ABCD3
- Known as:
- ABCD3
- Catalog number:
- 000927A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCD3
Related genes to: ABCD3
- Gene:
- ABCD3 NIH gene
- Name:
- ATP binding cassette subfamily D member 3
- Previous symbol:
- PXMP1
- Synonyms:
- PMP70, ZWS2
- Chromosome:
- 1p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-03-03
- Date modifiied:
- 2015-11-13
Related products to: ABCD3
Related articles to: ABCD3
- Diabetic kidney disease (DKD) is characterized by progressive tubular injury, yet the mechanisms linking metabolic stress to organelle dysfunction remain unclear. Here, utilizing human renal biopsies, db/db and high-fat diet with streptozotocin-induced diabetic mouse models, and cultured renal tubular epithelial cells (RTECs) exposed to 30 mM glucose, we demonstrate that impaired pexophagy drives peroxisomal dysfunction and tubular damage in DKD. Diabetic conditions induced marked accumulation of the peroxisomal membrane protein PMP70 (encoded by ABCD3/Abcd3) in RTECs, reflecting impaired peroxisomal turnover. We identified ubiquitin-specific peptidase 30 (USP30) as a contributor of this process. Expression profiling and localization analyses revealed that USP30 expression was significantly elevated in vivo and in vitro under high-glucose conditions and predominantly localized to RTECs. Global genetic depletion of USP30 restored peroxisomal function and metabolic homeostasis, enhanced pexophagy, and attenuated tubular injury. Mechanistically, USP30 antagonized the ubiquitination of the peroxisomal import receptor PEX5, thereby suppressing pexophagy. Furthermore, deletion of the essential autophagy factor ATG5 abolished the protective effects of USP30 deficiency. These findings reveal a critical role of USP30 mediated regulation of pexophagy in DKD and suggest that USP30 may serve as an experimental intervention target to alleviate tubular injury in DKD. - Source: PubMed
Publication date: 2026/08/21
Li JiaHua ChaoyangLi GuangpuZhai FurongRen JingjingPan ShaokangFeng QiWen JianguoLiu DongweiLiu ZhangsuoDuan Jiayu - This study systematically evaluated the anti-breast cancer potential and mechanisms of the cannabidiol (CBD) derivative MCPB-21. The structure of MCPB-21 was confirmed by nuclear magnetic resonance (NMR). The study analyzed differentially expressed genes associated with breast cancer using public databases and verified the binding affinity of MCPB-21 to glycogenin-2 (GYG2) through molecular docking. Additionally, the effects of MCPB-21 on apoptosis, invasion capacity, and lipid metabolism were evaluated in MDA-MB-231 and MCF-7 breast cancer cells using flow cytometry, Transwell invasion assays, cell proliferation assays, and Oil Red O staining. Western blot was employed to examine expression changes in proteins related to fatty acid β-oxidation and ferroptosis, including Acyl-CoA Oxidase 1 (ACOX1), ATP Binding Cassette Subfamily D Member 3 (ABCD3), ATP Binding Cassette Subfamily D Member 4 (ABCD4), Peroxisomal l-bifunctional enzyme (EHHADH), Carnitine palmitoyltransferase 1α (CPT1α), Glutathione Peroxidase 4 (GPX4), Solute Carrier Family 7 Member 11 (SLC7A11), and Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4). The role of fatty acid oxidation in ferroptosis was further analyzed using the ACOX1 inhibitor 10,12-Tricosadiynoic acid (500 nM). Additionally, the effects of MCPB-21 on fatty acid oxidation and ferroptosis were evaluated by interfering with GYG2 expression. Ferrostatin-1 (Fer-1) rescue experiments were conducted to verify the dependence of MCPB-21-induced cell death. Finally, the anti-tumor efficacy of various doses of MCPB-21 was compared to the control drug CBD. experimental results showed that MCPB-21 can affect the behavior of breast cancer cells by inducing cancer cell apoptosis, increasing reactive oxygen species (ROS) levels, and promoting lipid accumulation. At the same time, Western blot detection showed that MCPB-21 could downregulate key enzymes of fatty acid β-oxidation (ACOX1, ABCD3, ABCD4, EHHADH, CPT1α) and antioxidant factors (GPX4, SLC7A11), and upregulate the enzyme ACSL4 that promotes lipid peroxidation. Mechanistic studies further showed that MCPB-21 affects the expression of ACOX1 by regulating GYG2, inhibits fatty acid β-oxidation, and induces ferroptosis. At the same time, the combined use of ACOX1 inhibitors enhanced lipid accumulation and ROS levels, verifying its role in regulating fatty acid oxidation. In animal experiments, MCPB-21 (10 and 40 mg/kg) significantly inhibited the growth of nude mouse transplanted tumors, caused tumor tissue necrosis, inhibited the proliferation marker Ki67, and regulated the expression of ferroptosis-related proteins (GPX4 and SLC7A11 decreased, and ACSL4 increased). Immunohistochemical analysis showed that MCPB-21 had a stronger anti-tumor effect than CBD, mainly by regulating the fatty acid β-oxidation pathway to promote ferroptosis. In summary, MCPB-21 exhibits excellent anti-breast cancer potential. Its mechanism of action is mainly to achieve anti-tumor effects by inhibiting fatty acid β-oxidation and activating ferroptosis, which provides a theoretical basis and potential therapeutic strategy for the development of new anti-breast cancer drugs. - Source: PubMed
Publication date: 2026/07/15
Mao MengjieWang ChunyuLu YingchunTao QingxiuZeng LongLi JingLiu Bin - Tumor hypoxia promotes dedifferentiation and metabolic reprogramming in hepatocellular carcinoma (HCC), undermining normal liver functions. Here, we identify the E3 ubiquitin ligase RNF126 as a hypoxia-inducible "peroxisomal fate" switch that links the hypoxic microenvironment to loss of hepatocyte differentiation. Under hypoxia, HIF-2α drives RNF126 expression, which in turn ubiquitinates the peroxisomal membrane transporter ABCD3, triggering selective peroxisome autophagy (pexophagy) and depletion of peroxisomes. This organelle loss ablates very-long-chain fatty acid β-oxidation and hydrogen peroxide detoxification, erasing key hepatocyte differentiation features. We show that genetic RNF126 ablation restores peroxisomal functions and impairs hypoxic HCC growth. Leveraging these insights, we developed a small-molecule RNF126 inhibitor, D665-1412, which selectively blocks hypoxia-induced pexophagy. D665-1412 treatment stabilizes peroxisomes, normalizes lipid metabolism, and reactivates hepatocytic differentiation markers, thereby "redifferentiating" HCC cells and suppressing tumor progression in vitro and in vivo. Our findings establish the HIF-2α-RNF126-ABCD3 axis as a driver of HCC dedifferentiation and present organelle-targeted redifferentiation therapy as a promising approach for liver cancer. - Source: PubMed
Publication date: 2026/06/09
Su QiYang YichunRen JiayanZhang YuFu LijuanWu QingHan XuZhang Yanmin - High ammonia nitrogen stress significantly compromises the survival of under low-salinity conditions. However, existing studies predominantly focus on ammonia nitrogen responses under single stressors or normal seawater salinity. The molecular regulatory mechanisms, metabolic remodeling patterns, and key pathway interactions in shrimp subjected to high ammonia nitrogen stress under low-salinity environment remain unclear. In this study, we employed integrated transcriptomic and metabolomic analyses to unveil the underlying molecular responses and metabolic biomarkers in the gills of to ammonia stress under low-salinity conditions. First, . underwent low-salinity acclimation from 30‱ to 5‱ salinity and was then reared for one week to acclimate to the experimental environment. Subsequently, shrimp were treated with 42.32 mg/L ammonia nitrogen for a consecutive 96 h period. Integrated transcriptomic and metabolomic analyses elucidated the stress response patterns in the gills of under low-salinity ammonia nitrogen exposure. Specifically, 352, 802, and 140 differentially expressed genes (DEGs) were identified at 12 h, 48 h, and 96 h post-exposure, respectively. GO and KEGG enrichment analyses revealed that the significant DEGs were primarily enriched in six major pathways: autophagy, immune-related pathway, ABC transporter, fatty acid degradation and metabolism, metabolic pathway, and PPAR signaling pathway. Metabolomic profiling identified numerous differentially accumulated metabolites (DAMs) in both positive and negative ion modes, with significantly altered DAMs mainly consisting of organic acids and their derivatives, phospholipids, and other related metabolites. Key DAMs included taurine, guanosine, 1-palmitoyl-sn-glycero-3-phosphocholine, pseudouridine, and betaine. Integrative multi-omics analysis revealed that mediates stress responses by modulating five core pathways under low-salinity/high-ammonia-nitrogen dual stress: fatty acid degradation and metabolism (e.g., acyl-CoA dehydrogenase short chain (), acetyl-CoA acetyltransferase 2 ()), autophagy (e.g., autophagy-related protein 101-like ()), immune regulation pathway (e.g., V-type proton ATPase subunit H-like (), actin-5C-like ()), metabolic pathway (e.g., molybdopterin synthase catalytic subunit-like (), cytochrome P450 2U1-like ()), and ABC transporter (e.g., ATP-binding cassette sub-family D member 3-like (), ATP-binding cassette sub-family B member 10 ()). Through characterization of these core pathways, this study reveals the fundamental mechanisms by which responds to high ammonia nitrogen stress following low-salinity acclimation, providing a theoretical foundation for estuarine shrimp farming. - Source: PubMed
Publication date: 2026/04/13
Zhao YutongDing YangyangZhou FalinHu XiaojuanYang QibinCao Yucheng - Studies have shown that abnormal mitochondrial function is closely associated with the development and progression of colorectal cancer (CRC); however, prognostic models based on mitochondria-related genes are still lacking. We systematically analyzed the expression of mitochondrial-related genes in CRC patients and constructed and validated a mitochondrial gene risk prognostic model using various bioinformatics methods across the TCGA and GEO databases. We also investigated the effects of tumor microenvironment, immune cell infiltration, tumor mutation load, and drug sensitivity on patient prognosis. In addition, we overexpressed the ABCD3 gene using CRISPR-dCas9 technology and further explored the role of ABCD3 in cell proliferation and apoptosis by protein blotting and flow cytometry. The mitochondrial gene risk model was effective in predicting the prognosis of CRC patients, which showed that the high-risk group was significantly different from the low-risk group in terms of immune cell infiltration. Further analyses revealed a strong association between risk scores and clinicopathological features, immune infiltration, and drug sensitivity. We constructed a prognostic prediction model based on mitochondria-related genes and found that ABCD3 provides a novel biomarker for the individualized treatment of CRC. - Source: PubMed
Publication date: 2026/04/16
Chen ShuyuLi YouyueDing WenboYin YujuanXin XiaoqiWei XueyangBao SiqiPan BeiSun HuilingXu Mu