LRRK2 recruitment, activity, and function in organelles.

Abstract

Protein coding mutations in leucine-rich repeat kinase 2 (LRRK2) cause familial Parkinson's disease (PD), and noncoding variations around the gene increase the risk of developing sporadic PD. It is generally accepted that pathogenic LRRK2 mutations increase LRRK2 kinase activity, resulting in a toxic hyperactive protein that is inferred to lead to the PD phenotype. LRRK2 has long been linked to different membrane trafficking events, but the specific role of LRRK2 in these events has been difficult to resolve. Recently, several papers have reported the activation and translocation of LRRK2 to cellular organelles under specific conditions, which suggests that LRRK2 may influence intracellular membrane trafficking. Here, we review what is known about the role of LRRK2 at various organelle compartments.

• Authors: Luis Bonet-Ponce, Mark R Cookson
• Journal: The FEBS journal (FEBS J) Vol. 289 Issue 22 Pg. 6871-6890 (11 2022) ISSN: 1742-4658 [Electronic] England
• PMID: 34196120 (Publication Type: Journal Article, Review, Research Support, N.I.H., Intramural)
• Copyright: Published 2021. This article is a U.S. Government work and is in the public domain in the USA.

Chemical References

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

Topics

• Humans
• Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (genetics, metabolism)
• Parkinson Disease (pathology)
• Mutation
• Phenotype
• Organelles (genetics, metabolism)