Signaling inputs converge on nuclear effectors in TGF-beta signaling.
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.
ten Dijke
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P
Ludwig Institute for Cancer Research, Box 595, S-751 24 Uppsala, Sweden. ptdijke@nki.nl
Miyazono
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K
Heldin
C H
CH
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*
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