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- W4387356907 abstract "Notch receptors control tissue morphogenic processes that involve coordinated changes in cell architecture and gene expression, but how a single receptor can produce these diverse biological outputs is unclear. Here, we employ a 3D model of a human ductal epithelium to reveal tissue morphogenic defects result from loss of Notch1, but not Notch1 transcriptional signaling. Instead, defects in duct morphogenesis are driven by dysregulated epithelial cell architecture and mitogenic signaling which result from the loss of a transcription-independent, Notch1 cortical signaling mechanism that ultimately functions to stabilize adherens junctions and cortical actin. We identify that Notch1 localization and cortical signaling are tied to apical–basal cell restructuring and discover that a Notch1–FAM83H interaction underlies control of epithelial adherens junctions and cortical actin. Together, these results offer new insights into Notch1 signaling and regulation and advance a paradigm in which transcriptional and cell adhesive programs might be coordinated by a single receptor." @default.
- W4387356907 created "2023-10-06" @default.
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- W4387356907 date "2023-10-05" @default.
- W4387356907 modified "2023-10-17" @default.
- W4387356907 title "Notch1 cortical signaling regulates epithelial architecture and cell–cell adhesion" @default.
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- W4387356907 doi "https://doi.org/10.1083/jcb.202303013" @default.
- W4387356907 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37796194" @default.
- W4387356907 hasPublicationYear "2023" @default.
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