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
- BackgroundThe increasing global burden of obesity and type 2 diabetes mellitus (T2DM) poses a major public health challenge. Nutrigenomics has emerged as a promising approach for managing these metabolic diseases through specific gene-diet interactions.AimThis systematic review aimed to synthesize evidence on the effects of nutrigenomics in the prevention and management of obesity and T2DM in human populations.MethodsAn extensive search was performed across four databases from inception to June 2025. Eligibility criteria were: randomized controlled trials (RCTs), participants with obesity (body mass index (BMI): 25-40 kg/m), prediabetes, and/or diagnosed with T2DM, nutrigenomics-based dietary intervention studies, and reporting obesity or diabetes management as the primary outcome. Risk of bias (RoB) was assessed using the RoB visualization tool. Narrative evidence synthesis was done owing to heterogeneity in study populations, genotypes, diet-gene associations, and outcome measures.SummaryOf 1278 articles screened, six RCTs met the eligibility criteria. The included studies demonstrated that nutrigenomics-based dietary interventions and related molecular responses may influence obesity and T2DM-related outcomes. Specific genetic variants, including , Melatonin receptor 1B (, Circadian locomotor output cycles kaput (, and PP2C domain-containing protein phosphatase 1K (, as well as molecular response markers such as and , were associated with changes in weight, BMI, waist circumference, and insulin sensitivity following dietary interventions. RoB analysis revealed that only one study (16.7%) demonstrated low RoB. The findings suggest a potential role for nutrigenomics in the prevention and management of obesity and T2DM; however, more robust and standardized RCTs are needed. - Source: PubMed
Publication date: 2026/09/17
Mathur AnkitaNandi DhruvaBanerjee AnweshaMehta Vini - Type 2 Diabetes (T2D) and hypertension (HTN) are common comorbidities in severe COVID-19, yet their specific impact on proteomic recovery remains unclear. This study analyzed plasma protein signatures of critical COVID-19 patients with and without these comorbidities (COVID-only group [COG] and COVID comorbid group [CTHG]) on the first and last days of ICU stay. Proteomic analysis revealed a systemic shift characterized by upregulated immune responses and downregulated metabolic processes at admission across all patients. Survival was fundamentally defined by the restoration of homeostasis; liver-derived proteins─including LPA, TTR, and AHSG─were initially suppressed but rebounded significantly in survivors. This homeostatic recovery was impaired in CTHG compared to COG, with CTHG survivors showing attenuated recovery of metabolic markers. Distinct mortality-associated signatures also emerged between groups. COG nonsurvivors exhibited liver failure and severe hemolysis marked by persistent suppression of haptoglobin (HP). In contrast, CTHG mortality was driven by lipid metabolism dysregulation, with CD5L and APOA2 levels dropping specifically in comorbid nonsurvivors, often accompanied by a paradoxical elevation in APOA4─likely reflecting impaired renal clearance rather than restored lipid homeostasis. These findings indicate that preexisting T2D and HTN hinder physiological resolution of metabolic and lipid dysregulation, providing proteomic evidence for distinct mortality risks associated with failure to restore metabolic homeostasis in comorbid COVID-19 patients. - Source: PubMed
Taleb SaraStephan NishaVemulapalli Praveen BabuSuhre KarsenHssain Ali AitSchmidt FrankChoi Sunkyu - Osteoporosis is a major health issue that has implications worldwide, both clinically and socioeconomically. Therefore, searching for informative bone health biomarkers that provide early information on bone changes and assess treatment efficacy is essential. Previously, our group used label-free proteomics and bioinformatic approaches to analyze the serum proteomic profile of postmenopausal women with normal bone mineral density (BMD), osteopenia, and osteoporosis. Based on their role in bone metabolism and literature review, a panel of 12 candidate serum biomarkers for low BMD was proposed. - Source: PubMed
Publication date: 2026/08/05
Aparicio-Bautista Diana IBecerra-Cervera AdrianaRivera-Paredez BereniceJiménez-Ortega Rogelio FLópez-Pérez Tania VSalmerón JorgeReyes-Grajeda J PabloHidalgo-Bravo AlbertoVelázquez-Cruz Rafael - Alkaptonuria (AKU) is a rare metabolic disorder caused by homogentisic acid accumulation and characterised by ochronosis, oxidative stress, chronic inflammation, and progressive connective tissue damage. This study aimed to define the circulating proteomic alterations associated with AKU and assess their relationship with nitisinone treatment. Plasma samples from 11 patients with AKU and 6 age- and sex-matched healthy controls were analysed by liquid chromatography coupled to tandem mass spectrometry using label-free quantification. Differentially abundant proteins were identified using thresholds of |logFC| ≥ 1 and Benjamini-Hochberg false discovery rate ≤ 0.01, followed by functional enrichment and treatment-stratified analyses. Twenty-two proteins were differentially abundant between AKU patients and controls. Complement components (C1R, C1S, C9, C4BPA, CPN2), fibronectin, clusterin, PGLYRP2, and haemoglobin subunits showed increased abundance, whereas most immunoglobulin chains, kallikrein, apolipoprotein A2, and alpha-1-antitrypsin showed decreased abundance. Functional enrichment highlighted complement activation, B-cell-mediated and humoral immune responses, immunoglobulin-related functions, platelet activation, and erythrocyte gas-exchange pathways. Correlation analysis linked several proteins, particularly CPN2, APOA2, C1R and C1S, to core biochemical parameters of disease activity. Treatment-stratified analysis identified fourteen proteins that remained significantly altered in both treated and untreated patients, forming a treatment-resistant core of the signature, while several complement-, coagulation-, and lipid-related proteins were significant only in one treatment subgroup. These findings define an AKU plasma proteomic signature dominated by complement activation and humoral immune alterations, together with extracellular matrix, erythrocyte-, and coagulation-associated changes. The persistence of most alterations across treatment groups suggests that residual systemic proteomic dysregulation remains despite nitisinone treatment. - Source: PubMed
Publication date: 2026/08/03
Finetti RebeccaVisibelli AnnaRoncaglia BiancaTrezza AlfonsoPeruzzi LuanaMarzocchi BarbaraSpiga OttaviaCicogni MattiaSalvini LauraTinti LauraCicaloni VittoriaCheleschi SaraRossi MarcoTinti CristinaSantucci Annalisa - Development of new-onset steatotic liver disease (SLD) has been increasingly observed after pancreatectomy. However, the pathophysiology of post-operative SLD remains poorly understood. This study aimed to clarify the risk factors for new-onset SLD after pancreatectomy and verify the utility of monitoring plasma apolipoprotein A2-isoforms (apoA2-i) as a potentially promising biomarker for evaluating pancreatic exocrine function. - Source: PubMed
Publication date: 2026/01/08
Matsushita AkiraOno TakashiYoshimori DaigoHamaguchi AkiraMurokawa TakahiroUeda JunjiShimizu TetsuyaKawano YoichiYoshioka MasatoKawashima MampeiNakamura YoshiharuNagashima KengoHasegawa YutaKiriyama TomonariTakeuchi KeikoKashiro AyumiHonda KazufumiYoshida Hiroshi