Protein,PRDX1
- Known as:
- Protein,PRDX1
- Catalog number:
- 38163
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- Protein PRDX1
Related genes to: Protein,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: Protein,PRDX1
Related articles to: Protein,PRDX1
- Influenza A virus (IAV) is a major respiratory pathogen with the potential to invade the central nervous system (CNS), leading to neurological complications. However, the mechanisms underlying IAV neurotropism and its impact on neuronal cells remain poorly understood. This study is aimed at establishing a reliable in vitro model using differentiated SH-SY5Y human neuroblastoma cells to investigate IAV infection in the CNS, with a specific focus on oxidative stress and matrix metalloproteinases (MMPs) production. - Source: PubMed
Publication date: 2026/05/18
Prezioso CarlaDe Angelis MartaLimongi DoloresMarinelli Anna MariaFrezza FlavioNencioni LuciaPalamara Anna TeresaChecconi Paola - Ischemic stroke (IS), a predominant cerebrovascular disorder contributing to global disability and mortality, characterizes by a complex, multi-tiered cascade of pathological processes. As the primary innate immune cells within the central nervous system (CNS), microglia exhibit dual functional characteristics following ischemic injury, switching dynamically between pro-inflammatory detrimental phenotypes and anti-inflammatory reparative phenotypes in response to temporal progression, cellular phenotypic transformation, and changes in the local microenvironment. Consequently, therapeutic strategies targeting microglia have garnered considerable research interest, challenging the traditional neuron-centric therapeutic approaches. Microglia display a wide range of phenotypes, and the traditional M1/M2 classification is overly simplistic, failing to capture the full spectrum of their functional diversity. In contrast, single-cell RNA sequencing (scRNA-seq) technology has surpassed the limitations of bulk sequencing, providing a robust tool for elucidating microglial heterogeneity. Recent studies utilizing animal models of stroke have identified several subsets distinct from the conventional M1/M2-like subsets, including but no limited to ischemic stroke-associated microglia (ISAM), SAM, microglia and SAM-foamy. The mechanisms underlying microglial heterogeneity encompass innate programming influenced by genetic background, dynamic remodeling of epigenetic modifications, metabolic reprogramming in response to extrinsic microenvironmental stress, and intercellular interaction networks. This review systematically examines, from the perspective of scRNA-seq, the biological functions of MG, the heterogeneity observed throughout their CNS life cycle development and regional homeostasis, the characteristics and regulatory mechanisms of heterogeneous microglial subpopulations following ischemic stroke, and potential therapeutic strategies and associated challenges. The aim is to provide a reference for the development of precise therapeutic strategies for IS. - Source: PubMed
Publication date: 2026/05/16
Tian DamanYang JiaoWang ZhifengLan JunfengShi TingXu ShuangfengZhao ManyanHe PengfenWang JianXing Liwei - Oxidative stress is considered to play a role in the etiopathogenesis of bipolar disorder. This study aimed to compare oxidative stress indicators among bipolar disorder patients in different mood states and healthy controls. - Source: PubMed
Publication date: 2026/05/18
Gökçen OnurKarataş Kader SemraAkkuş MerveDönmez FeyzaSezgin Ayşe KoçakGündüz Meliha KoldemirKaymak Güllü - Epithelial barrier disruption is a hallmark of allergic skin diseases. Sodium dodecyl sulfate (SDS), a surfactant in household cleaning products, is known to impair the barrier. - Source: PubMed
Publication date: 2026/05/17
Li ManruBabayev HuseynD'Avino PaoloZeyneloğlu CanBicer CerenYazici DuyguPat YagizSvedenhag PerGaudenzio NicolasAkdis Cezmi AMitamura Yasutaka - Ionizing radiation (IR) is a major cause of accelerated skeletal aging and severe bone loss, primarily by triggering oxidative stress and promoting premature senescence in bone marrow mesenchymal stem cells (BMSCs). This mechanism underscores a critical need for redox-based intervention. Peroxiredoxin 1 (Prdx1), a vital thiol peroxidase and redox sensor, is recognized for its potent anti-oxidative and anti-senescence capabilities. However, the precise function and underlying mechanism of Prdx1 in protecting BMSCs from IR-induced bone loss remain unexplored. Through Single-cell RNA-sequencing (scRNA-seq) and IR-induced bone loss mice model, we found that the Prdx1 expression in BMSCs exhibited a transient elevation in early stage after IR, while its expression was downregulated in late stage after IR. A prdx1-knockout mice (Prdx1) was constructed and exhibited aggravated bone loss after IR. Prdx1-derived primary BMSCs exhibited elevated oxidative stress and cellular senescence level, confirming a protective role for Prdx1. By high-throughput RNA-sequencing (RNA-seq), transcriptional factor prediction, molecular dynamic simulation, we verified that Prdx1 inhibited BMSCs oxidative stress injury via interacting with Pten and suppressing the Akt/FoxO signaling pathway. A BMSCs-specific E7 affinity peptide modified extracellular vesicle (EV) delivery system E7-EV was constructed to achieve targeted delivery of Prdx1 mRNA to BMSCs. E7-EV effectively suppressed IR-induced oxidative stress injury in vitro. Systemic administration of E7-EV effectively rescued IR-induced bone loss and demonstrated favorable biocompatibility in vivo. Our study identifies Prdx1 as a pivotal redox-regulated target in IR-induced BMSCs injury and introduces E7-EV as a novel, highly efficient, and safe gene therapy strategy for mitigating IR-induced bone loss. - Source: PubMed
Publication date: 2026/05/13
Zhai YuBian ZhiqunWei JiayingWang SiyaWang RuoyuCheng ShengwenLi XinhangCao LinhaiTang WenjingHe YiOuyang JianZeng YahuiZhang ShiyuZhao ChenLiu MinghanHuang Wei