Proteins