ArticleFEBS open bio2019
BAG6 deficiency induces mis-distribution of mitochondrial clusters under depolarization.
Article in FEBS open bio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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
8 citing papers in PubMed, 11 citations in OpenAlex.
- Spatial control of mitochondrial retrograde signaling by nuclear pore-associated contact sites.bioRxiv : the preprint server for biology · 2026Article
- RAB3A-mediated BAG6 translocation promotes non-small cell lung cancer tumorigenesis and progression.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Proteotoxic stresses stimulate dissociation of UBL4A from the tail-anchored protein recognition complex.The Biochemical journal · 2023Article
- BAG6 supports stress fiber formation by preventing the ubiquitin-mediated degradation of RhoA.Molecular biology of the cell · 2023Article
- BAG family proteins contributes to autophagy-mediated multidrug resistance of tumor.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Review
- Regulation of Parkin-dependent mitophagy by Bcl-2-associated athanogene (BAG) family members.Neural regeneration research · 2021Article
- Chronic treatment with the complex I inhibitor MPPThe Journal of biological chemistry · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of damaged mitochondria is implicated in a number of neurodegenerative disorders, including Parkinson's disease. Therefore, the machinery for mitochondrial quality control is important for the prevention of such diseases. It has been reported that Parkin- and p62/sequestosome 1 (SQSTM1)-mediated clustering and subsequent elimination of damaged mitochondria (termed mitophagy) are critical for maintaining the quality of mitochondria under stress induced by uncoupling agents such as carbonyl cyanide m-chlorophenyl hydrazone. However, the molecular mechanisms underlying mitochondrial translocation to the perinuclear region during mitophagy have not been adequately addressed to date. In this study, we found that BCL2-associated athanogene 6 (BAG6; also known as BAT3 or Scythe) is required for this process. Indeed, RNA interference-mediated depletion of endogenous BAG6 prevented Parkin-dependent relocalization of mitochondrial clusters to the perinuclear cytoplasmic region, whereas BAG6 knockdown did not affect the translocation of Parkin and p62/SQSTM1 to the depolarized mitochondria and subsequent aggregation. These results suggest that BAG6 is essential for cytoplasmic redistribution, but not for clustering, of damaged mitochondria.
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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.