Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Dynamic recruitment and activation of ALS-associated TBK1 with its target optineurin are required for efficient mitophagy.

Proceedings of the National Academy of Sciences of the United States of America - 14 Jun 2016

Moore Andrew S, Holzbaur Erika L F

Abstract excerpt

Mitochondria play an essential role in maintaining cellular homeostasis. The removal of damaged or depolarized mitochondria occurs via mitophagy, in which damaged mitochondria are targeted for degradation via ubiquitination induced by PTEN-induced putative kinase 1 (PINK1) and Parkin. Mitophagy receptors, including optineurin (OPTN), nuclear dot 52 kDa protein (NDP52), and Tax1-binding protein 1 (TAX1BP1), are...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amyotrophic Lateral Sclerosis
Share to Intracellular Signaling Peptides and Proteins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Membrane Transport Proteins

Share to Mitophagy

Share to Protein Kinases

Share to Reactive Oxygen Species

Share to Transcription Factor TFIIIA

Share to Ubiquitin-Protein Ligases

Source

Open in PubMed Open full text

Identifiers

PMID: 27247382
DOI: 10.1073/pnas.1523810113
PMCID: PMC4914160

Genes

OPTN
TBK1
PINK1
PTEN
TANK

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Dynamic recruitment and activation of ALS-associated TBK1 with its target optineurin are required for efficient mitophagy.PMID 27247382Read ↗

ALS- and FTD-associated missense mutations in TBK1 differentially disrupt mitophagy.Semantic proximity Read ↗

ALS and FTD-associated missense mutations in TBK1 differentially disrupt mitophagySemantic proximity Read ↗

Control of mitophagy initiation and progression by the TBK1 adaptors NAP1 and SINTBADSemantic proximity Read ↗

Temporal dynamics of PARK2/parkin and OPTN/optineurin recruitment during the mitophagy of damaged mitochondriaSemantic proximity Read ↗

Unconventional initiation of PINK1/Parkin mitophagy by OptineurinSemantic proximity Read ↗

Optineurin is an autophagy receptor for damaged mitochondria in parkin-mediated mitophagy that is disrupted by an ALS-linked mutation.Semantic proximity Read ↗

Integrated proteogenetic analysis reveals the landscape of a mitochondrial-autophagosome synapse during PARK2-dependent mitophagySemantic proximity Read ↗

Parkin coordinates mitochondrial lipid remodeling to execute mitophagySemantic proximity Read ↗

LC3/GABARAPs drive ubiquitin-independent recruitment of Optineurin and NDP52 to amplify mitophagySemantic proximity Read ↗

Role of Optineurin in the Mitochondrial Dysfunction: Potential Implications in Neurodegenerative Diseases and CancerSemantic proximity Read ↗

Parkin-dependent mitophagy occurs via proteasome-dependent steps sequentially targeting separate mitochondrial sub-compartments for autophagySemantic proximity Read ↗

Degradation of engulfed mitochondria is rate-limiting in Optineurin-mediated mitophagy in neurons.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.