ELISA Chicken,Gallus gallus,Peroxiredoxin-1,PRDX1
- Known as:
- Enzyme-linked immunosorbent assay test Chicken,Gallus gallus,Peroxiredoxin-1,PRDX1
- Catalog number:
- E2222c
- Product Quantity:
- 96T
- Category:
- -
- Supplier:
- EIAab
- Gene target:
- ELISA Chicken Gallus gallus Peroxiredoxin-1 PRDX1
Related genes to: ELISA Chicken,Gallus gallus,Peroxiredoxin-1,PRDX1
- Gene:
- PRDX1 NIH gene
- Name:
- peroxiredoxin 1
- Previous symbol:
- PAGA
- Synonyms:
- NKEFA
- Chromosome:
- 1p34.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-01
- Date modifiied:
- 2014-11-19
Related products to: ELISA Chicken,Gallus gallus,Peroxiredoxin-1,PRDX1
Related articles to: ELISA Chicken,Gallus gallus,Peroxiredoxin-1,PRDX1
- Keloids represent a pathological fibroproliferative disorder with high recurrence rates and limited therapeutic options. This study integrates multi-dataset transcriptomics (GSE158395, GSE188952, GSE92566, GSE173900) and machine learning algorithms (XGBoost, Random Forest, LASSO) to systematically investigate the role of lactylation modification in keloid pathogenesis. We identified 26 lactylation-related differentially expressed genes (15 upregulated, 11 downregulated) enriched in oxidative stress, immune response, and extracellular matrix pathways. Machine learning convergence revealed five lactylation hub genes (PRDX1, CSRP1, IFI16, CALD1, VIM), with PRDX1 exhibiting the highest diagnostic efficacy (AUC = 0.85). Immune infiltration analysis demonstrated significant correlations between hub genes and dysregulated immune cells. Experimental validation confirmed reduced PRDX1 expression in keloid tissues; its knockdown in fibroblasts elevated ROS levels and enhanced proliferation and migration. Regulatory network analysis predicted shared transcription factors (KLF12, NFKB1, MYC) governing hub genes, while drug screening prioritized three clinically actionable compounds (acetaminophen, valproic acid, vorinostat) targeting PRDX1. These findings establish lactylation as a critical regulator of keloid pathogenesis and identify PRDX1 as a promising therapeutic target. - Source: PubMed
Publication date: 2026/04/17
He RuizheSun MengzheLiu TiantianPeng YinboPeng LinboFang Yong - Acute liver injury (ALI) is a severe condition characterized by excessive hepatic inflammation and oxidative stress, yet effective therapeutic strategies remain limited. Dihydromyricetin (DMY), a natural flavonoid, possesses hepatoprotective properties, but the precise molecular mechanisms involving acetylation modifications underlying its effects are not fully understood. - Source: PubMed
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Hu HongWang ChenChen MengyanHan JinluSong YunChen ZikeZhao DeWang YugangYu HeguoShi Min - - Source: PubMed
Publication date: 2026/04/08
Lai WenjieZhu WeianWu JianjieHuang JiongduanLi XiaojuanLuo YunWang YuZeng HengdaLi MingqiangQiu XiaofuWen Xingqiao - Phospholipids are key regulators of immune metabolism, yet their specific influence on macrophage function remains incompletely defined. We investigated how phosphatidylethanolamine (PE) species with distinct acyl chains (PE18:0/22:6 and PE18:0/20:4) modulate RAW264.7 macrophages under resting and LPS-stimulated conditions using LC-MS/MS-based proteomics and metabolomics, followed by qPCR validation. LPS elicited a robust M1-like phenotype with strong upregulation of Ptgs2, Nos2, Nfkb1, and Nfkb2. PE supplementation alone did not induce a classical pro-inflammatory profile but significantly remodeled protein expression, enhancing antioxidant defenses, including catalase, Hmox1 and Prdx1. In the context of LPS activation, PE selectively attenuated inflammatory signaling by downregulating Nfkb1, Nfkb2, and Ptgs2 while further enhancing proteins linked to oxidative stress response (Prdx1 and Hmox1) and lipid metabolism (CD36 and Abcc1). qPCR corroborated these effects: both PE species reduced LPS-induced and mRNA levels while increasing , , and transcription. Metabolomics converged with these findings, indicating reinforced glutathione metabolism and context-dependent shifts in purine and amino-acid pathways consistent with a restrained inflammatory phenotype. Collectively, native PE species reprogram macrophage immunometabolism, mitigating LPS-driven inflammation while strengthening Nrf2-mediated antioxidant and immune-supportive pathways. - Source: PubMed
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