Ask about this productRelated genes to: ATP11B Blocking Peptide
- Gene:
- ATP11B NIH gene
- Name:
- ATPase phospholipid transporting 11B (putative)
- Previous symbol:
- -
- Synonyms:
- ATPIF, ATPIR, KIAA0956
- Chromosome:
- 3q26.33
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-25
- Date modifiied:
- 2016-10-05
Related products to: ATP11B Blocking Peptide
Related articles to: ATP11B Blocking Peptide
- Brain aging is accompanied by cognitive decline and an increased risk of neurodegenerative disease, with neuronal aging being a key causative factor. Studies have shown that the earliest damage to blood-brain barrier (BBB) integrity occurs in the hippocampus, leading to the abnormal accumulation of Fe²⁺;however, the mechanisms underlying subsequent neuronal aging remain unclear. Using single-cell and spatial transcriptomic analyses, this study focuses on the phospholipid flippase ATP11B. We found that ATP11B deficiency facilitates the transport of Fe²⁺ from ependymal cells to hippocampal neurons, activating the Hippo signaling pathway and inducing mitochondrial respiratory dysfunction and dynamic imbalance, which results in neuronal ferroptosis and exacerbation of aging phenotypes. Mechanistically, ATP11B blocks mitochondrial respiratory function by regulating the chromatin accessibility of KLF4 to mitochondrial respiratory chain complex genes. Simultaneously, it impairs the mitochondrial quality control system, resulting in elevated levels of reactive oxygen species(ROS) and enhanced neuronal aging. The mitochondria-associated metabolite, lactate, facilitates histone lactylation of ferroptosis and the key aging-related genes Acsl4, Trp53 and Cdkn1a via the TEAD-YAP complex, thereby promoting transcription. This research uncovers the molecular mechanism through which ATP11B mediates neuronal aging: regulating the iron transport-mitochondrial plasticity axis. This provides a novel avenue for targeting iron homeostasis to intervene in cognitive decline and neurodegenerative disease. - Source: PubMed
Publication date: 2026/04/20
Qi WenxinLiu QianDong NaijunSun XiuqiaoWu PeiruZhou JianxinSun RuiqiLiu YihaoZhao Robert ChunhuaWang Jiao - The neurovascular unit (NVU) represents a multicellular functional ensemble pivotal to the preservation of cerebral homeostasis, encompassing endothelial cells, pericytes, glial cells (astrocytes, microglia, oligodendrocytes), and neurons. This complex orchestrates the regulation of blood-brain barrier (BBB) integrity, cerebral blood flow (CBF), and the metabolic microenvironment requisite for neuronal viability and functional competence. Accumulating lines of evidence have underscored that NVU dysfunction constitutes a critical early pathological event in neurodegenerative disorders, including Alzheimer's disease (AD) and vascular dementia (VaD). The present review summarizes the structural composition and core physiological functionalities of the NVU, with particular emphasis on the emerging role of lipid metabolism dysregulation in mediating NVU impairment-an aberrant process encompassing lipid droplets, apolipoprotein E (APOE), ATPase phospholipid transporting 11B (ATP11B), triggering receptor expressed on myeloid cells 2 (TREM2), and ATP-binding cassette (ABC) transporters. We further delineate the mechanisms by which disrupted lipid homeostasis elicits neuroinflammation, amplifies oxidative stress, impairs amyloid-β (Aβ) clearance, and precipitates BBB breakdown, ultimately culminating in cognitive decline. Simultaneously, this review examines controversies within the field, such as the specific role of apolipoprotein E ε4 allele (APOE4) in disease and highlights the significant pathophysiological differences between preclinical animal models and human diseases. Therapeutic strategies targeting lipid metabolism or the blood-brain barrier still face considerable challenges in clinical translation. Meanwhile, emerging tools such as lipidomics contribute to systematically analyzing the associated dysregulated lipid networks, thereby aiding in the identification of novel therapeutic targets. - Source: PubMed
Publication date: 2026/02/13
Li MengGeWang HuiYueTang ZhenYanYang ShuShengLin Li - Sepsis arises from a dysregulated host response to infection, leading to multiorgan inflammatory injury. Early diagnosis and treatment necessitate the identification of reliable immune biomarkers. This study investigated the relationship between aging, immunity, and sepsis by analyzing six human aging-related gene sets (656 genes). We identified 16 aging-related differentially expressed genes (DEGs) in sepsis. Among these, ATP11B, RBBP7, DOCK10, and NUP160 demonstrated the strongest connectivity with other genes and exhibited significant predictive power. Functional enrichment analysis (GO and KEGG) revealed distinct signaling pathway profiles between high-risk and low-risk sepsis groups (stratified based on risk scores). These dysregulated pathways, associated with multiple immune cells, were primarily linked to transcriptional dysregulation in cellular processes and cancer-related pathways. Experimental validation assays corroborated the roles of ATP11B and RBBP7. Collectively, our bioinformatic and experimental findings indicate that ATP11B, RBBP7, DOCK10, and NUP160 are implicated in the pathogenesis and progression of sepsis. But their potential for sepsis biomarkers still requires further verification. - Source: PubMed
Publication date: 2025/12/04
Sun XueyiGeng ShaoleiWang ZeyuanChen Qingjiang - Liver hepatocellular carcinoma (LIHC) is a leading cause of cancer-related mortality, with an immunosuppressive tumor microenvironment (TME) contributing to therapeutic resistance. Although neutrophils are recognized as key regulators of LIHC progression, their functional heterogeneity and metabolic drivers are not yet fully understood. - Source: PubMed
Publication date: 2025/10/23
Liu XingchaoZhang YinghuiHe YangkeLiang Liang - Parkinson's disease (PD) is a progressive neurodegenerative disorder lacking definitive diagnostic tests. To identify new diagnostic biomarkers, we employed glycoproteomics-mass spectrometry (MS) to investigate dynamic changes in protein -glycosylation across the serum, urine, and saliva of PD patients. Our comparative analysis of differentially expressed glycoproteins (DEGs) between PD patients and healthy controls (HCs) revealed distinct patterns. Specifically, ATPase phospholipid transporter 11B (ATP11B) was significantly upregulated in the serum of PD patients, while urine and saliva showed an opposite trend. Other key findings included elevated myeloperoxidase (MPO) in urine and clusterin (CLU) in serum. Zinc-α-2-glycoprotein (AZGP1), detected in all three biofluids, displayed increased sialylation and core fucosylation in serum but decreased levels in the saliva and urine of PD patients, along with a distinct bifucosylation pattern in saliva. These glycoprotein expression changes were further validated using enzyme-linked immunoassay (ELISA). Pathway analysis indicated that these DEGs are primarily involved in inflammatory response, complement activation, and synaptic plasticity, suggesting that glycosylation dysregulation may contribute to PD progression by modulating neuroinflammation and protein homeostasis. This study represents the first comprehensive analysis of multibiofluid -glycosylation in PD. The findings offer potential biomarkers and provide insights into the molecular mechanisms of the disease, which could ultimately inform early diagnosis and the development of targeted therapies. - Source: PubMed
Publication date: 2025/10/30
Zhao LingboHou ChunyanGao YuJin HongLiu Chun-FengLi ShuweiMa JunfengYang Shuang