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- Title
Editorial: LRRK2—Fifteen Years From Cloning to the Clinic.
- Authors
Rideout, Hardy; Greggio, Elisa; Kortholt, Arjan; Nichols, R. Jeremy
- Abstract
Kuwahara and Iwatsubo discuss how LRRK2 signaling to multiple Rab GTPases implicate LRRK2 kinase dysfunction as a driver of endolysosomal pathomechanisms in PD. Along these lines, Cabezudo et al. discuss how mutant LRRK2-driven inflammation may trigger PD starting from peripheral organs such as the gut and immune circulating cells, according to a multiple-hit hypothesis for PD. Keywords: LRRK2; Parkinson's disease; lysosome; endosome; biomarker; kinase; alpha-synuclein; phosphorylation EN LRRK2 Parkinson's disease lysosome endosome biomarker kinase alpha-synuclein phosphorylation 1 4 4 04/14/22 20220411 NES 220411 In the time since the identification of LRRK2 at the PARK8 locus as the responsible gene mutated in a common autosomal dominantly inherited form of Parkinson's disease (Paisan-Ruiz et al., [8]; Zimprich et al., [10]), it has become increasingly evident that activity of this protein plays a crucial role in disease pathogenesis of Parkinson's disease (PD). Phosphorylation of LRRK2 S910/S935 within the N-terminus of LRRK2 has been shown to be important for binding to 14-3-3 and regulating the cellular localization of LRRK2.
- Subjects
DARDARIN; MOLECULAR cloning
- Publication
Frontiers in Neuroscience, 2022, Vol 16, p1
- ISSN
1662-4548
- Publication type
Article
- DOI
10.3389/fnins.2022.880914