ATG4D
- Known as:
- ATG4D
- Catalog number:
- Y214138
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATG4D
Related genes to: ATG4D
- Gene:
- ATG4D NIH gene
- Name:
- autophagy related 4D cysteine peptidase
- Previous symbol:
- AUTL4, APG4D
- Synonyms:
- APG4-D
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-11
- Date modifiied:
- 2016-02-23
Related products to: ATG4D
Related articles to: ATG4D
- The immunotoxicity of microplastic pollution in aquatic species is an issue of growing concern. However, the time course and mechanistic crosstalk underlying microplastic-induced hepatic injury remain poorly defined. This study examined the temporal hepatic response of Nile tilapia (Oreochromis niloticus) to 100 nm polystyrene microplastics (PS) over a 21-day exposure period, covering acute (7 days) and sub-chronic (14 and 21 days) phases. Histopathological evaluation showed no obvious liver lesions in exposed fish relative to controls at 7 days post-exposure (dpe). In contrast, progressive tissue damage marked by enhanced inflammatory cell infiltration was apparent at 14 and 21 dpe. PS exposure triggered time-dependent oxidative stress, with reactive oxygen species (ROS) and malondialdehyde (MDA) levels significantly increased and superoxide dismutase (SOD) activity decreased at 14 and 21 dpe. Ultrastructural analysis using transmission electron microscopy (TEM) further revealed distinct mitochondrial swelling and a notable increase in autophagosome numbers within hepatocytes at 7 and 14 dpe. Transcriptomic profiling indicated a biphasic dysregulation affecting both autophagy and inflammatory pathways. Specifically, autophagy-related pathways were significantly upregulated by 7 dpe, which preceded the marked activation of innate immune signaling pathways, such as NOD-like receptors (NLR) and mitogen-activated protein kinase (MAPK) signaling, observed at 14 dpe. After prolonged exposure to 21 dpe, both autophagic and inflammatory pathways were downregulated. qPCR confirmed this time-dependent expression profile for key genes associated with autophagy (sqstm1, map1lc3b, atg4d, atg5, becn1) and immune (il1β, nlrp3, tgfβ, map3k7, tnfa, tnfb, myd88) function. Pharmacological inhibition of autophagy by 3-methyladenine (3-MA) markedly abrogated the activation of NLR and MAPK signaling genes at 14 dpe, confirming a causal regulatory link between autophagy and innate immunity. Collectively, these findings suggest that microplastic exposure triggers a sequential immunotoxic transition in the fish liver. The early induction of autophagy may support subsequent immune activation, which eventually shifts to a broad suppression of immune pathways under sustained stress. This study offers new insight into the dynamic interaction between autophagy and innate immunity during microplastic-induced hepatotoxicity and highlights the potential risk of immunosuppression after long-term microplastic exposure. - Source: PubMed
Publication date: 2026/04/16
Wang FeilongGuo XiaomengGuo NaFan XiaolongXu HaiyanLi YuanyuanGao TianChen YixinZhao ChangleSun LinaWang DeshouXie XinWu Fengrui - Orthodontic tooth movement (OTM) requires a delicate balance between osteoclastic bone resorption and osteoblastic bone formation. Excessive mechanical stress disrupts this coupling, leading to alveolar bone loss. Lycium barbarum glycopeptide (LbGP), a natural bioactive compound with antioxidant and immunomodulatory properties, has been reported to regulate bone metabolism. However, its precise mechanism in orthodontic bone remodeling remains unclear. - Source: PubMed
Publication date: 2026/02/05
Lai ShuangZeng ChuanjieFu YizheMu Yandong - Immune checkpoint inhibitors have transformed melanoma therapy but frequently cause immune-related adverse events (irAEs), including colitis, that limit treatment. Reliable biomarkers predicting toxicity remain lacking. - Source: PubMed
Publication date: 2026/01/27
Reschke RobinBudde PetraZucht Hans-DieterMangana JohannaDummer ReinhardPfoehler ClaudiaWistuba-Hamprecht KilianWeide BenjaminHakim-Meibodi Lara-ElenaMeier FriedegundSchulz CarstenRichter JasminBräutigam ManualGutjahr ClaudiaSchulz-Knappe PeterHassel Jessica C - 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 - Colorectal cancer (CRC), which has high mortality and increasing morbidity is a major concern worldwide. The autophagy pathway plays a crucial role in carcinogenesis and drug resistance in this disease. Epigenetic modification is one of the main regulatory mechanisms for this pathway. This study aimed to investigate the impact of promoter methylation as one of the epigenetic modifications on the expression of autophagy-associated genes (ATGs) ( and ) in 21 CRC patients from southern Iran. The tissue DNA and RNA were extracted by standard phenol-chloroform extraction method and A BIOZOL RNA isolation kit, respectively. The methylation status and transcript levels of desired genes were ascertained using the methylation-specific PCR and quantitative real-time PCR methods, respectively. In the majority of studied patients, the relative mRNA expressions of were significantly higher in CRC tissues compared to normal ones. There was no significant relationship between the methylation of the genes and clinicopathological features of CRC patients. Interestingly, in most of the patients, the promoter hypermethylation of the , , and genes led to their high mRNA expression. Although promoter hypermethylation usually suppresses gene expression, the cancer type, stage, and compensatory mechanisms may reverse this association. This highlights the complexity of the epigenetic regulation of , , and genes in CRC. Further large-scale studies will contribute to discovering the exact influences of methylation in CRC carcinogenesis and thereby may thereby provide novel targets and biomarkers for this lethal illness. - Source: PubMed
Niknam MaryamNaghibalhossaini FakhraddinHosseini Seyed VahidZamani MozhdehMokarram Pooneh