Ask about this productRelated genes to: OSBPL11 antibody
- Gene:
- OSBPL11 NIH gene
- Name:
- oxysterol binding protein like 11
- Previous symbol:
- -
- Synonyms:
- ORP-11, ORP11, FLJ13012, FLJ13164
- Chromosome:
- 3q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-28
- Date modifiied:
- 2016-10-05
Related products to: OSBPL11 antibody
Related articles to: OSBPL11 antibody
- Arsenic exposure remains a leading environmental health concern. MicroRNA (miRNA) dysregulation may provide a mechanistic link to arsenic-related diseases, yet the associations of arsenic species and arsenic methylation capacity with miRNA profiles in plasma and leukocytes remain largely unexplored. In a community-based population of 160 Chinese adults, we characterized the miRNA signatures of urinary arsenic species [arsenate, As(V); arsenite, As(III); monomethylarsonate, MMA; dimethylarsinate, DMA], their summed concentration (ƩAs), and arsenic methylation capacity. We further explored their potential origins, target genes, and functional pathways using RNA-seq data and public databases. After adjusting for multiple comparisons (FDR < 0.15), we identified 80 plasma miRNAs and 9 leukocyte miRNAs associated with As(V), 2 leukocyte miRNAs associated with inorganic arsenic [iAs = As(V) + As(III)], 6 plasma miRNAs associated with MMA, and 2 plasma miRNAs associated with secondary methylation index (SMI = DMA/MMA). Notably, 65 % (52/80) of the As(V)-related plasma miRNAs were located in chromosome 14q32. Most of these identified plasma miRNAs showed high enrichment in lymphocytes and arsenic-target organs, such as adrenal gland and brain. In miRNA-mRNA co-expression analysis, the identified miRNAs primarily targeted NRBF2, NUP50, OSBPL11, and SIRPD, and may be involved in pathways related to cancer, inflammation and immune function, and oxidative stress. Our findings provided novel insights into the miRNA regulatory mechanisms involved in arsenic exposure response at low to moderate levels. - Source: PubMed
Publication date: 2025/12/22
Wang YaxinLi WendingLi WeiyaWang YufeiXu XuedanYuan RuochenZhang XiaoQu JingliLong PinpinWang HaoHe MeianZhang XiaominWu TangchunYuan Yu - Sustained activation of the spindle assembly checkpoint (SAC) arrests cells in mitosis, resulting in mitotic cell death; therefore, SAC-activating drugs have been developed and clinically used as anti-cancer agents. However, some mitotic cells exhibit mitotic slippage, an event of mitotic exit without SAC satisfaction, and less sensitivity to these drugs. For developing efficient anti-cancer therapy, it is required to reveal the mechanism underlying the cell fate determination between cell death and mitotic slippage. In this study, we found that oxysterol-binding protein-like 11 (OSBPL11) is important for cell fate determination during mitotic arrest. OSBPL11 knockdown accelerates mitotic slippage and instead represses cell death during mitotic arrest by treatment with the Eg5 inhibitor S-trityl-l-cysteine (STLC), although the duration from mitotic entry to slippage or death is not altered. OSBPL11 knockdown exhibits a similar phenotype in paclitaxel-treated cells. Cyclin B1 levels are decreased in OSBPL11-knockdown mitotic cells. Treatment with the APC/C inhibitor proTAME mitigates both the decrease in the cyclin B1 levels and the acceleration of mitotic slippage caused by OSBPL11 knockdown. Although the OSBPL11 wild type could mitigate the acceleration of mitotic slippage and the repression of cell death induced by OSBPL11 knockdown, mutants lacking the lipid transport and lipid binding activities could not. Furthermore, OSBPL11 knockdown promotes survival upon STLC and paclitaxel treatments. These results suggest that OSBPL11 represses mitotic slippage and accelerates cell death during mitotic arrest in a manner dependent on both lipid transport and lipid binding activities, promoting the cytotoxic effect of SAC-activating drugs. - Source: PubMed
Publication date: 2025/11/26
Kawaji AyakaYuki RyuzaburoSaito YouheiNakayama Yuji - Rosai-Dorfman disease is an uncommon histiocytic neoplasm that is often self-limiting; however, rarely, it exhibits aggressive behavior and may undergo biological transformation to histiocytic sarcoma. Pathogenic genetic drivers of Rosai-Dorfman disease include recurrent genetic abnormalities in , , and Mutation of is a well-known oncogenic driver in histiocytic neoplasms, including up to 50% of Langerhans cell histiocytosis lesions, Erdheim-Chester disease, and adult and juvenile xanthogranuloma. However, mutations have been documented in only 4 reported Rosai-Dorfman disease specimens, and none were rearrangements. Herein, we report the first instance of Rosai-Dorfman disease with :: gene rearrangement, a unique gene fusion, and describe its clinicopathological features. - Source: PubMed
Publication date: 2025/08/19
Alvarez-Lesmes JessicaRosenberg AndrewCassidy Daniel P - Vitamin D deficiency is prevalent in Africa, but its genetic determinants are understudied. We report a genome-wide analysis of 25-hydroxyvitamin D (25(OH)D) concentrations in 3670 children from five countries across Africa with replication in four diaspora African ancestry populations (n=21,610). We identify a previously unreported locus at genome-wide significance in West African populations: (Oxysterol Binding Protein Like 11, lead variant, rs2979356, p=8.01 × 10). and molecular docking assays showed that OSBPL11 is a vitamin D binding protein likely involved in the intracellular binding of vitamin D metabolites. knockdown mice have increased fat, reduced triglycerides and improved glucose tolerance, and rs2979356 was associated with cardiometabolic health in adults of African ancestry. We also identify previously reported loci determining vitamin D status. Our study advances understanding of vitamin D genetics in Africa and indicates a novel function for in intracellular binding and transport of vitamin D metabolites. - Source: PubMed
Publication date: 2025/05/31
Mogire Reagan MMuriuki John MuthiiBayimenye Ruth FionaMentzer Alexander JChong AmandaGouveia Mateus HBentley Amy RBand GavinKing'ori PaulineMitchell RuthWebb Emily LSengupta DhritiEkunwe LynetteNdungu Francis MMorovat AlirezaMacharia Alex WCutland Clare LHemani GibranSirima Sodiomon BRamsay MichèleFigueiredo Camila APrentice Andrew MMadhi Shabir ARaffield Laura MSandhu Manjinder SBejon PhilipSmith George DaveyElliott Alison MWilliams Thomas NRotimi CharlesBourne Christina RBurgett AnthonyAdeyemo AdebowaleAtkinson Sarah H - With the global aging population, the incidence of aging-related diseases such as Alzheimer's disease (AD) and atherosclerosis (AS) is increasing. AS has also been identified as a key risk factor for AD. However, the conjoint molecular mechanisms driving these diseases remain unclear. This study first used bioinformatics analysis to analyze gene expression data in the cortex of AD patients and plaques of AS patients. We identified OSBPL11 as a gene whose expression co-increased under both conditions, and it is expressed in macrophages in AS patients and astrocytes in AD patients. Further validation was conducted through patient sample collection and an ApoE mouse model. Strikingly, our findings suggest that OSBPL11 plays a role in the development of both AS and AD, and that there is increased co-localization of OSBPL11 with macrophages and astrocytes. This discovery offers new insights into the association between AS and AD and offers a new target for the treatment AS and AD. - Source: PubMed
Publication date: 2025/05/23
Zhang HuayuChen YanyuXu QianWu XuanshuangHe NaiqiRen ZhongWang GuixueTang ZhihanXiang QiongLiu Lushan