APOH MaxPab mouse polyclonal antibody (B01)
- Known as:
- APOH MaxPab mouse pab (anti-) (B01)
- Catalog number:
- H00000350-B01
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- APOH MaxPab mouse polyclonal antibody (B01)
Related genes to: APOH MaxPab mouse polyclonal antibody (B01)
- Gene:
- APOH NIH gene
- Name:
- apolipoprotein H
- Previous symbol:
- B2G1
- Synonyms:
- BG
- Chromosome:
- 17q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1987-09-11
- Date modifiied:
- 2015-12-17
- Gene:
- HCG18 NIH gene
- Name:
- HLA complex group 18
- Previous symbol:
- -
- Synonyms:
- FLJ31598, FLJ25550, Em:AB014087.1
- Chromosome:
- 6p22.1
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2004-06-15
- Date modifiied:
- 2018-05-16
- Gene:
- HCG19P NIH gene
- Name:
- HLA complex group 19 pseudogene
- Previous symbol:
- -
- Synonyms:
- AB014085.4
- Chromosome:
- 6p21.3
- Locus Type:
- pseudogene
- Date approved:
- 2004-06-15
- Date modifiied:
- 2014-11-19
- Gene:
- PRR3 NIH gene
- Name:
- proline rich 3
- Previous symbol:
- -
- Synonyms:
- CAT56, Em:AB014077.1, Em:AB023052.2
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-21
- Date modifiied:
- 2016-10-05
- Gene:
- RANP1 NIH gene
- Name:
- RAN pseudogene 1
- Previous symbol:
- -
- Synonyms:
- Em:AB014080.2
- Chromosome:
- 6p22.1
- Locus Type:
- pseudogene
- Date approved:
- 2003-07-02
- Date modifiied:
- 2019-01-22
Related products to: APOH MaxPab mouse polyclonal antibody (B01)
Related articles to: APOH MaxPab mouse polyclonal antibody (B01)
- Chronic kidney disease (CKD) is a major health burden, yet its underlying mechanisms and early predictors remain poorly understood. - Source: PubMed
Publication date: 2026/07/09
Ru DongmeiWang XinyueXiao CongmeiCheng ManjingZhou FuxianMamuti ReziwanguliXi YueDeng KuiWang JiaoXu LinZheng Ju-ShengChen Yu-Ming - Cetaceans face the risk of thromboembolism due to diving and decompression responses. However, cetaceans maintain normal blood circulation. This study explores the molecular mechanisms cetaceans use to mitigate diving-associated hemostatic challenges during diving. Forty-six species were analyzed, including 18 cetaceans, 9 artiodactyls, and 19 other terrestrial mammals. Thirty-nine anticoagulant genes and proteins were examined, identifying 6 genes (ANXA2, ANXA5, FGA, FGB, PLAUR, and PLG) with conserved evolution, 4 genes (ANXA2, PDGFB, SH2B3, THBS1) with positive selection, and 12 proteins (APOH, FGA, FGB, FGG, GP1BA, PLAU, PRKCD, PRKG1, SERPINF2, SERPING1, TMPRSS6, and TMX1) with specific amino acid sites in cetaceans. Ancestral state reconstruction revealed independent evolution of deep diving behavior in different cetacean lineages, particularly within Odontoceti. Correlation analysis linked the evolution of the APOE gene with diving depth, suggesting its role in diving adaptation. These analyses suggest that cetaceans may help reduce the risk of thrombosis during diving by lowering platelet activity, enhancing fibrinolysis, and modulating the coagulation cascade. These analyses suggest that cetaceans may mitigate diving-associated thrombotic risk by modulating platelet activity, fibrinolysis, and the coagulation cascade. Overall, this study identifies candidate anticoagulant-related genes and amino acid substitutions for future functional validation of hemostatic adaptation in cetaceans. - Source: PubMed
Publication date: 2026/07/06
Lv WenjunCao LiZhang YaXu ShixiaRen Wenhua - Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality. Angiogenesis drives HCC progression, but reliable biomarkers remain limited. - Source: PubMed
Publication date: 2026/06/20
Zhu ZhanweiGuo CaoShen HongZeng ShanLi Namei - 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 - Cannabidiol (CBD) is increasingly being used in veterinary medicine; however, its systemic molecular effects in dogs remain poorly characterized. This study employed label-free quantitative proteomics to compare the serum proteomic responses of healthy dogs ( = 18) after 30 days of oral CBD delivery via three distinct matrices: hemp by-product feed pellets (F), CBD-infused oil (O), and semi-solid treat (SN). The verified chronic doses differed among the groups. Multivariate analysis revealed distinct formulation-specific proteomic signatures, with the F group clustered separately from the O and SN groups. Despite dose and matrix variations, all groups shared a core metabolic response characterized by downregulation of apolipoproteins (APOA4, APOC3, APOC1, and APOH) and upregulation of hemoglobin subunits (HBA and HBB), indicating CBD-mediated modulation of lipid metabolism and redox homeostasis. The high-exposure groups (O, SN) uniquely exhibited upregulation of proteins involved in vascular integrity and tissue scaffolding (e.g., TGFB1, PDGFRB, and VWF), while the SN group also showed induction of immunomodulatory and cytoprotective markers, such as clusterin (CLU). These findings demonstrate that the CBD delivery matrix critically influences systemic bioavailability and the scope of proteomic remodeling. Although all formulations engage core metabolic pathways, high-bioavailability formats induce additional signatures suggestive of vascular stabilization and stress resilience, providing a molecular rationale for optimizing CBD-based therapeutic formulations in canine medicine. - Source: PubMed
Publication date: 2026/05/13
Theerapan WutthiwongLimsuwan SasithornRattanasrisomporn JatupornPloypetch SekkarinTansakul Natthasit