PMID:12543979

Citation	Tang, Y, Katuri, V, Dillner, A, Mishra, B, Deng, CX and Mishra, L (2003) Disruption of transforming growth factor-beta signaling in ELF beta-spectrin-deficient mice. Science 299:574-7
Abstract	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.
Links	PubMed Online version:10.1126/science.1075994
Keywords	Abnormalities, Multiple; Animals; Carrier Proteins/metabolism; Cell Membrane/metabolism; Cell Nucleus/metabolism; Contractile Proteins/metabolism; DNA-Binding Proteins/metabolism; Embryonic and Fetal Development; Gene Targeting; Genes, fos; Liver/abnormalities; Liver/embryology; Liver/metabolism; Mice; Mice, Knockout; Microfilament Proteins/metabolism; Microscopy, Confocal; Mutation; Phenotype; Phosphorylation; Platelet-Derived Growth Factor/pharmacology; Signal Transduction; Smad2 Protein; Smad3 Protein; Smad4 Protein; Spectrin/genetics; Spectrin/metabolism; Trans-Activators/metabolism; Transcriptional Activation; Transforming Growth Factor beta/metabolism; Transforming Growth Factor beta/pharmacology; Tumor Cells, Cultured
edit table

Annotations

Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
edit table

References

See Help:References for how to manage references in GONUTS.