gp130 mAb;mouse (RMbeta2)
- Known as:
- gp130 mAb;mouse (RMbeta2)
- Catalog number:
- ASACSA-710E
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- gp130 mAb;mouse (RMbeta2)
Related genes to: gp130 mAb;mouse (RMbeta2)
- Gene:
- ENPP3 NIH gene
- Name:
- ectonucleotide pyrophosphatase/phosphodiesterase 3
- Previous symbol:
- PDNP3
- Synonyms:
- PD-IBETA, gp130RB13-6, B10, CD203c
- Chromosome:
- 6q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-10
- Date modifiied:
- 2016-10-05
Related products to: gp130 mAb;mouse (RMbeta2)
Related articles to: gp130 mAb;mouse (RMbeta2)
- There is a common basis of the diabetic nephropathy (DN) and diabetic retinopathy (DR), but the common genes of DN and DR were unclear. - Source: PubMed
Publication date: 2026/04/28
He JuanZhang DandanWang Yan - Nonsteroidal anti-inflammatory drugs (NSAID) are the second most frequent cause of drug-induced hypersensitivity after β-lactam antibiotics. Diagnosing cross-intolerance reactions to NSAIDs remains challenging because conventional allergy tests are not useful and drug provocation tests (DPT), the current criterion standard, are resource-intensive and carry risk of severe reactions. Basophil activation testing (BAT) has emerged as a potential ex vivo diagnostic alternative. This study aimed to evaluate the diagnostic utility of the BAT for cross-intolerance reactions to NSAIDs among Vietnamese patients, including the identification of optimal drug type, concentration, and cutoff values. This validation study used a case-control design that involved 38 patients previously diagnosed with cross-intolerance to NSAIDs and 34 healthy controls. The diagnosis of NSAID cross-intolerance was established according to the international consensus guidelines, based on a detailed clinical history and, when indicated, a DPT. Both groups underwent BAT by using two NSAIDs at two concentrations each: acetylsalicylic acid (ASA) at 1.25 mg/mL and 0.5 mg/mL, and ketorolac at 1.25 mg/mL and 0.5 mg/mL. Flow cytometric analysis was performed to assess basophil activation based on CD63 and CD203c expression. ASA 1.25 mg/mL showed the best BAT diagnostic performance for cross-intolerance, achieving 55.3% sensitivity and 91.2% specificity by using cutoffs of ≥4% activated basophils and stimulation index (SI) ≥ 1.5. BAT demonstrates moderate sensitivity but high specificity for NSAID cross-intolerance, particularly when ASA is used as the stimulant. These findings support BAT as a complementary confirmatory tool in selected patients at high risk, although negative results do not exclude hypersensitivity and DPT remains necessary when diagnostic confirmation is required. Further validation in clinically relevant populations is needed before routine clinical implementation. - Source: PubMed
Nguyen Anh QuynhNguyen Ha Thi NgocHo Nhan ThiVu Mai ThiPham Yen Thi HaiMai Hien ThiNguyen Han Hoang KimHoang Oanh ThiNguyen Nguyet Thi MinhChu Hieu Chivan Nunen SherylCraig Timothy JohnNguyen Tu DacNguyen Dinh Van - ATP acting on P2X3 receptors contributes to carotid body (CB) hyperexcitability in spontaneously hypertensive rats (SHRs). We investigated whether this reflects altered ATP release and/or impaired ATP metabolism. Using in vitro CB preparations, we quantified ATP release in Wistar rats and SHRs (n = 10 each) and found significantly greater ATP release in SHRs (P = 0.00062). Intracellular ATP depletion in dissociated glomus cells was similar between strains (n = 4 each). Morphometric analysis revealed a disproportionate increase in glomus tissue, measured as tyrosine hydroxylase-positive area, in juvenile SHRs compared with Wistar rats (n = 8 each; P = 5.44 × 10 ). This enlargement was associated with upregulated Epas1 mRNA (n = 8 each), encoding HIF‑2α, a driver of CB hyperplasia. Transcripts for ATP‑degrading enzymes Enpp1, Enpp3 and Entpd2 were also downregulated in SHRs (n = 8 each), suggesting reduced extracellular ATP breakdown. Electrophysiological recordings in vitro and reflex testing in situ showed that topical ATP or α,β‑methylene-ATP applied to the CB evoked tachypnoea and sympathoexcitation in both strains, but SHRs displayed a greater sympathetic reflex (n = 4 each; P = 0.037), indicating increased sensitivity to purinergic stimulation. In contrast, testing adenosine transmission revealed no difference between strains; adenosine did not contribute to CB hyperexcitability in SHRs (n = 11 each; P = 0.53). Overall, increased ATP release in SHRs likely reflects CB enlargement from glomus cell expansion, compounded by reduced ATP‑degrading enzyme expression, thereby enhancing purinergic drive and chemoreflex sensitivity. KEY POINTS: The carotid bodies (CBs) of spontaneously hypertensive rats (SHRs) release more ATP than those of Wistar rats. Glomus cell expansion underpins CB hyperplasia and contributes to increased ATP release in juvenile SHRs. Upregulated Epas1 (i.e. HIF-2α) gene expression is likely responsible for CB hyperplasia in SHRs. ATP transmission is linked to exacerbated chemoreflex sympathoexcitation. Adenosine transmission does not contribute to CB hyperexcitability in SHRs. - Source: PubMed
Publication date: 2026/04/19
Felippe Igor S APauza AudrysGold Olivia M SShen XinBrognara FernandaNonu Rosanna RobertsPen Dylan KBose AabharikaBardsley Emma NPonnampalam Anna PMoraes Davi J APaton Julian F R - The Swine hepatitis E virus (SHEV) ORF3 protein is pivotal in pathogenesis, yet its regulation of host metabolic homeostasis via endogenous RNA networks remains unclear. This study aimed to elucidate how the SHEV ORF3-mediated circRNA-miRNA network modulates riboflavin metabolism and triggers the aberrant activation of the ko05212 pathway, while also evaluating their physical interactions using AlphaFold 3 structural simulations. To achieve this, high-throughput RNA sequencing, KEGG pathway analysis, and AlphaFold 3 structural simulations were employed to elucidate the circRNA-miRNA-mRNA regulatory network and potential physical interactions. Transcriptomics revealed a "dual activation" of Riboflavin metabolism and Pancreatic cancer pathways. Specifically, we identified an "ENPP Isozyme Switch," where upregulated hsa_circ_0077855 sponges miR-181a-2-3p, relieving repression of the metabolic enzyme ENPP3 and proto-oncogene KRAS. Furthermore, AlphaFold 3 simulations yielded an extremely low interface predicted Template Modeling score (ipTM = 0.08), refuting direct physical binding, and ORF3 was found to suppress the m6A eraser FTO, suggesting host epigenetic instability. Consequently, SHEV ORF3 induces metabolic remodeling through a dual "epigenetic-post-transcriptional" mechanism: disrupting m6A homeostasis via FTO suppression and constructing a pathogenic ceRNA network via the ENPP3/miR-181a/KRAS axis. These findings highlight the critical role of non-coding RNAs in driving the virus-induced "pre-pathological state". - Source: PubMed
Publication date: 2026/03/09
Luo WeihaoLi JiyaWu ShengpingWang LingjieYin YulongCao XinWang LeliJiao Hanwei - Clear-cell renal cell carcinoma (ccRCC) is an immune-desert tumor. This study investigates the role of ectonucleotide pyrophosphatase/phosphodiesterase 3 (ENPP3) as a potential therapeutic target and immune-checkpoint enzyme in ccRCC. - Source: PubMed
Publication date: 2026/02/19
Ma JiaxingWu YayunLin GuangzhengSun XinGeng HaoZhang TaoYu Dexin