Optineurin is an autophagy receptor for damaged mitochondria in parkin-mediated mitophagy that is disrupted by an ALS-linked mutation

scientific journal article

Optineurin is an autophagy receptor for damaged mitochondria in parkin-mediated mitophagy that is disrupted by an ALS-linked mutation is …
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scholarly articleQ13442814

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P819ADS bibcode2014PNAS..111E4439W
P356DOI10.1073/PNAS.1405752111
P3181OpenCitations bibliographic resource ID747191
P932PMC publication ID4210283
P698PubMed publication ID25294927
P5875ResearchGate publication ID266627141

P2093author name stringErika L. F. Holzbaur
Yvette C. Wong
P2860cites workPINK1 is selectively stabilized on impaired mitochondria to activate ParkinQ21145802
PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1Q24297155
Optineurin links myosin VI to the Golgi complex and is involved in Golgi organization and exocytosisQ24300284
Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagyQ24300975
p62/SQSTM1 is required for Parkin-induced mitochondrial clustering but not mitophagy; VDAC1 is dispensable for bothQ24301629
Phosphorylation of the autophagy receptor optineurin restricts Salmonella growthQ24304447
Mutations in the parkin gene cause autosomal recessive juvenile parkinsonismQ24309753
p62/SQSTM1 binds directly to Atg8/LC3 to facilitate degradation of ubiquitinated protein aggregates by autophagyQ24312147
A subdomain of the endoplasmic reticulum forms a cradle for autophagosome formationQ24315723
A role for NBR1 in autophagosomal degradation of ubiquitinated substratesQ24316135
Parkin is recruited selectively to impaired mitochondria and promotes their autophagyQ24317471
Hereditary early-onset Parkinson's disease caused by mutations in PINK1Q24337084
Optineurin negatively regulates TNFalpha- induced NF-kappaB activation by competing with NEMO for ubiquitinated RIPQ24337587
LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processingQ24597817
Mechanisms of mitophagyQ27310261
Adult-onset primary open-angle glaucoma caused by mutations in optineurinQ28217964
Huntingtin interacts with a family of WW domain proteinsQ28279245
The regulation of autophagosome dynamics by huntingtin and HAP1 is disrupted by expression of mutant huntingtin, leading to defective cargo degradationQ28591685
Autophagosome formation from membrane compartments enriched in phosphatidylinositol 3-phosphate and dynamically connected to the endoplasmic reticulumQ29614500
Mutations of optineurin in amyotrophic lateral sclerosisQ29614836
The TBK1 adaptor and autophagy receptor NDP52 restricts the proliferation of ubiquitin-coated bacteriaQ29615619
Landscape of the PARKIN-dependent ubiquitylome in response to mitochondrial depolarizationQ29615622
Proteasome and p97 mediate mitophagy and degradation of mitofusins induced by ParkinQ29615623
Drosophila parkin requires PINK1 for mitochondrial translocation and ubiquitinates mitofusinQ29615625
PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagyQ29616005
PINK1-dependent recruitment of Parkin to mitochondria in mitophagyQ29620567
Autophagosomes initiate distally and mature during transport toward the cell soma in primary neuronsQ30425491
Autophagy receptors link myosin VI to autophagosomes to mediate Tom1-dependent autophagosome maturation and fusion with the lysosomeQ30525665
VCP is essential for mitochondrial quality control by PINK1/Parkin and this function is impaired by VCP mutationsQ30540665
The mitochondrial fusion-promoting factor mitofusin is a substrate of the PINK1/parkin pathwayQ33552320
Nix is critical to two distinct phases of mitophagy, reactive oxygen species-mediated autophagy induction and Parkin-ubiquitin-p62-mediated mitochondrial primingQ34107322
p62/SQSTM1 cooperates with Parkin for perinuclear clustering of depolarized mitochondriaQ34269257
Organization and dynamics of human mitochondrial DNA.Q34320137
Bit-by-bit autophagic removal of parkin-labelled mitochondriaQ34369366
Genome-wide association study identifies variants at CSF1, OPTN and TNFRSF11A as genetic risk factors for Paget's disease of boneQ35552797
Cellular and molecular biology of optineurinQ36905164
Mitochondria removal by autophagyQ37831014
Mitochondria and ALS: implications from novel genes and pathways.Q38019306
Maintenance of retinal ganglion cell mitochondrial functions as a neuroprotective strategy in glaucoma.Q38045590
Mitochondrial dynamics in neurodegenerationQ38060435
The LC3 interactome at a glanceQ38171884
Ubiquitin-independent function of optineurin in autophagic clearance of protein aggregatesQ40710483
Alterations in the common fragile site gene Parkin in ovarian and other cancersQ44653680
Novel monoclonal antibodies demonstrate biochemical variation of brain parkin with age.Q48199015
Chromophore-assisted light inactivation (CALI) using the phototoxic fluorescent protein KillerRed.Q50690849
Familial-associated mutations differentially disrupt the solubility, localization, binding and ubiquitination properties of parkin.Q51387140
Structures containing Atg9A and the ULK1 complex independently target depolarized mitochondria at initial stages of Parkin-mediated mitophagy.Q54534151
P4510describes a project that usesImageJQ1659584
P433issue42
P407language of work or nameEnglishQ1860
P921main subjectmitochondrionQ39572
amyotrophic lateral sclerosisQ206901
OptineurinQ7098997
autophagyQ288322
parkin-mediated stimulation of mitophagy in response to mitochondrial depolarizationQ22282659
P304page(s)E4439–4448
P577publication date2014-10-21
P1433published inProceedings of the National Academy of Sciences of the United States of AmericaQ1146531
P1476titleOptineurin is an autophagy receptor for damaged mitochondria in parkin-mediated mitophagy that is disrupted by an ALS-linked mutation
P478volume111

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cites work (P2860)
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