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  4. NUFIP1 is a ribosome receptor for starvation-induced ribophagy

NUFIP1 is a ribosome receptor for starvation-induced ribophagy

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sword-2020-01-30T14:11:15.original.xml (130 B)
Original SWORD entry document
Author(s)
Wyant, Gregory A.
•
Abu-Remaileh, Monther
•
Frenkel, Evgeni M.
•
Laqtom, Nouf N.
•
Dharamdasani, Vimisha
•
Lewis, Caroline A.
•
Chan, Sze Ham
•
Sabatini, David M.
Date Issued
April 26, 2018
Journal
Science
Publisher
American Association for the Advancement of Science (AAAS)
Citation
Wyant, Gregory A. et al. "NUFIP1 is a ribosome receptor for starvation-induced ribophagy." Science 360 (2018): 751-758 © 2018 The Author(s)
Version
Author's final manuscript
Abstract
The lysosome degrades and recycles macromolecules, signals to the master growth regulator mTORC1 [mechanistic target of rapamycin (mTOR) complex 1], and is associated with human disease.We performed quantitative proteomic analyses of rapidly isolated lysosomes and found that nutrient levels and mTOR dynamically modulate the lysosomal proteome. Upon mTORC1 inhibition, NUFIP1 (nuclear fragile Xmental retardation-interacting protein 1) redistributes from the nucleus to autophagosomes and lysosomes. Upon these conditions, NUFIP1 interacts with ribosomes and delivers them to autophagosomes by directly binding to microtubule-associated proteins 1A/1B light chain 3B (LC3B).The starvation-induced degradation of ribosomes via autophagy (ribophagy) depends on the capacity of NUFIP1 to bind LC3B and promotes cell survival.We propose that NUFIP1 is a receptor for the selective autophagy of ribosomes.
Subjects
Multidisciplinary
MIT Department
Whitehead Institute for Biomedical Research
Massachusetts Institute of Technology. Department of Biology
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
Persistent DSpace Link
https://hdl.handle.net/1721.1/124713
DOI of Published Version
https://doi.org/10.1126/science.aar2663
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