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- W2014519647 abstract "DCC (deleted in colorectal cancer) is postulated to function as transmembrane receptor for the axon and cell guidance factor netrin-1. We report here that the DCC cytoplasmic domain binds to proteins encoded by mammalian homologs of the Drosophila seven in absentia (sina) gene, as well as Drosophila Sina. Sina has a critical role in R7 photoreceptor development and shows upward of 85% amino acid identity with its mammalian homologs (termed Siahs), but the function of the Sina/Siah proteins has not been defined. We sought, therefore, to characterize further their interaction with DCC. Immunofluorescence studies suggested the Sina/Siah proteins localized predominantly in the cytoplasm and in association with DCC. DCC was found to be ubiquitinated and the Sina/Siah proteins regulated its expression. Proteasome inhibitors blocked the effects of Sina/Siah on DCC, and the Sina/Siah proteins interacted with ubiquitin-conjugating enzymes (Ubcs). A mutant Siah protein lacking the amino-terminal Ubc-binding sequences complexed with DCC, but did not degrade it. The in vivo interaction between Sina/Siah and DCC was confirmed through studies of transgenic Drosophila lines in which DCC and Sina were ectopically expressed in the eye. Taken together, the data imply that the Sina/Siah proteins regulate DCC and perhaps other proteins via the ubiquitin-proteasome pathway." @default.
- W2014519647 created "2016-06-24" @default.
- W2014519647 creator A5018482931 @default.
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- W2014519647 creator A5090966682 @default.
- W2014519647 date "1997-10-15" @default.
- W2014519647 modified "2023-09-25" @default.
- W2014519647 title "Mammalian homologs of <i>seven in absentia</i> regulate DCC via the ubiquitin–proteasome pathway" @default.
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- W2014519647 doi "https://doi.org/10.1101/gad.11.20.2701" @default.
- W2014519647 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/316613" @default.
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