Human Apolipoprotein A2 ELISA , APOA2
- Known as:
- Human Apolipoprotein A2 Enzyme-linked immunosorbent assay test , APOA2
- Catalog number:
- E01A0510
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Apolipoprotein A2 ELISA APOA2
Related genes to: Human Apolipoprotein A2 ELISA , APOA2
- Gene:
- APOA2 NIH gene
- Name:
- apolipoprotein A2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-04-26
Related products to: Human Apolipoprotein A2 ELISA , APOA2
Related articles to: Human Apolipoprotein A2 ELISA , APOA2
- Pancreatic ductal adenocarcinoma (PDAC) is associated with high mortality rates therefore early diagnosis and treatment is essential in reducing mortality. Blood tests that can identify high-risk individuals is an unmet medical need. In this pilot observational study, remnant samples from routine clinical lab orders were tested on 265 patients presenting with abdominal pain and/or presence of pancreatitis, pancreatic cyst, gall stones, abdominal infections (due to herpes or H. pylori), hepatic cirrhosis/hepatitis, non-pancreatic cancer, or pre-, new onset, controlled and uncontrolled diabetes. - Source: PubMed
Publication date: 2026/07/21
Wu Alan H BOng Chui MeiAlamillo MelissaClark ZakaryWong ChristinJung Giman - - Source: PubMed
Publication date: 2026/07/07
Esmaeily ZahraSotoudeh GityRafiee MasoumehKoohdani Fariba - Several studies have investigated the clinical and immunological aspects of medication-related osteonecrosis of the jaw (MRONJ). However, the underlying immunological mechanisms and signaling pathways involved in its pathophysiology remain incompletely understood. This systematic review and meta-analysis, complemented by bioinformatics analyses, aimed to identify proteomic biomarkers associated with MRONJ. - Source: PubMed
Publication date: 2026/06/10
Deróbio Helena OliveiraSouza Isabela Dos ReisCaldeira François Isnaldo DiasBasso Fernanda GonçalvesPansani Taisa Nogueira - Tendon disease is a highly prevalent musculoskeletal disorder characterized by extracellular matrix (ECM) disorganization and fibroblast activation, contributing to fibrotic tissue healing and impaired function. While extracellular vesicles (EVs) have emerged as key mediators of intercellular communication and drivers of fibrosis in various tissues, their role in tendon pathology remains poorly understood. In this study, we developed a physiologically relevant 3D in vitro model that recapitulates biophysical features of healthy and fibrotic tendon microenvironments to investigate EV-mediated contributions to tendon remodeling. Primary tendon-derived cells on diseased scaffolds had increased proliferation, higher collagen III and fibronectin protein expression, and inferior cellular alignment. Proteomic profiling of EVs revealed temporally regulated, microenvironment-dependent cargo reflective of disease progression in vitro. Diseased EVs were enriched in cytoskeletal, ECM-remodeling, and inflammatory proteins, including vimentin (VIM), Annexin A2 (ANXA2), MMP2, and INHBA, suggesting an EV-mediated role in promoting matrix remodeling, fibroblast activation, and chronic inflammation. Notably, the temporal analysis demonstrated the late-stage emergence of stress-responsive and myofibroblast-associated proteins such as ENO1 and DES, underscoring the model's ability to capture the progressive nature of tendon pathology. In contrast, EVs from the healthy mimetic model demonstrated cargo associated with metabolic homeostasis and lipid transport, including APOA2 and CKM. Collectively, these findings highlight the utility of our tendon model as a dynamic platform for studying tendon pathology and establishing EVs as both sensitive indicators of microenvironmental state and potential mediators of fibrotic progression. This work provides a foundation for future studies exploring the diagnostic and therapeutic potential of EVs in tendinopathy. - Source: PubMed
Publication date: 2026/04/24
Shama Kariman AGreenberg Zachary FMeyler Evangeline MBrown Emily MHe MeiTaylor Brittany L - Apolipoprotein A2 (APOA2) is a component of several plasma lipoproteins, yet its physiological and pathological functions remain unclear. Conflicting data regarding its effects on plasma lipid levels and cardiovascular risk indicate that APOA2 activity may be context dependent. Here, we employed adenovirus-mediated gene transfer of human APOA2 into male C57BL/6, ldlr, and apoe mice fed a western-type diet for 2 weeks to investigate in parallel its impact on lipoprotein metabolism and atherogenesis under different conditions of dyslipidemia and atherosclerotic burden. In normolipidemic C57BL/6 mice, APOA2 expression raised plasma VLDL/LDL cholesterol and triglycerides, consistent with inhibition of lipoprotein lipase activity. In HDL density fractions, cholesterol was unaffected while triglycerides increased. In contrast, APOA2 expression in ldlr mice reduced cholesterol and triglyceride levels across all major lipoprotein fractions, including HDL density fractions. Similarly, in apoe mice, APOA2 expression markedly lowered VLDL cholesterol and triglycerides, though cholesterol and triglycerides in LDL and HDL density fractions were increased. Interestingly, following oral administration of olive oil containing [C]-cholesterol and [H]-triolein to ldlr mice, APOA2 expression enhanced tracer deposition in the aorta and aortic root. Corroborating this finding, immunohistochemical analysis of aortic root cryosections from both ldlr and apoe mice revealed increased staining for APOA2 and APOB in APOA2-expressing animals, suggesting augmented accumulation of APOB-containing lipoproteins in the arterial wall. Collectively, these findings support a pro-atherogenic role for APOA2. Although under dyslipidemic conditions APOA2 may superficially appear protective by lowering circulating APOB-containing lipoproteins, mechanistic evidence indicates that it promotes vascular retention of APOB-containing particles, thereby accelerating atherogenesis. - Source: PubMed
Zvintzou EvangeliaFenyo Ioana MadalinaIonita RaduKakafoni GeorgiaDumitrescu MadalinaAlemi MariaDaraban Bianca SanzianaMarinos KonstantinosGafencu Anca VioletaKypreos Kyriakos E