LRRK2 signaling in neurodegeneration: two decades of progress.


Journal

Essays in biochemistry
ISSN: 1744-1358
Titre abrégé: Essays Biochem
Pays: England
ID NLM: 0043306

Informations de publication

Date de publication:
22 12 2021
Historique:
received: 26 08 2021
revised: 13 11 2021
accepted: 23 11 2021
pubmed: 14 12 2021
medline: 8 4 2022
entrez: 13 12 2021
Statut: ppublish

Résumé

Leucine-rich repeat kinase 2 (LRRK2) is a complex GTPase/kinase orchestrating cytoskeletal dynamics and multiple steps of the endolysosomal pathway through interaction with a host of partners and phosphorylation of a subset of Rab GTPases. Mutations in LRRK2 cause late-onset Parkinson's disease (PD) and common variants in the locus containing LRRK2 have been associated with sporadic PD, progressive supranuclear palsy as well as a number of inflammatory diseases. This review encompasses the major discoveries in the field of LRRK2 pathobiology, from the initial gene cloning to the latest progress in LRRK2 inhibition as a promising therapeutic approach to fight neurodegeneration.

Identifiants

pubmed: 34897411
pii: 230434
doi: 10.1042/EBC20210013
doi:

Substances chimiques

LRRK2 protein, human EC 2.7.11.1
Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 EC 2.7.11.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

859-872

Informations de copyright

© 2021 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.

Auteurs

Lucia Iannotta (L)

Department of Biology, University of Padova, Padova, Italy.

Elisa Greggio (E)

Department of Biology, University of Padova, Padova, Italy.

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Classifications MeSH