Results 1 to 10 of about 226,005 (247)

AMBRA1 is able to induce mitophagy via LC3 binding, regardless of PARKIN and p62/SQSTM1 [PDF]

open access: yesCell Death and Differentiation, 2014
Damaged mitochondria are eliminated by mitophagy, a selective form of autophagy whose dysfunction associates with neurodegenerative diseases. PINK1, PARKIN and p62/SQTMS1 have been shown to regulate mitophagy, leaving hitherto ill-defined the ...
Flavie Strappazzon   +2 more
exaly   +6 more sources

Parkin interacts with Ambra1 to induce mitophagy [PDF]

open access: yes, 2011
Mutations in the gene encoding Parkin are a major cause of recessive Parkinson's disease. Recent work has shown that Parkin translocates from the cytosol to depolarized mitochondria and induces their autophagic removal (mitophagy). However, the molecular
Cornelissen, Tom   +6 more
core   +2 more sources

Synergistic recruitment of UbcH7~Ub and phosphorylated Ubl domain triggers parkin activation [PDF]

open access: yes, 2018
The E3 ligase parkin ubiquitinates outer mitochondrial membrane proteins during oxidative stress and is linked to early-onset Parkinson’s disease. Parkin is autoinhibited but is activated by the kinase PINK1 that phosphorylates ubiquitin leading to ...
Aguirre, Jacob D.   +9 more
core   +1 more source

The Interplay among PINK1/PARKIN/Dj-1 Network during Mitochondrial Quality Control in Cancer Biology: Protein Interaction Analysis [PDF]

open access: yes, 2018
PARKIN (E3 ubiquitin ligase PARK2), PINK1 (PTEN induced kinase 1) and DJ-1 (PARK7) are proteins involved in autosomal recessive parkinsonism, and carcinogenic processes.
Lucas, Millikin, Narendra, Santel, Zhang
core   +2 more sources

Parkin function in Parkinson's disease [PDF]

open access: yes, 2018
Parkinson's disease (PD) is the second most common neurodegenerative disease, and is characterized by involuntary shaking, muscle rigidity, and the progressive loss of dopaminergic neurons.
Arkinson, Connor, Walden, Helen
core   +1 more source

Broad activation of the ubiquitin-proteasome system by Parkin is critical for mitophagy [PDF]

open access: yes, 2011
Parkin, an E3 ubiquitin ligase implicated in Parkinson's disease, promotes degradation of dysfunctional mitochondria by autophagy. Using proteomic and cellular approaches, we show that upon translocation to mitochondria, Parkin activates the ubiquitin ...
Anh H. Pham   +49 more
core   +3 more sources

Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin [PDF]

open access: yes, 2010
Loss of the E3 ubiquitin ligase Parkin causes early onset Parkinson's disease, a neurodegenerative disorder of unknown etiology. Parkin has been linked to multiple cellular processes including protein degradation, mitochondrial homeostasis, and autophagy;
A. J. Whitworth   +28 more
core   +2 more sources

The PINK1/Parkin pathway: a mitochondrial quality control system? [PDF]

open access: yes, 2009
Significant insight into the mechanisms that contribute to dopaminergic neurodegeneration in Parkinson disease has been gained from the analysis of genes linked to rare heritable forms of parkinsonism such as PINK1 and parkin, loss-of-function mutations ...
Pallanck, L.J., Whitworth, A.J.
core   +1 more source

Olfaction in Parkin single and compound heterozygotes in a cohort of young onset Parkinson's disease patients [PDF]

open access: yes, 2016
Background Parkin related Parkinson's disease (PD) is differentiated from idiopathic PD by absent or sparse Lewy bodies, and preserved olfaction. The significance of single Parkin mutations in the pathogenesis of PD is debated.
Bajaj, N. P.   +14 more
core   +2 more sources

Binding to serine 65-phosphorylated ubiquitin primes Parkin for optimal PINK1-dependent phosphorylation and activation [PDF]

open access: yes, 2015
This is the author accepted manuscript. The final version is available from EMBO Press via the DOI in this recordMutations in the mitochondrial protein kinase PINK1 are associated with autosomal recessive Parkinson disease (PD).
Alessi, Dario R   +16 more
core   +3 more sources

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