CLIA Bos taurus,Bovine,Peroxiredoxin-1,PRDX1
- Known as:
- CLIA Bos taurus,Bovine,Peroxiredoxin-1,PRDX1
- Catalog number:
- U2222b
- Product Quantity:
- 96T
- Category:
- -
- Supplier:
- EIAab
- Gene target:
- CLIA Bos taurus Bovine Peroxiredoxin-1 PRDX1
Related genes to: CLIA Bos taurus,Bovine,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: CLIA Bos taurus,Bovine,Peroxiredoxin-1,PRDX1
(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala13)-Apelin-13 (human, bovine, mouse, rat) 98% C63H107N23O16S CAS: 568565-11-7(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala96)-Myelin Basic Protein (87-99) (human, bovine, rat) 98% C70H110N20O17 CAS:(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(b_Asp3)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (b_Asp3)_Aviptadil SumFormula C147H238N44O42S(b_Asp3)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (b_Asp3)_Aviptadil SumFormula C147H238N44O42S(D-Ala2,Met5)-β-Casomorphin (1-5) amide (bovine) 98% C31H42N6O6S CAS:(D-Lys16)-ACTH (1-24) (human, bovine, rat)
(D-Lys16)-Tetracosactide 98% C136H210N40O31S CAS: 494750-52-6(D-Lys16)-ACTH (1-24) human, bovine, mouse, ovine, porcine, rabbit, rat(D-Lys16)-ACTH (1-24) human, bovine, mouse, ovine, porcine, rabbit, rat(D-Lys16)-ACTH (1-24) human, bovine, mouse, ovine, porcine, rabbit, rat Related articles to: CLIA Bos taurus,Bovine,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
Publication date: 2026/04/04
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
Publication date: 2026/04/08
Maurício TatianaNeves BrunoDomingues M RosárioDomingues Pedro - - Source: PubMed
Publication date: 2026/04/02
Xue XiangHuang ChangbaoChen JuanDing WeichaoRen YiZhang WeiLi QuanYang ZhizhouSun Zhaorui