SUBCELLULAR LOCALIZATION
| intracellular
|
|
| intracellular,cytoplasm,organelle,mitochondria,outer
|
|
| intracellular,cytoplasm,organelle,membrane
|
|
| intracellular,cytoplasm,organelle,endoplasmic reticulum
|
|
| intracellular,cytoplasm,organelle,Golgi
|
|
| intracellular,cytoplasm,cytosolic
|
|
| intracellular,cytoplasm,cytoskeleton,microtubule,centrosome
|
| text
| centriolar |
|
within the mitochondrial organelle of proliferating cells, but in the cytosol and Golgi in brain tissues |
|
translocating to uncoupled mitochondria to induce their autophagy  |
|
dominantly located in cytosol, whereas it is also located in mitochondria |
|
upon mitochondrial damage, translocates to mitochondria to mediate their selective elimination by autophagic degradation |
|
translocates from the cytosol to depolarized mitochondria and induces their autophagic removal (mitophagy) |
| basic FUNCTION
| involved in the protein degradation as a ubiquitin-protein ligase (E3 activity) collaborating with UBE2L3 |
|
may be promoting the degradation of substrates localized in mitochondria and involved in the late mitochondrial phase of ceramide-mediated cell-death |
|
ubiquitinating SYT11 and regulating the turn-over of SYT11 |
|
playing an important role for aggresome formation in neuronal cells |
|
promoting the degradation of the synaptic vesicle-associated protein PNUTL1 (CDCREL1) |
|
involved in the regulation of mitochondrial transcription/replication other than the ubiquitin-mediated protein degradation system in proliferating cells |
|
suppresses MAO expression (and may limit the production of reactive oxygen species generated by MAO in dopamine oxidation and would, thus, be beneficial to the survival of dopaminergic neurons) |
|
functions as an autophagy inhibitory protein via its interaction with Beclin 1, and the autophagy level maintained by BCL2 is compatible with cell survival, rather than cell death |
|
activates signaling through the IkappaB kinase (IKK)/nuclear factor kappaB (NF-kappaB) pathway |
|
modulating the expression of KIF11 through the Hsp70-JNK-c-Jun signaling pathway |
|
promotes DNA repair and protects against genotoxicity, (potential pathogenic mechanism in Parkinson disease) |
|
involved in the cellular homeastasis of a series of proteins by modulating their ubiquitylation and thereby controlling their subsequent degradation by the proteasome |
|
regulates PINK1 stabilization via direct interaction with PINK1, and operates through a common pathway with PINK1 in the pathogenesis of early-onset Parkinson disease |
|
playing a role in directly supporting mitochondrial function and protecting mitochondrial genomic integrity from oxidative stress |
|
involved in regulation of Wnt signaling and may protects dopaminergic neurons against excessive Wnt signaling and CTNNB-induced cell death |
|
ubiquitin ligase-independent function of parkin in the control of transcription and a functional link between parkin and TP53 that is altered by PARK2 mutations |
|
together with PINK1, modulates mitochondrial trafficking, especially to the perinuclear region, a subcellular area associated with autophagy |
|
tumor suppressor gene whose haploinsufficiency cooperates with mutant APC in colorectal carcinogenesis |
|
with PINK1 are intimately involved in preventing mitochondrial dysfunction |
|
mono-ubiquitinates BCL2 and regulates autophagy via BCL2 |
|
Parkin, but not its E3 ligase-deficient mutants, mono-ubiquitinates BCL2 to stabilize it, resulting in an increase of its binding to Beclin 1, thereby repressing autophagy in normal conditions or starvation |
|
PINK1 and PARK2 are thus required for the removal of damaged mitochondria in dopaminergic cells, and inhibition of this pathway may lead to the accumulation of defective mitochondria which may contribute to Parkinson disease pathogenesis |
|
restoration of autophagy in PINK1-silenced cells by PARK2 reverses ATP synthesis inhibition and the ubiquitination of MFN1 and MFN2 play a role in PINK1/PARK2-mediated mitophagy |
|
PARK2 and EIF4E act in a common pathway, likely modulating cap-dependent translation initiation events |
|
PARK7 works in parallel to the PINK1/PARK2 pathway to maintain mitochondrial function in the presence of an oxidative environment |
|
promotes MDM2-arrestin interaction but inhibits arrestin ubiquitination, and parkin mutations differentially affect the stimulation of MDM2 binding |
|
has a potential role in the interorganellar crosstalk between the ER and mitochondria to promote cell survival under stress, suggesting that both ER and mitochondrial stress can contribute to the pathogenesis of Parkinson disease |
|
regulates degradation of outer and inner mitochondrial membrane proteins differently through proteasome- and mitophagy-dependent pathways |
|
could be a key factor that regulates cellular homeostasis through mitochondrial turnover in both an autophagy-dependent and a proteasome-dependent manner |
|
ARIH1 and PARK2 functioning via a HECT-like mechanism whereby RING1 harbours the E2-binding site and RING2 harbours the active-site cysteine |
|
involved in ubiquitination of AMBRA1 |
