LRRK2 and membrane trafficking: nexus of Parkinson's disease.
Journal
BMB reports
ISSN: 1976-670X
Titre abrégé: BMB Rep
Pays: Korea (South)
ID NLM: 101465334
Informations de publication
Date de publication:
Sep 2019
Sep 2019
Historique:
received:
27
06
2019
pubmed:
7
8
2019
medline:
17
3
2020
entrez:
7
8
2019
Statut:
ppublish
Résumé
Recent evidence from genetics, animal model systems and biochemical studies suggests that defects in membrane trafficking play an important part in the pathophysiology of Parkinson's disease (PD). Mutations in leucine-rich repeat kinase 2 (LRRK2) constitute the most frequent genetic cause of both familial and sporadic PD, and LRRK2 has been suggested as a druggable target for PD. Although the precise physiological function of LRRK2 remains largely unknown, mounting evidence suggests that LRRK2 controls membrane trafficking by interacting with key regulators of the endosomal-lysosomal pathway and synaptic recycling. In this review, we discuss the genetic, biochemical and functional links between LRRK2 and membrane trafficking. Understanding the mechanism by which LRRK2 influences such processes may contribute to the development of disease-modifying therapies for PD. [BMB Reports 2019; 52(9): 533-539].
Substances chimiques
Leucine-Rich Repeat Serine-Threonine Protein Kinase-2
EC 2.7.11.1
Types de publication
News
Langues
eng
Sous-ensembles de citation
IM
Pagination
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