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The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.

A Role for NBR1 in Autophagosomal Degradation of Ubiquitinated Substrates

Kirkin, Vladimir, Lamark, Trond, Sou, Yu-Shin, Bjørkøy, Geir, Nunn, Jennifer L., Bruun, Jack-Ansgar, Shvets, Elena, McEwan, David G., Clausen, Terje H., Wild, Philipp, Bilusic, Ivana, Theurillat, Jean-Philippe, Øvervatn, Aud, Ishii, Tetsuro, Elazar, Zvulun, Komatsu, Masaaki, Dikic, Ivan, Johansen, Terje·2009·Molecular Cell
DOI 10.1016/j.molcel.2009.01.020
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Abstract

Autophagy is a catabolic process where cytosolic cellular components are delivered to the lysosome for degradation. Recent studies have indicated the existence of specific receptors, such as p62, which link ubiquitinated targets to autophagosomal degradation pathways. Here we show that NBR1 (neighbor of BRCA1 gene 1) is an autophagy receptor containing LC3- and ubiquitin (Ub)-binding domains. NBR1 is recruited to Ub-positive protein aggregates and degraded by autophagy depending on an LC3-interacting region (LIR) and LC3 family modifiers. Although NBR1 and p62 interact and form oligomers, they can function independently, as shown by autophagosomal clearance of NBR1 in p62-deficient cells. NBR1 was localized to Ub-positive inclusions in patients with liver dysfunction, and depletion of NBR1 abolished the formation of Ub-positive p62 bodies upon puromycin treatment of cells. We propose that NBR1 and p62 act as receptors for selective autophagosomal degradation of ubiquitinated targets.

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Crossref · 10.1016/j.molcel.2009.01.020

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10 of 10 references verified0 citation errors · 0 not checkable

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  • GFP-LC3 is more stable than GFP-SQSTM1 or GFP-NBR1.

    “Although GFP-LC3 can be used as a reporter for flow cytometry, it is more stable (which is not necessarily ideal for flux measurements) than GFP-SQSTM1 or GFP-NBR1 (NBR1 is an autophagy receptor with structural similarity to SQSTM1 [496]).”

    From Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1 (2021) · cites this paper as [496]

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 19

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Metadata

Authors
Kirkin, V., Lamark, T., Sou, Y.-S., Bjørkøy, G., Nunn, J. L., Bruun, J.-A., Shvets, E., McEwan, D. G., Clausen, T. H., Wild, P., Bilusic, I., Theurillat, J.-P., Øvervatn, A., Ishii, T., Elazar, Z., Komatsu, M., Dikic, I., & Johansen, T.
Venue
Molecular Cell
Publisher
Elsevier BV
Published
2009-02
Volume
33
Issue
4
Pages
505-516
ISSN
1097-2765
DOI
10.1016/j.molcel.2009.01.020
Cited by
1,065
References
10
Language
en
Licence

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