Content
Burbulla Lab
[2022] [2021] [2020] [2019] [2018] [2017] [2016] [2014] [2013] [2012] [2011] [2010]
- Mitochondrial Phenotypes in Parkinson's Diseases-A Focus on Human iPSC-Derived Dopaminergic Neurons. (Review)
- Identification of ASCL1 as a determinant for human iPSC-derived dopaminergic neurons.
- Mendelian Randomisation Study of Smoking, Alcohol, and Coffee Drinking in Relation to Parkinson's Disease.
- Direct targeting of wild-type glucocerebrosidase by antipsychotic quetiapine improves pathogenic phenotypes in Parkinson's disease models.
- Modeling Brain Pathology of Niemann-Pick Disease Type C Using Patient-Derived Neurons.
- The Convergence of Alpha-Synuclein, Mitochondrial, and Lysosomal Pathways in Vulnerability of Midbrain Dopaminergic Neurons in Parkinson's Disease. (Review)
- Gelator length precisely tunes supramolecular hydrogel stiffness and neuronal phenotype in 3D culture.
- A patient-based model of RNA mis-splicing uncovers treatment targets in Parkinson's disease.
- Variants in Miro1 Cause Alterations of ER-Mitochondria Contact Sites in Fibroblasts from Parkinson's Disease Patients.
- Dopamine metabolism by a monoamine oxidase mitochondrial shuttle activates the electron transport chain.
- A modulator of wild-type glucocerebrosidase improves pathogenic phenotypes in dopaminergic neuronal models of Parkinson's disease.
- The role of dopamine in the pathogenesis of GBA1-linked Parkinson's disease. (Review)
- Conversion of Quinazoline Modulators from Inhibitors to Activators of β-Glucocerebrosidase.
- Iron overload is accompanied by mitochondrial and lysosomal dysfunction in WDR45 mutant cells.
- Acid ceramidase inhibition ameliorates α-synuclein accumulation upon loss of GBA1 function.
- Functional Impairment in Miro Degradation and Mitophagy Is a Shared Feature in Familial and Sporadic Parkinson's Disease.
- Activation of β-Glucocerebrosidase Reduces Pathological α-Synuclein and Restores Lysosomal Function in Parkinson's Patient Midbrain Neurons.
- Micropatterning Facilitates the Long-Term Growth and Analysis of iPSC-Derived Individual Human Neurons and Neuronal Networks.
- Detection of Free and Protein-Bound ortho-Quinones by Near-Infrared Fluorescence.
- Knockdown of Hsc70-5/mortalin induces loss of synaptic mitochondria in a Drosophila Parkinson's disease model.
- A novel heterozygous OPA3 mutation located in the mitochondrial target sequence results in altered steady-state levels and fragmented mitochondrial network.
- Genetic correction of a LRRK2 mutation in human iPSCs links parkinsonian neurodegeneration to ERK-dependent changes in gene expression.
- The use of primary human fibroblasts for monitoring mitochondrial phenotypes in the field of Parkinson's disease.
- Guidelines for the use and interpretation of assays for monitoring autophagy.
- Loss of mortalin function in PD - supporting the mitochondrial pathway of neurodegeneration. (Book chapter)
- Dissecting the role of the mitochondrial chaperone mortalin in Parkinson's disease: functional impact of disease-related variants on mitochondrial homeostasis.
- Balance is the challenge--the impact of mitochondrial dynamics in Parkinson's disease. (Review)
- Reduced basal autophagy and impaired mitochondrial dynamics due to loss of Parkinson's disease-associated protein DJ-1.