APOF ELISA kit
- Known as:
- APOF Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-APOF-Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- APOF ELISA kit
Related genes to: APOF ELISA kit
- Gene:
- APOF NIH gene
- Name:
- apolipoprotein F
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-16
- Date modifiied:
- 2016-10-05
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- Perfluorooctane sulfonate (PFOS), a persistent member of the per- and polyfluoroalkyl substances family, has been increasingly associated with adverse carcinogenic effects; however, the molecular basis by which PFOS may contribute to prostate cancer (PCa) initiation and progression remains poorly defined. In this study, we aimed to systematically elucidate the mechanisms underlying PFOS-associated prostate carcinogenesis, with particular emphasis on the identification of actionable molecular targets and metabolically relevant pathways. By integrating network toxicology, transcriptomic differential analysis, weighted gene co-expression network analysis, multi-algorithm machine learning, single-cell and spatial transcriptomics, metabolomics, and structural modeling, we identified a four-gene core signature consisting of APOF, B3GAT1, CGREF1, and ENTPD5. Among these candidates, ENTPD5 emerged as the most prominent PFOS-associated target, showing marked enrichment in epithelial compartments across both single-cell and spatial datasets. Further integrative analyses converged on purine metabolism as a shared pathogenic vulnerability, and increased ENTPD5 expression was accompanied by elevated adenine abundance, supporting the existence of an ENTPD5-centered metabolic axis. Molecular docking and molecular dynamics simulations further suggested stable binding of PFOS to ENTPD5. In addition, immunohistochemical evidence consistently confirmed ENTPD5 upregulation in prostate cancer tissues. Collectively, our findings support a PFOS-ENTPD5-adenine mechanistic axis that may promote prostate cancer initiation and progression through purine metabolic reprogramming, and provide a potential foundation for the development of exposure-related biomarkers and preventive intervention targets in PCa. - Source: PubMed
Publication date: 2026/06/19
Lei YinLei PanShen GuohangLi XingbinTang HaotongWang RuoyanDai Yupei - Post-COVID-19 condition (PCC) is often accompanied by endocrine and immune dysregulation. Growth hormone (GH)deficiency has been reported in PCC patients, but its systemic effects remain poorly defined. - Source: PubMed
Publication date: 2026/06/03
Bai GuirongXie XiaominLi ShitingJi WenruiLi HuanHe YantingZhang LiLi LingPei SiqiYang YazhiWu YawenPing Rui - Pancreatic ductal adenocarcinoma (PDAC) represents a highly fatal malignancy with a huge public health burden. There is a critical need to better understand its etiology for developing innovative strategies for effective prevention and treatment. Leveraging genetic variants as instrumental variables, Mendelian randomization and proteome-wide association study have identified dozens of protein biomarkers associated with PDAC risk, yet potential nonlinear associations have largely been underexplored. In this study, we applied a nonlinear modeling approach, combining two-stage sliced inverse regression (2SIR) with nonlinear transformations via adjusted inverse regression (AIR), to investigate associations between genetically predicted protein concentrations in plasma and PC risk, by integrating blood proteome and genome data from the INTERVAL study (n = 3301), and a large genome-wide association study of PC risk (8275 cases and 6723 controls). We identified 25 genetically predicted proteins associated with PDAC risk after multiple comparison correction, including 22 that had been previously reported using linear modeling methods, and an additional three novel proteins (APOF, CCL15, and CHIT1). Importantly, there has been some level of evidence in the literature supporting potentially important roles of some of these novel proteins in PDAC development. Our study underscores the importance of accounting for nonlinear relationships in uncovering novel proteins associated with PDAC risk. If validated in further studies, our findings could improve the understanding of PDAC pathogenesis and inform future therapeutic and risk assessment strategies to reduce the burden from this deadly cancer. - Source: PubMed
Publication date: 2026/06/01
Zhu JingjingWu ChongMoaven OmeedYamazaki HajimeWei YumengDai BenWu Lang - Psoriasis is a complex immune-mediated disease closely linked to multiple systemic comorbidities. Although Mendelian randomization (MR) studies have been widely applied to investigate its potential risk factors, existing evidence remains fragmented and sometimes contradictory, limiting clinical translation. This study aimed to systematically consolidate MR findings on psoriasis and to develop an interactive online platform to support clinical decision-making. We systematically searched PubMed, Embase, and Web of Science for psoriasis-related MR studies published up to December 31, 2025, and performed a structured organization and evidence synthesis of the eligible studies. We also developed the MR-PsO Atlas platform using R and Shiny, integrating evidence retrieval, comparative analysis, and exploratory meta-integration where basic comparability was met. A total of 346 MR articles were included, from which 1046 causal associations were extracted. Overall, the findings support an association between disrupted lipid metabolism-particularly elevated LDL-C and certain phospholipid species-and increased psoriasis risk. The results also suggest possible causal links between psoriasis and psychiatric conditions such as depression, and identify IFNLR1 and APOF as potential novel therapeutic targets. For controversial findings, including those related to blood lipids and cancer risk, we further evaluated directional consistency across studies through exploratory meta-integration and discussion of heterogeneity. In addition, the MR-PsO Atlas platform has been successfully deployed and is openly accessible for the retrieval, comparison, and visualization of causal evidence. This study systematically collated published MR evidence on psoriasis and constructed a corresponding evidence atlas to support the retrieval, comparison and interpretation of causal findings. The results highlight multidimensional pathogenic mechanisms ranging from metabolism to immunity. The MR-PsO Atlas platform provides a practical tool for integrating genetic evidence with clinical practice and may help advance precision prevention and management of psoriasis. - Source: PubMed
Lu Jin-YuZeng WenlingWang KexinZhou JunlinPan WenhaoFan QiaomingYang QingyiLiu MantingRen Kai-Fang - Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a systemic disorder shaped by genetic variants and network-level interactions beyond obesity and insulin resistance. This study aimed to define the genetic and proteomic architecture of MASLD by integrating GWAS and plasma proteomic profiling from the UK Biobank. Genome-wide association analyses were conducted under additive and dominant models, with functional annotations performed using SIFT, PolyPhen-2, PROVEAN, REVEL, CADD, MutationTaster, and conservation metrics (GERP++, phyloP, phastCons, and B-statistic). Differential protein expression was assessed using the Olink platform, and STRING was applied for protein-protein interaction analysis. MASLD patients showed male predominance and significant differences in hepatic (AST, ALT, GGT, PDFF), metabolic (glucose, triglycerides, TyG index), and inflammatory markers (CRP, neutrophils, NLR, CAR). GWAS confirmed (rs738409, I148M) and (rs58542926, E167K) as major risk variants, while and showed weaker but conserved associations. Proteomics revealed downregulation of IGFBP2, IGFBP1, PON3, CKB, and APOF and upregulation of CPM, IGSF9, GUSB, ACY1, AFM, LEP, and GSTA1/3. PPI analysis identified ADIPOQ, LEP, FGF21, and ADH1B as central hubs in metabolic and inflammatory regulation. MASLD should be regarded as a network disease involving lipid metabolism, insulin/IGF signaling, mitochondrial function, and ECM-inflammatory pathways. These findings highlight and as major genetic drivers, while , , and peripheral proteins contribute regulatory roles, suggesting novel biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/04/28
Kang Sang WookKim Su KangBan Ju YeonPark Min Su