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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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SNT-2 interacts with ERK2 and negatively regulates ERK2 signaling in response to EGF stimulation.

The control of cellular responses with fibroblast growth factors and neurotrophins is mediated through membrane-linked docking proteins, SNT (suc1- binding neurotrophic target)-1/FRS2alpha and SNT-2/FRS2beta. ERK1/2 are members of the mitogen-activated protein kinase family that regulate diverse cellular activities in response to various stimuli. Here, we demonstrate that SNT-2 does not become tyrosine phosphorylated significantly in response to EGF but forms a complex with ERK2 via the region of 186-252 amino acid residues, and the complex formation is enhanced upon EGF stimulation. SNT-2 downregulates ERK2 phosphorylation, suppresses and delays ERK2 nuclear accumulation which occurs following EGF stimulation. In contrast, the mutant SNT-2 which carries deletion of 186-252 amino acids and lacks ERK2 binding does not have these effects. These observations suggest that SNT-2 negatively regulates ERK2 signaling activated via EGF stimulation through direct binding to ERK2.[1]

References

  1. SNT-2 interacts with ERK2 and negatively regulates ERK2 signaling in response to EGF stimulation. Huang, L., Gotoh, N., Zhang, S., Shibuya, M., Yamamoto, T., Tsuchida, N. Biochem. Biophys. Res. Commun. (2004) [Pubmed]
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