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- W2056564957 abstract "The ability to balance self-renewal and differentiation is a hallmark of stem cells. In Drosophila neural stem cells (NSCs), Numb/Notch (N) signaling plays a key role in this process. However, the molecular and cellular mechanisms underlying Numb function in a stem cell setting remain poorly defined. Here we show that α-Adaptin (α-Ada), a subunit of the endocytic AP-2 complex, interacts with Numb through a new mode of interaction to regulate NSC homeostasis. In α-ada mutants, N pathway component Sanpodo and the N receptor itself exhibited altered trafficking, and N signaling was up-regulated in the intermediate progenitors of type II NSC lineages, leading to their transformation into ectopic NSCs. Surprisingly, although the Ear domain of α-Ada interacts with the C terminus of Numb and is important for α-Ada function in the sensory organ precursor lineage, it was dispensable in the NSCs. Instead, α-Ada could regulate Sanpodo, N trafficking, and NSC homeostasis by interacting with Numb through new domains in both proteins previously not known to mediate their interaction. This interaction could be bypassed when α-Ada was directly fused to the phospho-tyrosine binding domain of Numb. Our results identify a critical role for the AP-2-mediated endocytosis in regulating NSC behavior and reveal a new mechanism by which Numb regulates NSC behavior through N. These findings are likely to have important implications for cancer biology." @default.
- W2056564957 created "2016-06-24" @default.
- W2056564957 creator A5003671931 @default.
- W2056564957 creator A5068128871 @default.
- W2056564957 date "2012-05-01" @default.
- W2056564957 modified "2023-09-26" @default.
- W2056564957 title "Interaction of Notch Signaling Modulator Numb with α-Adaptin Regulates Endocytosis of Notch Pathway Components and Cell Fate Determination of Neural Stem Cells" @default.
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- W2056564957 doi "https://doi.org/10.1074/jbc.m112.360719" @default.
- W2056564957 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3366835" @default.
- W2056564957 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22474327" @default.
- W2056564957 hasPublicationYear "2012" @default.
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