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Disruption of transforming growth factor-beta signaling in ELF beta-spectrin-deficient mice.

Disruption of the adaptor protein ELF, a beta-spectrin, leads to disruption of transforming growth factor-beta (TGF-beta) signaling by Smad proteins in mice. Elf-/- mice exhibit a phenotype similar to smad2+/-/smad3+/- mutant mice of midgestational death due to gastrointestinal, liver, neural, and heart defects. We show that TGF-beta triggers phosphorylation and association of ELF with Smad3 and Smad4, followed by nuclear translocation. ELF deficiency results in mislocalization of Smad3 and Smad4 and loss of the TGF-beta-dependent transcriptional response, which could be rescued by overexpression of the COOH-terminal region of ELF. This study reveals an unexpected molecular link between a major dynamic scaffolding protein and a key signaling pathway.

Pubmed ID: 12543979

Authors

  • Tang Y
  • Katuri V
  • Dillner A
  • Mishra B
  • Deng CX
  • Mishra L

Journal

Science (New York, N.Y.)

Publication Data

January 24, 2003

Associated Grants

  • Agency: NIDDK NIH HHS, Id: R01 DK56111
  • Agency: NIDDK NIH HHS, Id: R01 DK58637
  • Agency: NIDDK NIH HHS, Id: R03 DK53861

Mesh Terms

  • Abnormalities, Multiple
  • Animals
  • Carrier Proteins
  • Cell Membrane
  • Cell Nucleus
  • Contractile Proteins
  • DNA-Binding Proteins
  • Embryonic and Fetal Development
  • Filamins
  • Gene Targeting
  • Genes, fos
  • Liver
  • Mice
  • Mice, Knockout
  • Microfilament Proteins
  • Microscopy, Confocal
  • Mutation
  • Phenotype
  • Phosphorylation
  • Platelet-Derived Growth Factor
  • Signal Transduction
  • Smad2 Protein
  • Smad3 Protein
  • Smad4 Protein
  • Spectrin
  • Trans-Activators
  • Transcriptional Activation
  • Transforming Growth Factor beta
  • Tumor Cells, Cultured