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The G2019S variant of leucine-rich repeat kinase 2 (LRRK2) alters endolysosomal trafficking by impairing the function of the GTPase RAB8A

Rivero-Ríos, Pilar, Romo-Lozano, María, Madero-Pérez, Jesús, Thomas, Andrew P., Biosa, Alice, Greggio, Elisa, Hilfiker, Sabine·2019·Journal of Biological Chemistry
DOI 10.1074/jbc.ra118.005008PMC PMC6442034
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  • The deficits in endolysosomal trafficking/degradation of the EGFR caused by RAB10 inactivation are accompanied by accumulation of the receptor in a RAB4-positive recycling compartment and by a decrease in the levels of active, GTP-bound RAB7A.

    “The deficits in endolysosomal trafficking/degradation of the EGFR by RAB10 inactivation are accompanied by the accumulation of the receptor in a RAB4-positive recycling compartment, and by a decrease in the levels of active, GTP-bound RAB7A, identical to what we previously described for pathogenic LRRK2 expression or knockdown of RAB8A [30,31].”

    From Distinct Roles for RAB10 and RAB29 in Pathogenic LRRK2-Mediated Endolysosomal Trafficking Alterations (2020) · cites this paper as [31]

  • Pathogenic LRRK2 expression impairs endolysosomal degradative trafficking and endocytic recycling of EGFR, with decreased active GTP-bound RAB7A and accumulation of the receptor in a RAB4-positive recycling compartment.

    “Pathogenic LRRK2 expression was found to impair the endolysosomal degradative trafficking as well as the endocytic recycling of the EGFR, with a concomitant decrease in the levels of active, GTP-bound RAB7A, and an accumulation of the receptor in a RAB4-positive recycling compartment [30,31].”

    From Distinct Roles for RAB10 and RAB29 in Pathogenic LRRK2-Mediated Endolysosomal Trafficking Alterations (2020) · cites this paper as [31]

  • RAB7A does not serve as a substrate for the LRRK2 kinase activity in vitro or in intact cells.

    “RAB7A does not serve as a substrate for the LRRK2 kinase activity in vitro or in intact cells [12,18,31]”

    From Distinct Roles for RAB10 and RAB29 in Pathogenic LRRK2-Mediated Endolysosomal Trafficking Alterations (2020) · cites this paper as [31]

  • All alterations due to pathogenic LRRK2 expression were mimicked by knockdown of RAB8A and rescued by expression of active RAB8A, suggesting they are mediated at least in part by RAB8A inactivation.

    “All alterations due to pathogenic LRRK2 expression were mimicked by knockdown of RAB8A and rescued by expression of active RAB8A, suggesting that they are mediated, at least in part, by RAB8A inactivation [31].”

    From Distinct Roles for RAB10 and RAB29 in Pathogenic LRRK2-Mediated Endolysosomal Trafficking Alterations (2020) · cites this paper as [31]

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Research works printed but not linked: 68

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Metadata

Authors
Rivero-Ríos, P., Romo-Lozano, M., Madero-Pérez, J., Thomas, A. P., Biosa, A., Greggio, E., & Hilfiker, S.
ORCID
Romo-Lozano, María
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2019-03
Volume
294
Issue
13
Pages
4738-4758
ISSN
0021-9258
DOI
10.1074/jbc.ra118.005008
PMC
PMC6442034
Cited by
83
References
4
Language
en
Licence
Funders
  • Michael J. Fox Foundation for Parkinson's Research (10255)
  • Ministerio de Economía y Competitividad (SAF2017–89402-R)

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