Ask about this productRelated genes to: ATG4A Blocking Peptide
- Gene:
- ATG4A NIH gene
- Name:
- autophagy related 4A cysteine peptidase
- Previous symbol:
- AUTL2, APG4A
- Synonyms:
- -
- Chromosome:
- Xq22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-05
- Date modifiied:
- 2016-02-23
Related products to: ATG4A Blocking Peptide
Related articles to: ATG4A Blocking Peptide
- Platelet activation is a key contributor to myocardial ischemia/ reperfusion (MI/R) injury. Although hydroxysafflor yellow A (HSYA) possesses cardioprotective and antiplatelet properties, its specific mechanisms in modulating platelet activation during MI/R remain unclear. - Source: PubMed
Publication date: 2026/04/21
Zhang YaqiWang ZhihuiLi RuotongLiu ZhiweiZhang RuiLi RuoyunWang MinSun Guibo - Members of the mammalian Atg8-protein family (ATG8), including the MAP1LC3/LC3 and GABARAP subfamilies, play essential roles in selective macroautophagy/autophagy. However, their functional distinctions during viral infection remain poorly understood. Here, we show that S-adenosyl-L-methionine (SAM)-binding viral proteins, such as nsp14 from coronavirus and NP868R from African swine fever virus (ASFV), reprogram autophagy by shifting antiviral LC3B activity toward GABARAP-mediated mitophagy in an ATG4A-dependent manner. Mechanistically, the SAM-binding motif allows these viral proteins to stabilize mRNA, thereby increasing ATG4A expression and redirecting autophagic flux from LC3B-mediated virophagy to GABARAP-dependent mitophagy. This shift suppresses innate immune responses by targeting both MAVS-dependent interferon signaling and virophagy, ultimately enhancing viral replication. Collectively, our findings uncover a previously unrecognized immune evasion strategy in which SAM-binding viral proteins rewire autophagy from antiviral to proviral pathways. ACTB: actin beta; ATG: autophagy related genes; ASFV: African swine fever virus; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CQ: chloroquine; CS: citrate synthase; ExoN: exoribonuclease; GABARAP: GABA type A receptor-associated protein; IFN: type I interferon; IFNB: interferon beta; IPEC-J2: intestinal porcine epithelial cell line-J2; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAVS: mitochondrial antiviral signaling protein; MT-CO2/COX2: mitochondrially encoded cytochrome c oxidase II; nsp14: nonstructural protein 14; OPTN: optineurin; PEDV: porcine epidemic diarrhea virus; RNMT/N7-MTases: RNA guanine-7 methyltransferase; SAM: S-adenosyl-L-methionine; SQSTM1/p62: sequestosome 1; TAX1BP1: Tax1 binding protein 1; TCID: 50% tissue culture infective dose; TOMM70: translocase of outer mitochondrial membrane 70; TOMM20: translocase of outer mitochondrial membrane 20; WT: wild-type. - Source: PubMed
Publication date: 2026/01/01
Li YahuiZhu YaWang FeiYing XuezhiZhao ChenchenSi WeiZhong JiepengYin WeiLin LuluLi JianYan YanZhou JiyongHu Boli - Cordycepin (COR) is a compound extracted from Cordyceps sinensis. We found that COR exacerbates the acute anaemia induced by 5' fluorouracil (5-FU). Healthy mice were intraperitoneally injected with COR at doses of 2, 4, or 8 mg/kg for 10 consecutive days, which produced a slight decrease in the red cell distribution width in the peripheral blood and a reduction in the erythroblast levels in the spleen. Furthermore, COR (8 mg/kg) treatment delayed reticulocyte recovery when 5-FU was used to induce anaemia. A single 5-FU dose decreased the levels of reticulocytes and erythroblasts compared with those in the control mice; this decrease was more pronounced when COR was also administered. The percentage of reticulocytes was lower in the bone marrow of COR-treated mice than in the 5-FU group. COR treatment inhibited erythroid differentiation, characterised by a decrease in the proportion of erythroblasts and low mRNA levels of Hba, Hbb, Uros, Gata-1, and Epb42, compared with the control mice; these effects were reversed by treatment the AMPK inhibitor, compound C. COR treatment also reduced the mitochondrial membrane potential. Mitochondrial matrix genes, such as those involved in haeme synthesis (Alas-2), metabolic enzymes (Pck2 and Mthfd2), the respiratory chain (Ndufs7), and autophagy (Atg4a and Atg4d) were downregulated in the COR-treated erythroid precursors. Compound C reversed the COR-induced decrease in the mitochondrial membrane potential as well as Alas-2, Pck2, Atg4a, and Atg4d mRNA levels. COR treatment substantially delayed reticulocyte recovery in the peripheral blood and reduced the number of erythroblasts in the spleen following 5-FU-induced anaemia. The mechanism of action of COR involves inhibiting erythroid differentiation via activating AMPK. - Source: PubMed
Publication date: 2025/10/11
Yang LeiKong SiqiShi HailanXu LiangyuWei ZichenChen YafengFang Lei - Osteosarcoma is one of the most prevalent malignant tumors in pediatric cancer, with survival rates remaining stagnant for over a decade, particularly among patients with metastatic disease. Thus, identifying novel therapeutic targets is critical for improving clinical outcomes. The ATG4 family (ATG4A, ATG4B, ATG4C, and ATG4D) encodes proteases essential for autophagy, a process implicated in cancer progression and drug resistance. However, the role of ATG4 proteins in osteosarcoma remains unclear. This study showed that silencing ATG4 family members using small interfering RNA (siRNA) induced G1-phase cell cycle arrest and promoted cell death in osteosarcoma cells. Among them, ATG4D knockdown significantly impaired cell migration and invasion. Consistently, stable knockdown of ATG4D via short hairpin RNA (shRNA) reduced cell motility and tumorsphere formation. Moreover, ATG4D depletion enhanced autophagic markers, including LC3B-II puncta and p62 protein levels, and sensitized osteosarcoma cells to starvation and chemotherapy-induced cell death. In vivo, osteosarcoma cells harboring ATG4D-targeting shRNA exhibited reduced tumor growth and elevated apoptosis in xenografted mice compared to control cells. Clinically, ATG4D protein expression was elevated in osteosarcoma tissues compared to normal bone cells, with higher levels correlating with poor overall survival, particularly in patients older than 10 years or with tumors located in the lower limbs. These findings suggest that ATG4D may serve as a potential diagnostic biomarker and therapeutic target for osteosarcoma. - Source: PubMed
Liu Pei-FengYang Shan-WeiYang Wen-HsinHuang Shu-FangTsai Ching-YangHsu Chien-JenTseng Ho-HsingLee Cheng-HsinShu Chih-Wen - Low nitrogen (LN) stress is a major limiting factor affecting crop growth and productivity. Understanding the genetic basis of LN tolerance is essential for improving nitrogen use efficiency in . A genome-wide association study (GWAS) was conducted on a panel of 275 accessions using a semi-automated hydroponic system to evaluate five seedling traits-leaf number (NL), shoot length (SL), root length (RL), shoot fresh weight (SFW), and root fresh weight (RFW)-under LN conditions. The system ensured environmental uniformity and high-throughput phenotyping. Significant phenotypic variation was observed across accessions, and correlation analysis suggested that RFW and SFW are key traits associated with LN tolerance. GWAS identified 71 significant SNPs, with 20 candidate genes located near these loci. Gene Ontology analysis revealed enrichment in nitrogen compound transport functions. Several genes such as , , and were implicated in nitrogen uptake, transport, remobilization, and stress adaptation. This study highlights the polygenic nature of LN tolerance and the importance of precise phenotyping in detecting stable genetic signals. The identified candidate genes are involved in nitrogen metabolism, autophagy, RNA processing, and amino acid transport, with transcriptomic evidence supporting the LN-responsive expression of . Comparative analysis with previous studies revealed unique SNP loci, likely due to differences in germplasm, nitrogen levels, and experimental design. These findings broaden our understanding of the genetic mechanisms underlying LN tolerance and provide promising targets for breeding varieties with improved nitrogen use efficiency. - Source: PubMed
Publication date: 2025/07/07
Chen JingdongXie LingliHou XianfeiYang RuiLiu JinDai XigangXue TianyuanYin ShuaiXu BenboZhang XuekunZeng ChangliXu Jinsong