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Novel determinants of NOTCH1 trafficking and signaling in breast epithelial cells. | LitMetric

AI Article Synopsis

  • - The Notch signaling pathway is crucial for communication between cells and is important for development and maintaining tissue health; when it goes wrong, it can lead to issues like congenital disorders and cancers.
  • - Researchers developed methods to track how the human NOTCH1 receptor behaves in breast cells and conducted a large screening of 2,749 genes to find new Notch regulators that could be targeted for drug development.
  • - They discovered 39 new molecules that affect NOTCH1, with some enhancing its function by aiding its movement within the cell, while others can inhibit it and can be targeted with drugs, suggesting potential new treatments for diseases related to Notch signaling.

Article Abstract

The evolutionarily conserved Notch signaling pathway controls cell-cell communication, enacting cell fate decisions during development and tissue homeostasis. Its dysregulation is associated with a wide range of diseases, including congenital disorders and cancers. Signaling outputs depend on maturation of Notch receptors and trafficking to the plasma membrane, endocytic uptake and sorting, lysosomal and proteasomal degradation, and ligand-dependent and independent proteolytic cleavages. We devised assays to follow quantitatively the trafficking and signaling of endogenous human NOTCH1 receptor in breast epithelial cells in culture. Based on such analyses, we executed a high-content screen of 2,749 human genes to identify new regulators of Notch that might be amenable to pharmacologic intervention. We uncovered 39 new NOTCH1 modulators for NOTCH1 trafficking and signaling. Among them, we find that and act as positive NOTCH1 regulators by promoting endocytic trafficking and NOTCH1 maturation in the Golgi apparatus, respectively, whereas serves as a negative regulator that can be modulated by pharmacologic inhibition. Our findings might be relevant in the search of new strategies to counteract pathologic Notch signaling.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11633778PMC
http://dx.doi.org/10.26508/lsa.202403122DOI Listing

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