title: Signaling inputs converge on nuclear effectors in TGF-beta signaling.
abstract: Recent studies have consolidated the pivotal role of Smads as intracellular effectors of TGF-beta family members. Upon binding to their specific type I and type II serine/threonine kinase receptors, each family member activates a particular subset of Smad proteins. Activated, receptor-regulated Smads form hetero-oligomeric complexes with common-partner Smads that translocate into the nucleus, where they control the expression of target genes in a cell-type-specific manner. Smads appear to function not only as nuclear effectors for TGF-beta family members, but as signal integrators within an extensive intracellular network.
authors.affiliation: Ludwig Institute for Cancer Research, Box 595, S-751 24 Uppsala, Sweden. ptdijke@nki.nl
authors.forename: P
authors.initials: P
authors.lastname: ten Dijke
authors.forename: K
authors.initials: K
authors.lastname: Miyazono
authors.forename: C H
authors.initials: CH
authors.lastname: Heldin
mesh_terms: D000818:Animals; D004247:DNA / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism*; D012097:Repressor Proteins / Q000378:metabolism*; D015398:Signal Transduction; D051899:Smad2 Protein; D051900:Smad3 Protein; D051905:Smad6 Protein; D015534:Trans-Activators / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism*; D016212:Transforming Growth Factor beta / Q000378:metabolism*
chemical_list: D004268:DNA-Binding Proteins; D012097:Repressor Proteins; D051899:Smad2 Protein; D051900:Smad3 Protein; D051905:Smad6 Protein; D015534:Trans-Activators; D014157:Transcription Factors; D016212:Transforming Growth Factor beta; D004247:DNA