Receptor expression modulates the specificity of transforming growth factor-β signaling pathways

• Published in: Genes to cells : devoted to molecular & cellular mechanisms Vol. 14; no. 4; pp. 469 - 482
• Main Authors: Murakami, Masaru, Kawachi, Hiroyuki, Ogawa, Kenji, Nishino, Yoshii, Funaba, Masayuki
• Format: Journal Article
• Language: English
• Published: Malden, USA Malden, USA : Blackwell Publishing Inc 01.04.2009; Blackwell Publishing Inc
• Subjects: Activin Receptors, Type I - genetics; Activin Receptors, Type I - metabolism; Animals; Blotting, Western; Bone Morphogenetic Protein 2 - pharmacology; Cell Line; Cell Line, Tumor; Cercopithecus aethiops; COS Cells; Dose-Response Relationship, Drug; Gene Expression; HeLa Cells; Humans; Imidazoles - pharmacology; Immunoprecipitation; Mice; Phosphorylation - drug effects; Protein-Serine-Threonine Kinases - genetics; Protein-Serine-Threonine Kinases - metabolism; Pyridines - pharmacology; Receptors, Transforming Growth Factor beta - genetics; Receptors, Transforming Growth Factor beta - metabolism; Reverse Transcriptase Polymerase Chain Reaction; RNA Interference; Signal Transduction; Smad Proteins, Receptor-Regulated - genetics; Smad Proteins, Receptor-Regulated - metabolism; Transforming Growth Factor beta1 - pharmacology

In current models of transforming growth factor-β (TGF-β) family signaling, type II receptors activate specific activin receptor-like kinase (ALK) type I receptors. These serine/threonine kinases activate ligand-dependent receptor regulated (R)-Smad by phosphorylating carboxy-terminal serines. We fo...