PRDX1
- Known as:
- PRDX1
- Catalog number:
- Y214076
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PRDX1
Related genes to: 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: PRDX1
anti-PRDX1 / Peroxiredoxin 1 (Internal)Anti-PRDX1 AntibodyAnti-PRDX1 AntibodyAnti-PRDX1, Goat Polyclonal to PRDX1, Isotype , Host GoatAntibodies: PRDX1 HOST: Goat Clonality: pAbAntibody to Peroxiredoxin 1 (PRDX1) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitAntibody to Peroxiredoxin 1 (PRDX1) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitAntigens PRDX1, 1-199aa, Human, His tagged , Recombinant, E.coliBiotin-linked Antibody to Peroxiredoxin 1 (PRDX1); Reactivity: Homo sapiens (Human) Clonality: Polyclonal Source: RabbitBos taurus,Bovine,Peroxiredoxin-1,PRDX1Bovine peroxiredoxin 1 (PRDX1) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine Peroxiredoxin-1(PRDX1) ELISA kitBovine Peroxiredoxin-1(PRDX1) ELISA kit SpeciesBovineChicken peroxiredoxin 1 (PRDX1) ELISA kit, Species Chicken, Sample Type serum, plasmaChicken Peroxiredoxin-1(PRDX1) ELISA kit Related articles to: PRDX1
- 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
MaurÃcio TatianaNeves BrunoDomingues M RosárioDomingues Pedro - - Source: PubMed
Publication date: 2026/04/02
Xue XiangHuang ChangbaoChen JuanDing WeichaoRen YiZhang WeiLi QuanYang ZhizhouSun Zhaorui - Microglia play a crucial role in the progression of neuroinflammation following traumatic brain injury (TBI). Interleukin-3 (IL-3), a significant regulatory factor, has been involved in the pathogenesis of various diseases, yet its effects on neuroinflammation post-TBI through microglia remain unclear. Here, we evaluate the potential of IL-3 to alleviate neuroinflammation in microglia following TBI. Using the ABplex Multi-Metric Streaming Joint Analysis to detect inflammatory factors, we observed significantly elevated levels of IL-3 in cerebrospinal fluid, but not in blood samples, of patients with headaches and TBI. In addition, we found that administration of exogenous IL-3 within the brain reduced neuroinflammation and promoted functional recovery in rat TBI models. Mechanistically, we identified Peroxiredoxin-1 (PRDX1) as the target of IL-3 in microglia. Notably, the protective effects of IL-3 in TBI rats were abolished when PRDX1 was specifically knocked down in microglia. In conclusion, our experimental research demonstrates that IL-3 acts as a key modulator via regulating microglia polarization to inhibit neuroinflammation. IL-3 improves neurological function and prognosis in TBI rats by recruiting PRDX1 through IL-3R to modulate microglia polarization. Therefore, IL-3 may represent a novel therapeutic strategy for TBI. - Source: PubMed
Publication date: 2026/03/31
Huang NanaZhang QingchenChen YanruiYu DapengLiu RonghanKang JianningFang XiangZhang YingBian HongZhao YanxinYin YongchengZhang CeJia YanfeiChen QingfaFang YuepengLi ShangLi FangJin ZhengxinNing Bin