ArticleCell death and differentiation2022
The caspase-6-p62 axis modulates p62 droplets based autophagy in a dominant-negative manner.
Article in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 26 citations in OpenAlex.
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- Herbacetin ameliorates lipopolysaccharide-elicited inflammatory response by suppressing NLRP-3/AIM-2 inflammasome activation, PI3K/Akt/MAPKs/NF-κB redox inflammatory signalling, modulating autophagy and macrophage polarization imbalance.Molecular biology reports · 2024Article
- Caspase 6 promotes innate immune activation by functional crosstalk between RIPK1-IκBα axis in liver inflammation.Cell communication and signaling : CCS · 2023Article
- Effect and mechanism of pearl on ovarian function of rats with premature ovarian failure induced by tripterygium glycosides.Journal of traditional and complementary medicine · 2023Article
- Independent role of caspases and Bik in augmenting influenza A virus replication in airway epithelial cells and mice.Virology journal · 2023Article
- In Vitro Cytotoxic Effect of Aqueous Extracts from Leaves and Rhizomes of the SeagrassBiology · 2023Article
- Antigen Presentation and Autophagy in Teleost Adaptive Immunity.International journal of molecular sciences · 2022Review
- Article
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8 authors at 3 institutions in 2 countries.
Funding
Abstract
SQSTM1/p62, as a major autophagy receptor, forms droplets that are critical for cargo recognition, nucleation, and clearance. p62 droplets also function as liquid assembly platforms to allow the formation of autophagosomes at their surfaces. It is unknown how p62-droplet formation is regulated under physiological or pathological conditions. Here, we report that p62-droplet formation is selectively blocked by inflammatory toxicity, which induces cleavage of p62 by caspase-6 at a novel cleavage site D256, a conserved site across human, mouse, rat, and zebrafish. The N-terminal cleavage product is relatively stable, whereas the C-terminal product appears undetectable. Using a variety of cellular models, we show that the p62 N-terminal caspase-6 cleavage product (p62-N) plays a dominant-negative role to block p62-droplet formation. In vitro p62 phase separation assays confirm this observation. Dominant-negative regulation of p62-droplet formation by caspase-6 cleavage attenuates p62 droplets dependent autophagosome formation. Our study suggests a novel pathway to modulate autophagy through the caspase-6-p62 axis under certain stress stimuli.
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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.