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Conserved role for 14‐3‐3ϵ downstream of type I TGFβ receptors
Author(s) -
McGonigle Sharon,
Beall Melissa J.,
Feeney Erika L.,
Pearce Edward J.
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)02133-0
Subject(s) - smad , receptor , microbiology and biotechnology , biology , signal transduction , transforming growth factor , phosphorylation , schistosoma mansoni , transforming growth factor beta , r smad , smad2 protein , genetics , immunology , tgf alpha , growth factor , schistosomiasis , helminths
Schistosoma mansoni receptor kinase‐1 (SmRK1) is a divergent type I transforming growth factor β (TGFβ) receptor on the surface of adult parasites. Using the intracellular domain of SmRK1 as bait in a yeast two‐hybrid screen we identified an interaction with S. mansoni 14‐3‐3ϵ. The interaction which is phosphorylation‐dependent is not specific to schistosomes since 14‐3‐3ϵ also binds to TβRI, the human type I TGFβ receptor. 14‐3‐3ϵ enhances TGFβ‐mediated signaling by TβRI and is the first TβRI‐interacting non‐Smad protein identified that positively regulates this receptor. The interaction of 14‐3‐3ϵ with schistosome and human TβRI suggests a conserved, but previously unappreciated, role for this protein in TGFβ signaling pathways.