Ask about this productRelated genes to: ATG10 antibody
- Gene:
- ATG10 NIH gene
- Name:
- autophagy related 10
- Previous symbol:
- APG10L
- Synonyms:
- DKFZP586I0418, FLJ13954
- Chromosome:
- 5q14.1-q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-28
- Date modifiied:
- 2018-02-13
Related products to: ATG10 antibody
Related articles to: ATG10 antibody
- Ammonia exposure can induce oxidative stress in aquatic animals. The p62 protein is a selective autophagy receptor that participates in protein degradation and oxidative stress regulation. In this study, the role of in the response of to ammonia exposure was investigated using RNA interference. The results showed that expression was significantly induced in the hepatopancreas, gills, and intestine of after ammonia exposure ( < 0.05). expression peaked at 6 h in the gills and 24 h in the intestine, whereas a biphasic response was observed in the hepatopancreas, with an initial peak at 12 h and a higher second peak at 48 h. In the RNAi experiment, knockdown altered the expression of antioxidant-related genes (, , and ) in a tissue-specific manner, with expression being prominently increased in the gills and intestine but not in the hepatopancreas under ammonia exposure. Autophagy-related genes ( and ) also showed time-dependent and tissue-specific expression changes after knockdown. The expression of apoptosis-related genes, including and , was tissue-specific and was generally lower in the dsRNA-+NH group than in the dsRNA-EGFP+NH group at most time points. Histopathological observations showed that hepatopancreatic acinar vacuolation and structural damage were alleviated, and the hepatopancreatic apoptosis rate was reduced in in the dsRNA-+NH group. These findings suggest that participates in the response of to ammonia exposure, possibly by regulating antioxidant defense, autophagy-related processes, and apoptosis, thereby affecting hepatopancreatic oxidative damage and tissue injury. - Source: PubMed
Publication date: 2026/06/04
Lu WeiLuo JunliangFeng LeyuanCai ShuanghuJian JichangYang Shiping - Cytokine storm, characterized by excessive release of pro-inflammatory cytokines, contributes to the severity and exacerbation of various diseases. Current therapies targeting individual cytokines prove inadequate due to the complex and multifactorial nature of inflammatory cascades. Here, we report human ATG10S, a novel isoform of the autophagy-related protein ATG10, as a potential inhibitor of cytokine storms. Using SARS-CoV-2 Spike (S) protein- or LPS-induced pro-inflammatory zebrafish and co-cultured human cell models, we found that ATG10S significantly reduced the expression of key pro-inflammatory cytokines (IFNA, IFNG, IL1B, IL6, TNF/TNFA, IL8, and CCL2), all transcriptionally regulated by MEF2A (myocyte enhancer factor 2A). Mechanistically, ATG10S bound directly to MEF2A at residues D61/D63, facilitating its selective autolysosomal degradation through MAP1LC3B/LC3B interaction, while it also competed with MAPK7/ERK5 for MEF2A binding to disrupt the TLR4-MAPK7-MEF2A signaling axis. This dual mechanism reduced both MEF2A protein levels and transcriptional activity, thereby attenuating cytokine overproduction. Importantly, ATG10S restored autophagic flux impaired by inflammatory stimuli and exhibited high specificity, sparing unrelated transcription factors. These findings established MEF2A as a critical regulator of the cytokine storm and revealed ATG10S as a distinctive macroautophagy/autophagy-linked immunomodulator that integrated selective autophagic degradation and transcriptional interference. Our study provides mechanistic insight into autophagy-mediated inflammatory regulation and highlights ATG10S as a promising therapeutic candidate for cytokine storm-associated diseases.: ATG: autophagy related; co-IP: co-immunoprecipitation; CQ: chloroquine; dpf: days post-fertilization; ELISA: enzyme-linked immunosorbent assay; hpi: hours post-injection; LC3B: microtubule-associated protein 1 light chain 3 beta; LIR: LC3-interacting region; LPS: lipopolysaccharide; MAPK7/ERK5: mitogen-activated protein kinase 7; MDMs: macrophages; MEF2A: myocyte enhancer factor 2A; MO: morpholino; S: spike protein; SQSTM1: sequestosome 1; TLR4: toll like receptor 4. - Source: PubMed
Publication date: 2026/05/26
Zhang Miao-QingWang Zheng-HaoZhang Jing-Pu - The macroautophagy/autophagy machinery has two ubiquitin-like (UBL) conjugation systems. The Atg8/MAP1LC3/GABARAP (yeast/human) and Atg12/ATG12 proteins are UBL substrates for Atg7/ATG7, a non-canonical E1 enzyme, that thioesterifies its substrates; however, autophagy requires a much greater amount of conjugated Atg8 (Atg8-PE) than Atg12 (Atg12-Atg5). Exactly how Atg7/ATG7 distinguishes between its two substrates to facilitate this differential biogenesis remains elusive. Here, analyses of recombinant complexes of yeast proteins reveal that the N termini of Atg8 and Atg12 are structural determinants for conjugation to Atg7, but play no role in conjugation to Atg3 or Atg10, non-canonical E2 enzymes. The disordered N terminus of Atg12 is a protector of the Atg12 C terminus and a negative regulator of Atg7-Atg12 conjugation and autophagy, whereas the N-terminal helical domain in Atg8 promotes autophagy and has a high avidity to Atg7. We show that balanced autophagy requires different specific N termini attached to the UBL domains, which are structural determinants for selective transfer to the native E2s. These findings deepen our understanding of the two autophagy UBL conjugation systems that is far from complete. - Source: PubMed
Publication date: 2026/05/15
Popelka HanaKlionsky Daniel J - Hydrogen sulfide (HS) is a colorless, toxic, asphyxiant gas. In recent years, industrial accidents involving HS exposure have frequently resulted in fatalities and disabilities. Acute respiratory distress syndrome (ARDS) poses a substantial burden on healthcare systems worldwide. The syndrome's heterogeneity and multifaceted pathogenesis, combined with a paucity of effective treatments, contribute to a persistently high mortality rate, which currently stands at 30-35%. The present study utilized metabolomics, transcriptomics, and CUT&Tag sequencing to explore ARDS pathogenesis, providing insights into its mechanisms and therapeutic targets for its treatment. Serum metabolomics for individuals with HS-induced ARDS identified lactate accumulation as a pivotal metabolic event that mediates changes in HS-induced ARDS biomarkers. Lactate, a potential biomarker of HS-induced ARDS, is associated with a poor prognosis. However, whether elevated lactate directly promotes HS-induced ARDS and the mechanisms underlying this effect remain unclear. Here, we demonstrate that lactate disrupts the alveolar epithelial barrier, thereby facilitating the development of ARDS. Mechanistically, lactate promotes histone H3K18 lactylation at the promoter for ATG10, a gene involved in the process of autophagy, driving its transcription and upregulating autophagy in alveolar epithelial cells, which results in disruption of the epithelial barrier. For rats, the reduction of lactate generation by a glycolytic inhibitor mitigates HS-induced ARDS, as evidenced by attenuated pulmonary edema. Our results show that the lactate-autophagy axis mediates HS-induced ARDS. Therefore, targeting the regulation of lactate production and/or autophagy is a therapeutic strategy for patients with HS-induced ARDS. - Source: PubMed
Publication date: 2026/05/07
Ling BingyuGeng PingFan BowenWu XiaolongYang YiLin JiahengLi WenjieLiu QizhanCheng ChengZhang JinsongWu Hao - Chlorophagy is an autophagy pathway that delivers chloroplast components into the vacuole for degradation, thus eliminating damaged chloroplasts. Chloroplast degradation is observed in Arabidopsis (Arabidopsis thaliana) mutants of MALTOSE-EXCESS 1 (MEX1), a maltose exporter in the chloroplast inner envelope membrane. However, whether autophagy is involved in the mex1 phenotypes is unknown. To extend our understanding of the signals that emanate from damaged chloroplasts and activate chlorophagy, we investigated how mex1 chloroplasts are degraded. Chlorotic mature leaves caused by maltose hyperaccumulation in mex1 plants contained swollen chloroplasts in the cytoplasm and degrading chloroplasts in the vacuole, together with heightened expression of autophagy-related (ATG) genes. The vacuolar degradation of mex1 chloroplasts required the core ATG proteins ATG7 and ATG10. ATG8-labeled structures accumulated on the surfaces of swollen mex1 chloroplasts. These findings indicate that maltose hyperaccumulation triggers chlorophagy via the core autophagy machinery. Notably, phenotypic analysis of mex1 atg double mutant plants suggested that excess chlorophagy aggravates the chlorosis seen in mex1 leaves. Transcriptome deep sequencing indicated that maltose-excess stress shares a similar transcriptomic response with high-light stress, which also triggers chlorophagy. Therefore, the signals inducing chlorophagy may be highly stimulated in mex1 leaves, making mex1 mutants effective tools for chlorophagy research. - Source: PubMed
Nakamura SakuyaWakazaki MayumiSato MayukoToyooka KiminoriNagano Atsushi JIshida HiroyukiHagihara ShinyaIzumi Masanori