Signaling inputs converge on nuclear effectors in TGF-beta signaling

Trends Biochem Sci. 2000 Feb;25(2):64-70. doi: 10.1016/s0968-0004(99)01519-4.


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.

Publication types

  • Review

MeSH terms

  • Animals
  • DNA / metabolism
  • DNA-Binding Proteins / metabolism*
  • Repressor Proteins / metabolism*
  • Signal Transduction*
  • Smad2 Protein
  • Smad3 Protein
  • Smad6 Protein
  • Trans-Activators / metabolism*
  • Transcription Factors / metabolism*
  • Transforming Growth Factor beta / metabolism*


  • DNA-Binding Proteins
  • Repressor Proteins
  • Smad2 Protein
  • Smad3 Protein
  • Smad6 Protein
  • Trans-Activators
  • Transcription Factors
  • Transforming Growth Factor beta
  • DNA