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
- The A2 β-casein variant has gained considerable interest in the dairy industry due to proposed health-related benefits, leading to an increasing frequency of the A2A2 genotype in dairy herds. Although the A1/A2 substitution in the β-casein gene (CSN2) does not directly affect gene regulation, previous transcriptomic studies have reported differences in mRNA isoform expression between A1A1 and A2A2 cows. Therefore, the objective of this study was to identify single nucleotide variants (SNVs) in A1A1 and A2A2 β-casein groups of cows using milk fat globule (MFG) RNA-seq data and to evaluate their predicted functional consequences. RNA sequencing was performed on MFG samples obtained from 14 lactating Holstein cows (A1A1, n = 7; A2A2, n = 7). Variants were classified according to their predicted effects as amino acid changing (AAC) variants, splice site effect (SSE) variants, or variants presenting both consequences. Additionally, variant data were integrated with previously reported mRNA isoform expression results, and only variants located in genes showing expression levels ≥ 0.2 FPKM were retained for further analysis. Candidate RNA-seq-derived variants differing between A1A1 and A2A2 β-casein genotype groups were identified in genes involved in mammary gland function and lactation, including mitochondrial function, lipid metabolism, vesicle trafficking and secretion, and RNA processing. Among the prioritized genes, A1A1 cows showed a greater representation of SNVs located in genes involved in mitochondrial oxidative phosphorylation (NDUFV2, NDUFAB1, COX7A2, and ATP5PF), while additional SNVs were identified in lipid metabolism-related genes (ACSL1, ATP10A, and MFGE8). In contrast, A2A2 group of cows showed a greater representation of SNVs located in genes involved in lipid metabolism (LPIN1, FASN, SPTLC2, and ATP11B) and vesicle trafficking and secretion (SEC31A, LRRK2, DBNL, EIPR1, and ABCG2). Overall, these findings provide additional insight into the molecular differences detected between A1A1 and A2A2 groups of cows. Although the predicted functional consequences of the identified variants are currently based on in silico analyses, the novel SNVs reported here constitute a valuable resource for future studies investigating the biological consequences associated with selection for the A2A2 β-casein genotype in Holstein dairy cattle. - Source: PubMed
Jiménez-Montenegro LucíaUrrutia OlaiaCánovas Ángela - Muscle fatigue, a potential risk factor for athlete injuries, lacks specific therapeutic targets and diagnostic biomarkers. This study aimed to identify biomarkers or targets for muscle fatigue to develop new diagnostic and treatment approaches. We utilized skeletal muscle and blood expression Quantitative Trait Loci data, employing the methods of Summary-data-based Mendelian Randomization (SMR) and Bayesian colocalization to identify genes that exhibit significant association with fatigue. DSigDB database and molecular docking method were used to predict potential drug candidates for the identified target genes and validated their interactions. Finally, the transcription levels of candidate genes were assessed in a muscle fatigue rat model using RT-qPCR. Using SMR and Bayesian colocalization analyses, we ultimately identified 24 genes stably associated with fatigue in skeletal muscle and 24 fatigue-related genes in blood, among which 6 common genes (ISYNA1, PABPC4, ZDHHC5, KATNAL1, UBOX5, and ATP11B) were found to serve as potential intervention targets for muscle fatigue and peripheral blood gene biomarkers. Several drugs associated with fatigue symptoms, including valproic acid, hesperidin, and cannabidiol were explored through DSigDB database and validated by molecular docking. RT-qPCR results confirmed that the transcriptional levels of Isyna1, Pabpc4, Zdhhc5, Katnal1, Ubox5, and Atp11b in the skeletal muscle of fatigue model rats were significantly altered compared to the control group (p = 0.020, p = 0.028, p = 0.001, p = 0.006, p = 0.027, p = 0.041). Our findings identified potential biomarkers or therapeutic targets for the diagnosis and treatment of fatigue, particularly muscle fatigue. - Source: PubMed
Publication date: 2026/05/25
Zhang YifeiZhang ZehanChen XiaoyaoDai MiaoZheng YuxiaoZhang WeiyueLi Feng - 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