ACOX2
- Known as:
- ACOX2
- Catalog number:
- 001027A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACOX2
Related genes to: ACOX2
- Gene:
- ACOX2 NIH gene
- Name:
- acyl-CoA oxidase 2
- Previous symbol:
- -
- Synonyms:
- BRCACOX, BRCOX, THCCox
- Chromosome:
- 3p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2016-06-01
Related products to: ACOX2
Related articles to: ACOX2
- Protein biomarkers are increasingly recognized as indicators of metabolic status, immune response, and reproductive performance in cattle. However, comparative data among different breeds commonly raised in Indonesia remain limited. - Source: PubMed
Publication date: 2026/08/04
Gustina SriHasbi HasbiAzis Ismah UlfiyahMaulana TulusHamsir Siti Nuraisya - Gastric cancer (GC) is a prevalent malignancy worldwide with high morbidity and mortality. Its insidious onset and lack of sensitive early biomarkers impede routine screening, so most patients present advanced or metastatic disease at first diagnosis, leading to poor prognosis and scarce curative options. Surgery, chemotherapy and targeted therapy serve as standard GC treatments, however their efficacy is restricted by metastasis, adverse reactions and drug resistance, which drives the rapid development of immune checkpoint inhibitor (ICI)-based immunotherapy. Although monoclonal antibodies targeting programmed cell death protein 1/programmed cell death 1 ligand 1 (PD-1/PD-L1) resulted in significant survival benefits for GC patients, some patients exhibited an ineffective response. Our previous study has shown that Weitiao No. 3 (WD-3) enhanced the efficacy of anti-PD-1 immunotherapy by regulating intestinal flora in gastric cancer (GC) mice, in this study, huPBMC-NOG-dKO mice and MGC803 cells were used for in vivo and in vitro functional validation to explore the regulatory mechanism of WD-3 in GC immunotherapy. 16 S rRNA sequencing analysis of mouse fecal samples demonstrated that WD-3 significantly enriched the intestinal abundance of and in GC model mice. Targeted serum metabolomics further verified that WD-3 markedly elevated serum isobutyric acid level in GC mice. Combined with HE staining and tumor growth monitoring, both the intestinal flora mixture consisting of and and isobutyric acid prominently enhanced the anti-tumor efficacy of PD-L1 inhibitors in GC mice. Mechanistically, RNA sequencing and qRT-PCR assays identified as the most significantly up-regulated gene in isobutyric acid-treated MGC803 cells. Functional experiments using CCK-8 assay and flow cytometry revealed that isobutyric acid inhibited the viability and induced apoptosis of MGC803 cells, and such phenotypic changes were effectively rescued by knockdown. Furthermore, results from the CytoTox 96 cytotoxicity assay and ELISA revealed that combined treatment with isobutyric acid and PD-L1 inhibitor elevated the levels of LDH, IL-2, TNF-α, IFN-γ, Perforin 1 and GzmB, while suppressing IL-8, PD-1 and TIM-3 expression in CD8⁺ T cells co-cultured with MGC803 cells. Notably, all these regulatory effects were abrogated when MGC803 cells were transfected with si-ACOX2. These results suggested that WD-3 modulated intestinal flora to elevate isobutyric acid level, thereby enhancing the inhibitory effect of PD-L1 inhibitor on tumor growth and boosting the anti-tumor activity of CD8⁺ T cells by up-regulating ACOX2 expression in GC. These findings may provide novel targets for improving anti-PD-L1 therapy against GC. - Source: PubMed
Publication date: 2026/07/15
Zhu HengzhouZhu XiaodanHuang XiaonaQian YiyangLi JiahuiZhang JiayingNiu DongJin Chunhui - The parotoid gland secretion of the medicinal toad () is the primary source of Chansu, a valuable traditional medicine. However, the lack of understanding regarding the biological regulation of venom synthesis limits the optimization of farming practices and quality control. Here, we integrated histology, lipidomics, transcriptomics, and untargeted metabolomics to delineate the regulatory mechanisms governing venom accumulation and biosynthesis, aimed at guiding aquaculture management. Histological results revealed that the parotoid gland is a highly regionalized organ, where structural maturity is positively correlated with toxin storage capacity, providing a morphological basis for determining optimal harvest timing. This structure is underpinned by a distinct lipid profile: high levels of triglycerides supply essential energy for massive venom production, while enriched ceramides and sphingomyelin form a specialized barrier to ensure high-quality venom encapsulation. Transcriptome analysis indicated that the upregulation of steroid and primary bile acid biosynthesis genes (e.g., , , , , and ) drives the synthesis of bioactive bufadienolides. Furthermore, we identified key enzymatic regulators─including CYP450s (, , ) and acetylases (, )─as potential genetic markers for identifying high-yielding venom. Collectively, these findings provide a scientific basis for establishing standardized farming protocols, advancing molecular breeding strategies for this important medicinal species, and achieving sustainable exploitation of toad venom. - Source: PubMed
Publication date: 2026/06/18
Wang YaxiYu XiaopingPeng JufangWang Hongyuan - Peroxisomal metabolism was long regarded as a housekeeping pathway with minimal involvement in cancer. Nonetheless, accumulating data demonstrate that peroxisomal lipid oxidation critically modulates genome stability and antitumor immunity. The acyl-CoA oxidase (ACOX) family-including ACOX1, ACOX2 and ACOX3-catalyzes the initial oxidative step of peroxisomal fatty acid β-oxidation, and governs lipid metabolism, redox homeostasis, as well as acyl-CoA-related post-translational modifications such as lysine crotonylation. Notably, ACOX2 has gained growing attention for its connections with DNA damage sensing, cGAS-STING activation and anticancer immunity. Dysregulated ACOX2 expression correlates with tumor progression, therapeutic response and clinical prognosis across various cancers, though direct functional evidence varies by tumor type. Mechanistically, ACOX2-related lipid metabolism maintains intracellular redox balance and stress adaptation, with its pathway-specific signaling still poorly defined. In clear cell renal cell carcinoma, ACOX2 binds MRE11 to destabilize the MRN complex, inducing cytosolic DNA buildup and cGAS-STING-mediated type I interferon signaling, while its universal role in other malignancies awaits validation. ACOX2 acts in a context-dependent fashion: it exerts tumor-suppressive effects in liver, prostate and lung cancers, yet facilitates metabolic adaptation and chemoresistance under therapeutic stress. This review summarizes ACOX2 as a key integrator of metabolism, immunity and genome integrity, and highlights its translational potential as a cancer biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/05/23
Zheng MeiguiZhao BaihuiChen XiuyingZhao Ying - Cholestatic liver disease (CLD) is a severe hepatobiliary disorder with limited treatment options. Although the natural compound Isoastragaloside II (IAS II) has been suggested to possess general hepatoprotective properties, its therapeutic efficacy against CLD has not been reported. In this study, the therapeutic potential and underlying mechanisms of IAS II for CLD were investigated using a murine model established by 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) feeding. It was demonstrated that DDC-induced cholestatic liver injury was significantly alleviated by IAS II treatment, as indicated by the normalization of key serum biochemical parameters. An integrated analysis of histopathological, protein, and gene expression data demonstrated that IAS II treatment effectively suppressed the ductular reaction, inhibited hepatic fibrosis, and attenuated inflammation. Analysis of 16S rRNA sequencing data revealed that IAS II treatment was accompanied by alterations in gut microbiota composition, including an enrichment of Bacteroides and a reduction in Lachnospiraceae_NK4A136_group. Antibiotic depletion experiments demonstrated that the hepatoprotective effects of IAS II were abrogated by gut microbiota depletion, confirming the essential role of the gut microbiota in its pharmacological action. At the molecular level, IAS II activated both the PPAR-α pathway (as indicated by transcriptomic analysis) and the FXR pathway (as confirmed by subsequent validation), which collectively resulted in a significant reduction in the hepatic accumulation of toxic bile acids (BAs). In vitro studies in LCA-induced HepG2 cells further revealed that the restoration of PPAR-α, ACOX2, FXR, and BSEP protein expression by IAS II required receptor activation, as these effects were blocked by specific inhibitors. In summary, to our knowledge, this study provides the first demonstration that a protective effect against DDC-induced cholestatic liver injury is conferred by IAS II through coordinated regulation of PPAR-α and FXR signaling, restoration of BA homeostasis, and in a gut microbiota-dependent manner, with these effects requiring the activation of both PPAR-α and FXR pathways, thereby identifying IAS II as a novel and promising therapeutic candidate for CLD. - Source: PubMed
Publication date: 2026/05/20
Luo LanLiu WeiQi ShenglanChen JiameiZhang HuaMu YongpingChen GaofengYuan Wei'anLiu PingZhang Linzhang