rHIV gp13, soluble Antigens - Infectious Disease
- Known as:
- rHIV gp13, soluble Antigens - Infectious Disease
- Catalog number:
- AGHIV-0255
- Product Quantity:
- 1-99 mg/ml/ea price
- Category:
- -
- Supplier:
- Arista Bio
- Gene target:
- rHIV gp13 soluble Antigens - Infectious Disease
Related genes to: rHIV gp13, soluble Antigens - Infectious Disease
- 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: rHIV gp13, soluble Antigens - Infectious Disease
1-Ethyl-3-(3-dimethylaminopropyl)carbodiimide Hydrochloride 〔Water Soluble Carbodiimide〕1-Ethyl-3-(3-dimethylaminopropyl)carbodiimide Hydrochloride 〔Water Soluble Carbodiimide〕1-Ethyl-3-(3-dimethylaminopropyl)carbodiimide Hydrochloride 〔Water Soluble Carbodiimide〕14.5 kDa translational inhibitor protein,Hrsp12,Perchloric acid soluble protein,Psp1,Rat,Rattus norvegicus,Ribonuclease UK1141‐Ethyl‐3‐(3‐dimethylaminopropyl)carbodiimide Hydrochloride 〔Water Soluble Carbodiimide〕1‐Ethyl‐3‐(3‐dimethylaminopropyl)carbodiimide Hydrochloride 〔Water Soluble Carbodiimide〕1‐Ethyl‐3‐(3‐dimethylaminopropyl)carbodiimide Hydrochloride 〔Water Soluble Carbodiimide〕3-hydroxy-3-methylglutaryl-Coenzyme A synthase 1 (soluble) primary antibody, Host: Rabbit4-1BB receptor, soluble (TNFRSF9) Human Host: E. coli TNFRSF9; ILA; 4-1BB; CD137; CDw1374-1BB receptor, soluble (TNFRSF9), Host: E. coli, Species: Human, Synonyms: TNFRSF9; ILA; 4-1BB; CD137; CDw13747 kDa autosomal chronic granulomatous disease protein,47 kDa neutrophil oxidase factor,Homo sapiens,Human,NCF1,NCF-1,NCF-47K,Neutrophil cytosol factor 1,Neutrophil NADPH oxidase factor 1,Nox organize5(6)-Carboxyfluorescein, Water Soluble Fluorophore Standard, 100mg5(6)-Carboxyfluorescein, Water Soluble Fluorophore Standard, 100mg5(6)_Carboxyfluorescein, Water Soluble Fluorophore Standard, 100mg71B10,Mouse,Mus musculus,PC1-like 3 protein,Pkd1l3,Polycystic kidney disease protein 1-like 3,Polycystin-1L3 Related articles to: rHIV gp13, soluble Antigens - Infectious Disease
- 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 - : Hepatocellular carcinoma (HCC) remains a major global health challenge with limited treatment options for advanced disease. Although immune checkpoint inhibitors (ICIs) have shown clinical benefits, response rates remain low, emphasizing the need for reliable biomarkers to guide patient selection. Given the critical role of metabolic reprogramming in immune modulation, this study aimed to identify a metabolic gene signature predictive of immunotherapy response in HCC. : Three independent transcriptomic datasets (GSE279750, GSE215011, and GSE235863) comprising 35 ICI-treated HCC samples were integrated after quality control and ComBat batch correction. Differentially expressed genes were identified using DESeq2 and limma, followed by integration of the meta-analysis results. Machine learning models, including LASSO regression and random forest algorithms, were applied for feature selection, and a logistic regression model was developed for predictive scoring. : A five-gene metabolic signature (PLPPR1, CNTN3, HOXA10, HAGLR, and ENPP3) demonstrated good discriminative ability between responders and non-responders, with consistent performance observed across internal validation analyses. Functional enrichment analysis revealed significant involvement of metabolic pathways, with HOXA10 linked to immune evasion and CNTN3 associated with immune activation. : This five-gene signature represents a biologically interpretable biomarker panel with potential utility for immunotherapy response stratification in HCC. The integrative analytical framework provides preliminary evidence supporting its value, warranting further validation in larger, independent clinical cohorts before clinical translation. - Source: PubMed
Publication date: 2025/12/26
Chao Hsu-WenLin Yi-Mei JoyWu Chen-Shiou - Lung adenocarcinoma (LUAD) is a common culprit of cancer-related deaths. Recent studies have revealed that succinylation-related genes (SRGs) are pivotal in cancer. However, the comprehensive characteristics and clinical significance of SRGs in LUAD occurrence are not clear. Therefore, our goal is to dig out the succinylation-related prognostic feature genes in LUAD. - Source: PubMed
Publication date: 2026/01/03
Li ZongyuLiu QingqingLu ErdanZhang TiantianZhu Yan