ABCB8
- Known as:
- ABCB8
- Catalog number:
- 000902A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCB8
Related genes to: ABCB8
- Gene:
- ABCB8 NIH gene
- Name:
- ATP binding cassette subfamily B member 8
- Previous symbol:
- -
- Synonyms:
- EST328128, M-ABC1, MABC1
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2015-11-13
Related products to: ABCB8
Related articles to: ABCB8
- Chromosome copy number variations are poorly understood drivers of human malignancies. -7/del(7q) is common in acute myeloid leukemia, confers a poor prognosis, and is thought to harbor several tumor suppressors. Previously, we identified the histone methyltransferase KMT2C as a tumor suppressor in this region. Here, through a differentiation CRISPR screen in hematopoietic stem and progenitor cells, we find that the mitochondrial iron transporter ABCB8 is essential for their differentiation. ABCB8 deficiency accelerates leukemogenesis in vivo and disrupts iron homeostasis, reducing cytoplasmic iron availability and impairing iron-dependent enzymes, including the histone demethylase KDM6A. Consequently, ABCB8 loss elevates H3K27me3 levels, repressing differentiation genes in an iron- and KDM6A-dependent manner. Notably, ABCB8 and KMT2C, neighboring genes on 7q, cooperatively regulate H3K27me3 to suppress leukemogenesis. Our findings reveal ABCB8 as a tumor suppressor in -7/del(7q) acute myeloid leukemia and uncover an epigenetic collaboration between neighboring tumor suppressors, driven by iron-mediated chromatin remodeling. - Source: PubMed
Publication date: 2026/07/10
Zheng JiananPeng YimanDeng XintongZhang LanxinWang ZhongwangChen XuelanLi HeLi YanxinZhang QiZheng LiuxianQi ZiyiWang LanLu MinCui WenguoWang LiWu YuZhao WeiliNiu TingChen ChongLiu Yu - Perioperative neurocognitive disorders (PND) are prevalent complications in elderly patients following surgery, characterized by cognitive decline and memory impairment. This study investigates the contribution of plasma-derived exosomal microRNA hsa-miR-3677-3p to PND pathogenesis via ABCB8 regulation and subsequent induction of neuronal ferroptosis. Exosomes were isolated from plasma of patients with delayed neurocognitive recovery (dNCR) and non-dNCR patients. Characterization confirmed successful exosome isolation, revealing distinct microRNA profiles between the two groups. MicroRNA sequencing identified 69 differentially expressed microRNAs, with hsa-miR-3677-3p significantly upregulated in dNCR patients. Functional enrichment analysis implicated these microRNAs in mitochondrial function and nervous system development. In vitro overexpression of hsa-miR-3677-3p mimicked the pathological phenotype, leading to downregulation of ABCB8, which resulted in iron dyshomeostasis and oxidative stress, marked by reduced antioxidant capacity, intracellular iron accumulation, elevated malondialdehyde (MDA), a decreased glutathione/glutathione disulfide (GSH/GSSG) ratio, and increased mitochondrial lipid peroxidation (MitoPerOx). Treatment with the ferroptosis inhibitor Ferrostatin-1 (Fer-1) attenuated these alterations, restoring mitochondrial function and reducing oxidative damage. Taken together, our findings indicate that exosomal hsa-miR-3677-3p modulates ABCB8-mediated ferroptosis in neurons, highlighting a novel insight into PND pathogenesis and potential therapeutic strategies. - Source: PubMed
Publication date: 2026/01/24
Sun YiyanZuo YuanyuanZhang JingyaWu YingXia XiaohuanLiu Jianhui - ATP-binding cassette B8 (ABCB8) is a mitochondrial iron exporter known to prevent iron-dependent oxidative stress in cardiomyocytes and endothelial cells. However, the role of ABCB8 in endothelial and vascular function remains unclear. Here, we identified ABCB8 as a key regulator of vascular homeostasis. We found that loss of ABCB8 in endothelial cells triggers a pro-inflammatory transcriptional program, marked by upregulation of TGF-β isoforms and activation of TGF-β signalling. We show that TGF-β functions as an iron effector that drives mitochondrial reactive oxygen species (ROS) and mitochondrial damage, revealing a new ABCB8-iron-TGF-β axis in endothelial cells. In endothelial-specific inducible Abcb8 knockout mice (Abcb8), ABCB8 deficiency leads to endothelial activation, pro-inflammatory transcriptional reprogramming of smooth muscle cells (SMCs), fibroblasts and immune cells. Combination of intravital imaging experiments with ex vivo treatment of aortae from Abcb8 with the iron chelator deferoxamine or TGF-β receptor I inhibitor SB431542 suggests that ABCB8 suppresses iron-dependent TGF-β-mediated vascular inflammation in the aorta. In agreement, endothelial ABCB8 deficiency exacerbates atherosclerosis and hypertension in Apoe knockout mice, uncovering a critical atheroprotective role for ABCB8 and supporting its therapeutic potential in vascular disease. - Source: PubMed
Publication date: 2025/10/26
Chaker Ahmed BeyRinaldi LucaGillham OliviaPerez-Ternero CristinaBosseboeuf EmyDyson NickiSmith Danielle SydneyArdehali HosseinFantin AlessandroChikh AnissaAhluwalia AmritaRaimondi Claudio - Humans have three known ATP-binding cassette (ABC) transporters in the inner mitochondrial membrane (ABCB7, ABCB8, and ABCB10). ABCB10, the most studied of them thus far, is essential for normal red blood cell development and protection against oxidative stress, and it was recently found to export biliverdin, a heme degradation product with antioxidant properties. The molecular mechanism underlying the function of ABC transporters remains controversial. Their nucleotide binding domains (NBDs) must dimerize to hydrolyze ATP, but capturing the transporters in such conformation for structural studies has been experimentally difficult, especially for ABCB10 and related eukaryotic transporters. Purified transporters are commonly studied in detergent micelles, or after their reconstitution in nanodiscs, usually at nonphysiological temperature and using nonhydrolyzable ATP analogs or mutations that prevent ATP hydrolysis. Here, we have used luminescence resonance energy transfer to evaluate the effect of experimental conditions on the NBD dimerization of ABCB10. Our results indicate that all conditions used for determination of currently available ABCB10 structures have failed to induce NBD dimerization. ABCB10 in detergent responded only to MgATP at 37°C, whereas reconstituted protein shifted toward dimeric NBDs more easily, including in response to MgAMP-PNP and even present NBD dimerization with MgATP at room temperature. The nanodisc's size affects the nucleotide-free conformational equilibrium of ABCB10 and the response to ATP in the absence of magnesium, but for all analyzed sizes (scaffold proteins MSP1D1, MSP1E3D1, and MSP2N2), a conformation with dimeric NBDs is clearly preferred during active ATP hydrolysis (MgATP, 37°C). These results highlight the sensitivity of this human ABC transporter to experimental conditions and the need for a more cautious interpretation of structural models obtained under far from physiological conditions. A dimeric NBD conformation that has been elusive in previous studies seems to be dominant during MgATP hydrolysis at physiological temperature. - Source: PubMed
Publication date: 2025/02/18
Zoghbi Maria ENouel Barreto AnnabellaHernandez Alex L - Targeting mitochondrial ferroptosis presents a promising strategy for mitigating myocardial ischemia-reperfusion (I/R) injury. This study aims to evaluate the efficacy of the mitochondrial-targeted ferroptosis inhibitor SS-31@Fer-1 (elamipretide@ferrostatin1) in reducing myocardial I/R injury. - Source: PubMed
Publication date: 2025/01/22
Zheng HaoOu JinboHan HuiLu QizhengShen Yunli