Results 31 to 40 of about 15,787 (93)

Mechanism of parkin activation by PINK1 [PDF]

open access: yesNature, 2018
Mutations in the E3 ubiquitin ligase parkin (PARK2, also known as PRKN) and the protein kinase PINK1 (also known as PARK6) are linked to autosomal-recessive juvenile parkinsonism (AR-JP)1,2; at the cellular level, these mutations cause defects in mitophagy, the process that organizes the destruction of damaged mitochondria3,4.
Gladkova, Christina   +3 more
openaire   +2 more sources

Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer disease [PDF]

open access: yes, 2017
Alzheimer disease (AD), Frontotemporal lobar degeneration (FTD), Amyotrophic lateral sclerosis (ALS) and Parkinson disease (PD) have a certain degree of clinical, pathological and molecular overlap.
Alexandra Medvedeva   +17 more
core   +4 more sources

TSPO interacts with VDAC1 and triggers a ROS-mediated inhibition of mitochondrial quality control [PDF]

open access: yes, 2014
The 18-kDa TSPO (translocator protein) localizes on the outer mitochondrial membrane (OMM) and participates in cholesterol transport. Here, we report that TSPO inhibits mitochondrial autophagy downstream of the PINK1-PARK2 pathway, preventing essential ...
Anholt R   +22 more
core   +3 more sources

PINK1/PARKIN signalling in neurodegeneration and neuroinflammation [PDF]

open access: yesActa Neuropathologica Communications, 2020
Abstract Mutations in the PTEN-induced kinase 1 (PINK1) and Parkin RBR E3 ubiquitin-protein ligase (PARKIN) genes are associated with familial forms of Parkinson’s disease (PD). PINK1, a protein kinase, and PARKIN, an E3 ubiquitin ligase, control the specific elimination of dysfunctional or superfluous mitochondria, thus fine-tuning ...
Peter M. J. Quinn   +3 more
openaire   +5 more sources

The selectivity and specificity of autophagy in drosophila [PDF]

open access: yes, 2012
Autophagy is a process of cellular self-degradation and is a major pathway for elimination of cytoplasmic material by the lysosomes. Autophagy is responsible for the degradation of damaged organelles and protein aggregates and therefore plays a ...
Chou   +27 more
core   +2 more sources

Circadian Rhythm Abnormalities in Parkinson's Disease from Humans to Flies and Back [PDF]

open access: yes, 2018
Clinical and research studies have suggested a link between Parkinson\u2019s disease (PD) and alterations in the circadian clock. Drosophila melanogaster may represent a useful model to study the relationship between the circadian clock and PD.
Bisaglia, Marco   +3 more
core   +1 more source

Anti-oxidants in Parkinson's disease therapy: a critical point of view [PDF]

open access: yes, 2016
Parkinson's disease (PD) is a degenerative neurological syndrome, which is characterized by the preferential death of dopaminergic (DAergic) neurons in the SubstantiaNigra.
Beltramini, Mariano   +3 more
core   +2 more sources

PINK1/Parkin direct mitochondria to autophagy [PDF]

open access: yesAutophagy, 2010
Mutations in PTEN-induced putative kinase 1 (PINK1) and PARK2/Parkin cause autosomal recessive forms of Parkinson disease. In mammalian cells, cytosolic Parkin is selectively recruited to depolarized mitochondria, followed by a stimulation of mitochondrial autophagy.
Cristofol, Vives-Bauza   +3 more
openaire   +2 more sources

PINK1 homozygous W437X mutation in a patient with apparent dominant transmission of parkinsonism. [PDF]

open access: yes, 2006
We analyzed the PINK1 gene in 58 patients with early-onset Parkinsonism and detected the homozygous mutation W437X in 1 patient. The clinical phenotype was characterized by early onset (22 years of age), good re- sponse to levodopa, early fluctuations ...
CRISCUOLO C   +10 more
core  

αSynuclein control of mitochondrial homeostasis in human-derived neurons is disrupted by mutations associated with Parkinson’s disease [PDF]

open access: yes, 2017
The etiology of Parkinson’s disease (PD) converges on a common pathogenic pathway of mitochondrial defects in which α-Synuclein (αSyn) is thought to play a role.
Alloatti, Matías   +12 more
core   +1 more source

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