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- W2052521454 abstract "Mutations that inactivate either merlin (mer) or expanded (ex) result in increased cell growth and proliferation in Drosophila. Both Mer and Ex are members of the Band 4.1 protein superfamily, and, based on analyses of mer ex double mutants, they are proposed to function together in at least a partially redundant manner upstream of the Hippo (Hpo) and Warts (Wts) proteins to regulate cell growth and division. By individually analyzing ex and mer mutant phenotypes, we have found important qualitative and quantitative differences in the ways Mer and Ex function to regulate cell proliferation and cell survival. Though both mer and ex restrict cell and tissue growth, ex clones exhibit delayed cell cycle exit in the developing eye, while mer clones do not. Conversely, loss of mer substantially compromises normal developmental apoptosis in the pupal retina, while loss of ex has only mild effects. Finally, ex has a role in regulating Wingless protein levels in the eye that is not obviously shared by either mer or hpo. Taken together, our data suggest that Mer and Ex differentially regulate multiple downstream pathways." @default.
- W2052521454 created "2016-06-24" @default.
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- W2052521454 creator A5017223407 @default.
- W2052521454 creator A5020659886 @default.
- W2052521454 creator A5055398277 @default.
- W2052521454 date "2007-04-01" @default.
- W2052521454 modified "2023-10-18" @default.
- W2052521454 title "The Drosophila tumor suppressors Expanded and Merlin differentially regulate cell cycle exit, apoptosis, and Wingless signaling" @default.
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- W2052521454 doi "https://doi.org/10.1016/j.ydbio.2006.12.021" @default.
- W2052521454 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1924969" @default.
- W2052521454 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17258190" @default.
- W2052521454 hasPublicationYear "2007" @default.
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