ArticleThe Journal of biological chemistry2015
Interaction of Phospholipase A/Acyltransferase-3 with Pex19p: A POSSIBLE INVOLVEMENT IN THE DOWN-REGULATION OF PEROXISOMES.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- The Phospholipase AJournal of lipid and atherosclerosis · 2026Review
- PLAAT2 suppresses gastric cancer progression by facilitating cMyc ubiquitination and inhibiting MEK/ERK signaling.Cell death & disease · 2026Article
- Recent Progress inInternational journal of molecular sciences · 2025Review
- Article
- Defunctionalizing intracellular organelles such as mitochondria and peroxisomes with engineered phospholipase A/acyltransferases.Nature communications · 2022Article
- Current Knowledge on Mammalian Phospholipase AMolecules (Basel, Switzerland) · 2022Review
- PLAAT1 inhibits type I interferon responseFrontiers in immunology · 2022Article
- Protein Dynamics Influence the Enzymatic Activity of Phospholipase A/Acyltransferases 3 and 4.Biochemistry · 2021Article
- Article
- Plasmalogens, platelet-activating factor and beyond - Ether lipids in signaling and neurodegeneration.Neurobiology of disease · 2020Review
- Updating Phospholipase ABiomolecules · 2020Review
- Plasmalogen loss caused by remodeling deficiency in mitochondria.Life science alliance · 2019Article
- Substantial Decrease in Plasmalogen in the Heart Associated with Tafazzin Deficiency.Biochemistry · 2018Article
- A reversible haploid mouse embryonic stem cell biobank resource for functional genomics.Nature · 2017Article
- Peroxisomal Dysfunction in Age-Related Diseases.Trends in endocrinology and metabolism: TEM · 2017Review
- Lipoquality control by phospholipase AProceedings of the Japan Academy. Series B, Physical and biological sciences · 2017Review
- The HRASLS (PLA/AT) subfamily of enzymes.Journal of biomedical science · 2015Review
- H-rev107 Regulates Cytochrome P450 Reductase Activity and Increases Lipid Accumulation.PloS one · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phospholipase A/acyltransferase (PLA/AT)-3 (also known as H-rev107 or AdPLA) was originally isolated as a tumor suppressor and was later shown to have phospholipase A1/A2 activity. We have also found that the overexpression of PLA/AT-3 in mammalian cells results in specific disappearance of peroxisomes. However, its molecular mechanism remained unclear. In the present study, we first established a HEK293 cell line, which stably expresses a fluorescent peroxisome marker protein (DsRed2-Peroxi) and expresses PLA/AT-3 in a tetracycline-dependent manner. The treatment with tetracycline, as expected, caused disappearance of peroxisomes within 24 h, as revealed by diffuse signals of DsRed2-Peroxi and a remarkable decrease in a peroxisomal membrane protein, PMP70. A time-dependent decrease in ether-type lipid levels was also seen. Because the activation of LC3, a marker of autophagy, was not observed, the involvement of autophagy was unlikely. Among various peroxins responsible for peroxisome biogenesis, Pex19p functions as a chaperone protein for the transportation of peroxisomal membrane proteins. Immunoprecipitation analysis showed that PLA/AT-3 binds to Pex19p through its N-terminal proline-rich and C-terminal hydrophobic domains. The protein level and enzyme activity of PLA/AT-3 were increased by its coexpression with Pex19p. Moreover, PLA/AT-3 inhibited the binding of Pex19 to peroxisomal membrane proteins, such as Pex3p and Pex11βp. A catalytically inactive point mutant of PLA/AT-3 could bind to Pex19p but did not inhibit the chaperone activity of Pex19p. Altogether, these results suggest a novel regulatory mechanism for peroxisome biogenesis through the interaction between Pex19p and PLA/AT-3.
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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.