ArticleFrontiers in cellular neuroscience2013
LRRK2: an éminence grise of Wnt-mediated neurogenesis?
Article in Frontiers in cellular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Glial Dysfunction and Memory Impairments in a Model of Pediatric Obstructive Sleep Apnea.Glia · 2026Article
- Synthetic Small Molecules as Regulators of In Vitro Multiplication inPlants (Basel, Switzerland) · 2026Article
- LRRK2 kinase activity is necessary for development and regeneration in Nematostella vectensis.Neural development · 2024Article
- Biphenotypic Cells and α-Synuclein Accumulation in Enteric Neurons of Leucine-Rich Repeat Kinase 2 Knockout Mice.Digestive diseases and sciences · 2024Article
- LRRK2 kinase activity is necessary for development and regeneration in Nematostella vectensis.Research square · 2023Article
- Molecular mechanisms of developmental pathways in neurological disorders: a pharmacological and therapeutic review.Open biology · 2022Review
- Deletion of lrrk2 causes early developmental abnormalities and age-dependent increase of monoamine catabolism in the zebrafish brain.PLoS genetics · 2021Article
- LRRK2 Biology from structure to dysfunction: research progresses, but the themes remain the same.Molecular neurodegeneration · 2019Review
- Centrality of Early Synaptopathy in Parkinson's Disease.Frontiers in neurology · 2018Review
- Back to the tubule: microtubule dynamics in Parkinson's disease.Cellular and molecular life sciences : CMLS · 2017Review
- Pathogenic LRRK2 variants are gain-of-function mutations that enhance LRRK2-mediated repression of β-catenin signaling.Molecular neurodegeneration · 2017Article
- Synaptopathies: synaptic dysfunction in neurological disorders - A review from students to students.Journal of neurochemistry · 2016Review
- Comparative Microarray Analysis of Proliferating and Differentiating Murine ENS Progenitor Cells.Stem cells international · 2016Article
- Protective LRRK2 R1398H Variant Enhances GTPase and Wnt Signaling Activity.Frontiers in molecular neuroscience · 2016Article
- Drosophila Mutant Model of Parkinson's Disease Revealed an Unexpected Olfactory Performance: Morphofunctional Evidences.Parkinson's disease · 2016Article
- A visual review of the interactome of LRRK2: Using deep-curated molecular interaction data to represent biology.Proteomics · 2015Review
- Neural stem cells in Parkinson's disease: a role for neurogenesis defects in onset and progression.Cellular and molecular life sciences : CMLS · 2015Review
- FIH-1 disrupts an LRRK1/EGFR complex to positively regulate keratinocyte migration.The American journal of pathology · 2014Article
- The regulation and deregulation of Wnt signaling by PARK genes in health and disease.Journal of molecular cell biology · 2014Review
- WISP1: Clinical insights for a proliferative and restorative member of the CCN family.Current neurovascular research · 2014Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The importance of leucine-rich repeat kinase 2 (LRRK2) to mature neurons is well-established, since mutations in PARK8, the gene encoding LRRK2, are the most common known cause of Parkinson's disease. Nonetheless, despite the LRRK2 knockout mouse having no overt neurodevelopmental defect, numerous lines of in vitro data point toward a central role for this protein in neurogenesis. Roles for LRRK2 have been described in many key processes, including neurite outgrowth and the regulation of microtubule dynamics. Moreover, LRRK2 has been implicated in cell cycle control, suggesting additional roles in neurogenesis that precede terminal differentiation. However, we contend that the suggested function of LRRK2 as a scaffolding protein at the heart of numerous Wnt signaling cascades provides the most tantalizing link to neurogenesis in the developing brain. Numerous lines of evidence show a critical requirement for multiple Wnt pathways in the development of certain brain regions, not least the dopaminergic neurons of the ventral mid-brain. In conclusion, these observations indicate a function of LRRK2 as a subtle yet critical mediator of the action of Wnt ligands on developing neurons. We suggest that LRRK2 loss- or gain-of-function are likely modifiers of developmental phenotypes seen in animal models of Wnt signaling deregulation, a hypothesis that can be tested by cross-breeding relevant genetically modified experimental strains.
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