APOA2 ELISA kit
- Known as:
- APOA2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-APOA2-p
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- APOA2 ELISA kit
Ask about this productRelated genes to: APOA2 ELISA kit
- 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
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- 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 - Non-alcoholic fatty liver disease (NAFLD) is a globally prevalent chronic liver disease, and its progression is closely associated with Kupffer cells (KCs). This study aims to characterize C-X-C motif chemokine ligand 9꞉secreted phosphoprotein 1 (CS) polarization in KCs and investigate its intercellular communication with endothelial cells (ECs) in NAFLD. - Source: PubMed
Lu YaoNi WenjuanChen RongcuiWang Wei - Apolipoprotein A-II, the second most abundant protein in HDL, plays a key role in HDL maturation and reverse cholesterol transport. It has a stronger affinity for lipids than apolipoprotein A-I (APOA1), which forms HDL's structural scaffold. Like APOA1, APOA2 mainly consists of amphipathic alpha helices that help it interact with lipid surfaces. Using computer modeling and mutagenesis, we developed a structural model for lipid-bound human APOA2. The protein's single disulfide bond restricts it to a belt-like configuration in discoidal HDL particles. Our model shows several key features: (i) most basic residues of APOA2 are in the hairpin loop; (ii) salt bridges and π-π interactions stabilize the structure; (iii) two high-lipid affinity helical regions are in each APOA2 monomer; and (iv) the hairpin structure facilitates interactions with other proteins like APOA1 or APOA2. Chemical crosslinking and MS/MS analysis identified 16 crosslinks; Fifteen of the 16 crosslinks are consistent with the double hairpin belt model, strongly supporting the proposal that the disulfide-dimer double hairpin belt is the primary structure of APOA2 in humans. - Source: PubMed
Publication date: 2026/07/27
He YiSong HyunYou YoungkiMelchior John TJones Martin KAller Stephen GDavidson W SeanHeinecke Jay WSegrest Jere P