ArticleCell death & disease2015
NBR1 is dispensable for PARK2-mediated mitophagy regardless of the presence or absence of SQSTM1.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Selective autophagy of intracellular organelles: recent research advances.Theranostics · 2021Pooled it
- The Metabolic Role of Mitochondria in the Perinatal Cardiac Development and Cardiovascular Diseases.Exploration (Beijing, China) · 2026Review
- ANKZF1 helps to eliminate stress-damaged mitochondria by LC3-mediated mitophagy.Cell death discovery · 2025Article
- Mechanisms and therapeutic implications of selective autophagy in nonalcoholic fatty liver disease.Journal of advanced research · 2025Review
- RNA modification: mechanisms and therapeutic targets.Molecular biomedicine · 2023Review
- Current opinions on mitophagy in fungi.Autophagy · 2023Review
- Parkin Insufficiency Accentuates High-Fat Diet-Induced Cardiac Remodeling and Contractile Dysfunction Through VDAC1-Mediated Mitochondrial CaJACC. Basic to translational science · 2022Article
- Parkin-dependent mitophagy occurs via proteasome-dependent steps sequentially targeting separate mitochondrial sub-compartments for autophagy.Autophagy reports · 2022Article
- Functions of autophagy in chloroplast protein degradation and homeostasis.Frontiers in plant science · 2022Review
- New insights into the interplay between autophagy and oxidative and endoplasmic reticulum stress in neuronal cell death and survival.Frontiers in cell and developmental biology · 2022Review
- Insights into the Pathogenesis of Neurodegenerative Diseases: Focus on Mitochondrial Dysfunction and Oxidative Stress.International journal of molecular sciences · 2021Review
- The Dawn of Mitophagy: What Do We Know by Now?Current neuropharmacology · 2021Review
- A novel selective autophagy receptor, CCDC50, delivers K63 polyubiquitination-activated RIG-I/MDA5 for degradation during viral infection.Cell research · 2021Article
- Mitophagy and the Brain.International journal of molecular sciences · 2020Review
- Mitophagy pathways in health and disease.The Journal of cell biology · 2020Review
- Decision between mitophagy and apoptosis by Parkin via VDAC1 ubiquitination.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- An antibody for analysis of autophagy induction.Nature methods · 2020Article
- Review
- The Marine DinoflagellateMarine drugs · 2018Article
- PINK1/Parkin-mediated mitophagy is activated in cisplatin nephrotoxicity to protect against kidney injury.Cell death & disease · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Degradation of malfunctional mitochondria by mitophagy is a pivotal component of mitochondrial quality control to maintain cellular homeostasis. Mitochondrial clearance through the PINK1/PARK2 pathway is mediated by autophagic adaptor proteins. Previous studies revealed a significant involvement, but not an absolute requirement for SQSTM1 in PARK2-dependent mitophagy, suggesting that the existence of redundant adaptor proteins may compensate for the loss of SQSTM1. Here we investigated whether NBR1, a functional homolog of SQSTM1, has a role in PARK2-mediated mitophagy, either alone or as a compensatory mechanism. We showed that NBR1 does not appear to be required for mitochondrial clustering following mitochondrial depolarization. Moreover, we demonstrated that deletion of NBR1 alone or in combination with SQSTM1 does not prevent the degradation of damaged mitochondria. Our data suggest that NBR1 is dispensable for PARK2-dependent mitophagy and additional autophagic adaptor proteins, other than NBR1, are responsible for mitochondrial degradation in cells depleted of SQSTM1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.