Kinase signaling pathways as potential targets in the treatment of Parkinson’s disease
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Summary
The current data and thoughts regarding LRRK2 and PINK1 are explored and further avenues of research are discussed to understand the pathologic effects of mutations at these loci and potential points of therapeutic intervention, such as within these kinases or in associated pathways.
- Type
- article
- Published
- 2007-12-01
- Cited by
- 22
- References
- 92
- OpenAlex
- https://openalex.org/W18067416
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:34172624
Keywords
Political science, Humanities, Philosophy
References
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- Lessons in Rational Drug Design for Protein Kinases
- Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism
- CEP-1347/KT-7515, an inhibitor of c-jun N-terminal kinase activation, attenuates the 1-methyl-4-phenyl tetrahydropyridine-mediated loss of nigrostriatal dopaminergic neurons In vivo.
- p38 MAP kinase activation by vascular endothelial growth factor mediates actin reorganization and cell migration in human endothelial cells
- A new locus for Parkinson's disease (PARK8) maps to chromosome 12p11.2–q13.1
- The Parkinson's disease-associated protein, leucine-rich repeat kinase 2 (LRRK2), is an authentic GTPase that stimulates kinase activity.
- GTP binding is essential to the protein kinase activity of LRRK2, a causative gene product for familial Parkinson's disease.
- A novel kinase cascade triggered by stress and heat shock that stimulates MAPKAP kinase-2 and phosphorylation of the small heat shock proteins.
- Progressive Degeneration of Human Mesencephalic Neuron-Derived Cells Triggered by Dopamine-Dependent Oxidative Stress Is Dependent on the Mixed-Lineage Kinase Pathway
- Parkinson's Disease: The LRRK2-G2019S mutation: opening a novel era in Parkinson's disease genetics
- Activation of apoptosis signal regulating kinase 1 (ASK1) and translocation of death‐associated protein, Daxx, in substantia nigra pars compacta in a mouse model of Parkinson's disease: protection by α‐lipoic acid
- Kinase activity is required for the toxic effects of mutant LRRK2/dardarin.
- Growth-suppressive effects of BPOZ and EGR2, two genes involved in the PTEN signaling pathway
- The R1441C mutation of LRRK2 disrupts GTP hydrolysis.
- Tau phosphorylation increases in symptomatic mice overexpressing A30P alpha-synuclein.
Cited by
- Sulforaphane Protects Cortical Neurons against Endogenous Neurotoxins in a Model of Parkinson’s Disease
- Kinases and kinase signaling pathways: potential therapeutic targets in Parkinson's disease.
- Review: Familial Parkinson's disease – genetics, clinical phenotype and neuropathology in relation to the common sporadic form of the disease
- Mechanisms in dominant parkinsonism; The toxic triangle of LRRK2, α-synuclein and tau
- Proteomic Identification of Plasma Protein Tyrosine Phosphatase Alpha and Fibronectin Associated with Liver Fluke, Opisthorchis viverrini, Infection
- LRRK2, a puzzling protein: insights into Parkinson’s disease pathogenesis
- The Chaperone Activity of Heat Shock Protein 90 Is Critical for Maintaining the Stability of Leucine-Rich Repeat Kinase 2
- Neuroprotective Effects of Carpinus tschonoskii MAX on 6-Hydroxydopamine-Induced Death of PC12 Cells
- From the cell to the clinic: a comparative review of the partial D₂/D₃receptor agonist and α2-adrenoceptor antagonist, piribedil, in the treatment of Parkinson's disease.
- Cystamine-tacrine dimer: a new multi-target-directed ligand as potential therapeutic agent for Alzheimer's disease treatment.
- Role of LRRK2 kinase activity in the pathogenesis of Parkinson's disease.
- Dysregulation of mTOR Signaling in Fragile X Syndrome
- Understanding the molecular basis of Parkinson’s disease, identification of biomarkers and routes to therapy
- Cancer and Neurodegeneration: Between the Devil and the Deep Blue Sea
- Differential protein-protein interactions of LRRK1 and LRRK2 indicate roles in distinct cellular signaling pathways
- The GTPase function of LRRK2.
- Sulforaphane protects cortical neurons against 5-S-cysteinyl-dopamine-induced toxicity through the activation of ERK1/2, Nrf-2 and the upregulation of detoxification enzymes.
- In silico, in vitro and cellular analysis with a kinome-wide inhibitor panel correlates cellular LRRK2 dephosphorylation to inhibitor activity on LRRK2
- Bcl-xL-mediated antioxidant function abrogates the disruption of mitochondrial dynamics induced by LRRK2 inhibition.
- Role and mechanism of action of leucine-rich repeat kinase 1 in bone
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