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Cited by 659

The DOI matches its Crossref record; 62 of the 62 references it cites were found in a registry or an index.

FYCO1 is a Rab7 effector that binds to LC3 and PI3P to mediate microtubule plus end–directed vesicle transport

Open access
Pankiv, Serhiy, Alemu, Endalkachew A., Brech, Andreas, Bruun, Jack-Ansgar, Lamark, Trond, Øvervatn, Aud, Bjørkøy, Geir, Johansen, Terje·2010·Journal of Cell Biology

Abstract

Autophagy is the main eukaryotic degradation pathway for long-lived proteins, protein aggregates, and cytosolic organelles. Although the protein machinery involved in the biogenesis of autophagic vesicles is well described, very little is known about the mechanism of cytosolic transport of autophagosomes. In this study, we have identified an adaptor protein complex, formed by the two autophagic membrane-associated proteins LC3 and Rab7 and the novel FYVE and coiled-coil (CC) domain–containing protein FYCO1, that promotes microtubule (MT) plus end–directed transport of autophagic vesicles. We have characterized the LC3-, Rab7-, and phosphatidylinositol-3-phosphate–binding domains in FYCO1 and mapped part of the CC region essential for MT plus end–directed transport. We also propose a mechanism for selective autophagosomal membrane recruitment of FYCO1.

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Metadata

Authors
Pankiv, S., Alemu, E. A., Brech, A., Bruun, J.-A., Lamark, T., Øvervatn, A., Bjørkøy, G., & Johansen, T.
Venue
Journal of Cell Biology
Published
2010-01-25
Volume
188
Issue
2
Pages
253-269
ISSN
  • 0021-9525 (ISSN-L)
  • 1540-8140
OpenAlex
W2165218453
Cited by
659
References
62
FWCI
22.22
Type
journal article
Language
en
Open access
hybrid

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The paper
Pankiv, S., Alemu, E. A., Brech, A., Bruun, J.-A., Lamark, T., Øvervatn, A., Bjørkøy, G., & Johansen, T. (2010). FYCO1 is a Rab7 effector that binds to LC3 and PI3P to mediate microtubule plus end–directed vesicle transport. Journal of Cell Biology. https://doi.org/10.1083/jcb.200907015

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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