ArticleMolecular biology of the cell2013
Notch signaling from the endosome requires a conserved dileucine motif.
Article in Molecular biology of the cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Endosomal trafficking protein TBC-2 modulates stress resistance and lifespan through DAF-16-dependent and independent mechanisms.Aging cell · 2023Article
- Endosomal trafficking protein TBC-2 is required for the longevity of long-lived mitochondrial mutants.Frontiers in aging · 2023Article
- Multiple Mechanisms of NOTCH1 Activation in Chronic Lymphocytic Leukemia: NOTCH1 Mutations and Beyond.Cancers · 2022Review
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- The Role of Intracellular Trafficking of Notch Receptors in Ligand-Independent Notch Activation.Biomolecules · 2021Review
- Notch3 in Development, Health and Disease.Biomolecules · 2020Review
- PI5P4Kγ functions in DTX1-mediated Notch signaling.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Glycogen synthase kinase 3β inhibition enhances Notch1 recycling.Molecular biology of the cell · 2018Article
- Progranulin promotes peripheral nerve regeneration and reinnervation: role of notch signaling.Molecular neurodegeneration · 2016Article
- Control of lysosomal biogenesis and Notch-dependent tissue patterning by components of the TFEB-V-ATPase axis in Drosophila melanogaster.Autophagy · 2016Article
- Ligand-Independent Mechanisms of Notch Activity.Trends in cell biology · 2015Review
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Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Notch signaling is reliant on γ-secretase-mediated processing, although the subcellular location where γ-secretase cleaves Notch to initiate signaling remains unresolved. Accumulating evidence demonstrates that Notch signaling is modulated by endocytosis and endosomal transport. In this study, we investigated the relationship between Notch transport itinerary and signaling capacity. In doing so, we discovered a highly conserved dileucine sorting signal encoded within the cytoplasmic tail that directs Notch to the limiting membrane of the lysosome for signaling. Mutating the dileucine motif led to receptor accumulation in cation-dependent mannose-phosphate receptor-positive tubular early endosomes and a reduction in Notch signaling capacity. Moreover, truncated receptor forms that mimic activated Notch were readily cleaved by γ-secretase within the endosome; however, the cleavage product was proteasome-sensitive and failed to contribute to robust signaling. Collectively these results indicate that Notch signaling from the lysosome limiting membrane is conserved and that receptor targeting to this compartment is an active process. Moreover, the data support a model in which Notch signaling in mammalian systems is initiated from either the plasma membrane or lysosome, but not the early endosome.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.