Arg2 ELISA kit
- Known as:
- Arg2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-Arg2-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- Arg2 ELISA kit
Related genes to: Arg2 ELISA kit
- Gene:
- ARG2 NIH gene
- Name:
- arginase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 14q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-08-06
- Date modifiied:
- 2014-11-19
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- The stems and leaves of (CPSL) are commonly treated as agricultural waste, yet they are rich in antioxidants and other bioactive compounds. In order to explore their applicability in livestock feeding, a systematic evaluation was conducted on the dose-dependent effects of CPSL on yak production traits and meat characteristics. A total of forty yaks were randomly allocated into four experimental groups, including a control group fed a basal diet and three treatment groups receiving the basal diet supplemented with 0.5%, 1.0%, or 2.0% CPSL. Results indicated that the 2.0% CPSL supplementation group exhibited the highest net meat yield while significantly improving meat processing suitability. Through transcriptomic profiling, 13 genes were found to be differentially expressed between the control and CPSL-treated groups, with functions related to myofiber formation and energy metabolic processes. A marked upregulation of insulin-sensitizing gene 1 (INSIG1) and arginase 2 (ARG2) was observed specifically in the group receiving the intermediate CPSL dose. Metabolomic profiling further revealed that 81 shared differentially abundant metabolites were primarily involved in the AMPK signaling and oxidative phosphorylation pathways. Collectively, CPSL not only fortifies yak beef production by optimizing growth and slaughter performance but also significantly enhances meat tenderness and processing adaptability through regulating core mechanisms governing redox hubs and energy metabolism. These findings offer novel insights into the high-value utilization of CPSL as a feed additive. - Source: PubMed
Publication date: 2026/04/03
Yang XueLi YihengShen RuhengDuan YufengSong RendeShi HongmeiKong XiangyingHua YongliZhang WangangZhang Li - Glucagon activates amino acid catabolism and gluconeogenesis in adults. Elevated glucagon concentrations in the fetus occur in pregnancy complications such as fetal growth restriction and hypoxia, yet the impact of chronic fetal hyperglucagonemia is unknown. Using chronically catheterized pregnant sheep, glucose tracers, and liver tissue biopsies, we investigated the effects of nine days of glucagon infusion at 5 or 50 ng·kg-1·min-1 in late-gestation fetal sheep that increased plasma glucagon concentrations by 800%. Glucagon-infused fetuses were euglycemic and exhibited lower plasma and hepatic amino acid concentrations. They also had increased hepatic mRNA expression of amino acid catabolism genes, including ARG2, GLS2, BCAT1, BCAT2, GLUL, HAL, UROC1, and PPARGC1A. Metabolite profiling in liver tissue revealed enrichment of pathways associated with amino acid degradation, elevated tri- and diphosphate nucleotides, and changes in fatty acid metabolites, supporting enhanced hepatic energy metabolism from amino acid oxidation. Hepatic glycogen content was reduced in glucagon-infused fetuses and the gluconeogenic genes PCK1 and G6PC1 were increased, though fetal glucose production was not detected. These findings demonstrate that in the fetal liver, chronic hyperglucagonemia activates amino acid catabolic pathways, indicating a physiological role for glucagon in regulating fetal amino acid homeostasis. These findings have implications for understanding fetal hepatic adaptations during chronic fetal hyperglucagonemia that can occur in the setting of fetal growth restriction or hypoxia. - Source: PubMed
Publication date: 2026/04/15
Tanner Amelia RCilvik Sarah NNguyen Marjorie ABrown Laura DAnthony Russell VWright Clyde JWesolowski Stephanie RRozance Paul J - Human solid tumors such as hepatocellular carcinomas (HCC) establish a complex immunosuppressive tumor microenvironment (TME) that undermines the efficacy of existing immunotherapies such as chimeric antigen receptor T (CAR T) cell therapy. To advance immunotherapy for HCC, it is crucial to delineate the molecular mechanisms that drive TME formation and immune evasion. - Source: PubMed
Publication date: 2026/04/09
Zhu LishengWu MengFeng BingbingZhang YuXu YangYu Lili - Erectile dysfunction (ED) is a multifactorial condition influenced by vascular, neuroendocrine, metabolic, and psychological factors. Growing evidence suggests that genetic variation may contribute to individual susceptibility, severity, and therapeutic response, particularly regarding nitric oxide (NO) signaling and vascular pathways. To systematically synthesize evidence on genetic biomarkers associated with the risk, severity, or therapeutic response of ED in adult men. - Source: PubMed
Publication date: 2026/03/24
Ferezin Letícia PerticarraraKayzuka CezarPaiva de Alcântara E Silva MaurielyTavares Peixeiro Cecilia NogueiraRondon-Pereira Vitória CarolinaTanus-Santos Jose EduardoLacchini Riccardo - Adenosine-to-inosine (A-to-I) mRNA editing alters genetic information post-transcriptionally and can impact protein sequence and function, yet its regulation in bacteria remains unclear. Here, we profiled A-to-I editing in across nutrient-rich Luria-Bertani (LB) and minimal M9 media and different growth phases. Our analysis expanded the repertoire of TadA-dependent A-to-I edited mRNAs to 27, including 12 novel sites, and revealed that editing levels were dynamic and markedly increased at the stationary phase in LB but not in M9. Editing levels were independent of mRNA expression yet correlated with tRNA-Arg2 downregulation, and overexpressing tRNA-Arg2 reduced mRNA editing, demonstrating substrate competition for TadA, the sole bacterial tRNA adenosine deaminase. Mutants with TadA-deficient editing or reduced tRNA-Arg2 expression displayed similar LB-specific growth defects. Moreover, tRNA-Arg2 expression, tRNA-Arg2-dependent codon usage, and tRNA-Arg2 editing were all elevated in LB compared to M9. These findings establish regulatory principles for bacterial RNA editing, implicate tRNA editing in nutrient-responsive fitness, and provide a framework to explore the physiological roles of mRNA editing.IMPORTANCEAdenosine-to-inosine (A-to-I) mRNA editing is a recently discovered post-transcriptional mechanism in bacteria, yet its regulation and physiological roles remain poorly understood. In this study, we expand the catalog of TadA-dependent mRNA editing events in and identify key regulatory factors influencing editing levels, including nutrient availability, growth phase, and tRNA-Arg2 expression. Linking altered tRNA-Arg2 levels and editing to growth defects specifically in rich medium further demonstrates that tRNA editing contributes to nutrient-responsive fitness. Together, these findings establish a framework to explore bacterial RNA editing as a regulated process with potential implications for environmental adaptation and cellular function. - Source: PubMed
Publication date: 2026/04/03
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