A Novel, Selective c-Abl Inhibitor, Compound 5, Prevents Neurodegeneration in Parkinson’s Disease

Efficacy of Nilotinib in Patients With Moderately Advanced Parkinson Disease

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Emerging therapies in Parkinson disease — repurposed drugs and new approaches

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Parkin interacting substrate zinc finger protein 746 is a pathological mediator in Parkinson’s disease

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Nilotinib Effects on Safety, Tolerability, and Potential Biomarkers in Parkinson Disease

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The c-Abl inhibitor, Radotinib HCl, is neuroprotective in a preclinical Parkinson’s disease mouse model

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Block of A1 astrocyte conversion by microglia is neuroprotective in models of Parkinson’s disease

(2018) Seung Pil Yun et al.   NATURE MEDICINE

Graphene quantum dots prevent α-synucleinopathy in Parkinson’s disease

(2018) Donghoon Kim et al.   Nature Nanotechnology

Identification of a highly neurotoxic α-synuclein species inducing mitochondrial damage and mitophagy in Parkinson’s disease

(2018) Diego Grassi et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Poly(ADP-ribose) drives pathologic α-synuclein neurodegeneration in Parkinson’s disease

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Involvement of c-Abl Kinase in Microglial Activation of NLRP3 Inflammasome and Impairment in Autolysosomal System

(2017) Vivek Lawana et al.   Journal of Neuroimmune Pharmacology

TMEM175 deficiency impairs lysosomal and mitochondrial function and increases α-synuclein aggregation

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c-Abl and Parkinson’s Disease: Mechanisms and Therapeutic Potential

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Activation of tyrosine kinase c-Abl contributes to α-synuclein–induced neurodegeneration

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Pathological  -synuclein transmission initiated by binding lymphocyte-activation gene 3

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Crystal structure of an SH2–kinase construct of c-Abl and effect of the SH2 domain on kinase activity

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c-Abl–p38α signaling plays an important role in MPTP-induced neuronal death

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c-Abl phosphorylates α-synuclein and regulates its degradation: implication for α-synuclein clearance and contribution to the pathogenesis of Parkinson's disease

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Addition of exogenous α-synuclein preformed fibrils to primary neuronal cultures to seed recruitment of endogenous α-synuclein to Lewy body and Lewy neurite–like aggregates

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Oxidative Stress-Induced Signaling Pathways Implicated in the Pathogenesis of Parkinson’s Disease

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The c-Abl inhibitor, Nilotinib, protects dopaminergic neurons in a preclinical animal model of Parkinson's disease

(2014) Senthilkumar S. Karuppagounder et al.   Scientific Reports

Ins and Outs of Kinase DFG Motifs

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Calcium Entry and  -Synuclein Inclusions Elevate Dendritic Mitochondrial Oxidant Stress in Dopaminergic Neurons

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Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss

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Clinical cardiac safety profile of nilotinib

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PARIS (ZNF746) Repression of PGC-1α Contributes to Neurodegeneration in Parkinson's Disease

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c-Abl in Neurodegenerative Disease

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Novel Regulation of Parkin Function through c-Abl-Mediated Tyrosine Phosphorylation: Implications for Parkinson's Disease

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Role of hERG potassium channel assays in drug development

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Phosphorylation by the c-Abl protein tyrosine kinase inhibits parkin's ubiquitination and protective function

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Lewy body dementia and Parkinson’s disease with dementia

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