Prdx1 Antibody
- Known as:
- Prdx1 Antibody
- Catalog number:
- 46-754
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- Prdx1 Antibody
Related genes to: Prdx1 Antibody
- 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 Antibody
Related articles to: Prdx1 Antibody
- To investigate the role of peroxiredoxin isoforms (Prdx) in the radioresistance of cancer cells, the expression of Prdx1-6, DNA repair genes, and apoptosis regulators was studied in human cancer cell lines with varying radiosensitivities (A549, Caco-2, and MCF-7) after exposure to ionizing radiation. A correlation was found between high constitutive Prdx1-6 expression levels and increased radioresistance. Predominantly cytosolic isoforms Prdx2 and Prdx6 demonstrated pronounced induction after irradiation, indicating their critical role in protecting against radiation-induced oxidative stress. Most radiosensitive A549 cells exhibited the lowest baseline Prdx expression and the most pronounced transcriptional changes after irradiation, whereas MCF-7 and Caco-2 cells had higher constitutive expression and a weaker response to radiation. Mitochondrial Prdx3 and Prdx5, as well as ER-localized Prdx4, exhibited relatively stable expression. A549 cells demonstrated the highest induction of DNA repair genes, which may indicate more severe DNA damage. In contrast, MCF-7 cells were characterized by high basal expression of repair genes and elevated γH2AX levels before irradiation, which may reflect their "readiness" for repair and explain their higher radioresistance. Furthermore, radioresistant MCF-7 cells had increased expression of anti-apoptotic genes (BCL2, MCL1, BIRC5), suppressing the mitochondrial apoptotic pathway. Meanwhile, A549 cells showed higher induction of pro-apoptotic genes (PUMA, NOXA, BAK1) and activation of caspase-3, which correlates with their increased radiosensitivity. Therefore, peroxiredoxins protect cells from radiation exposure, either by being constitutively expressed or by being highly inducible in response to radiation, and promote cell survival after irradiation. This makes them attractive targets for overcoming cancer cell radioresistance. - Source: PubMed
Publication date: 2026/05/22
Sharapov M GGoncharov R GKarmanova E EParfenyuk S BGlushkova O VLunin S M - This study evaluated whether resveratrol (RESV), alone or in combination with antifreeze protein type I (AFP I), improves slow freezing cryopreservation of in vivo-derived ovine embryos. Good-quality embryos recovered non-surgically from 35 superovulated ewes were assigned to three groups: AFP (0.1 µg/mL AFP I in the freezing solution), RESV (pre-incubation for 6 h in holding medium supplemented with 1 µM RESV before cryopreservation), or RESV + AFP (combined treatment). After thawing, embryos were cultured in vitro for 48 h and assessed for several endpoints. Resveratrol exposure (RESV and RESV + AFP) reduced intracellular levels of glutathione (GSH), reactive oxygen species (ROS), and ROS/GSH ratio after incubation (P < 0.05), without affecting mitochondrial activity. After thawing, embryos in the RESV + AFP group exhibited higher mitochondrial activity than the others (P < 0.05), accompanied by increased ROS/GSH ratios compared to AFP alone (P < 0.05). After culture, redox parameters did not differ across treatments. There was no difference in survival rates or dead cell index among groups (P > 0.05), but RESV + AFP presented the highest content of intracellular lipid (P < 0.05). Finally, expression of AQP3 and PRDX1 genes was downregulated in the AFP group compared with RESV, with no difference between RESV and RESV + AFP (P > 0.05). Altogether, combining RESV with AFP I enhanced post-thaw mitochondrial activity but disrupted redox homeostasis and increased lipid accumulation, without improving embryo survival or hatching. These findings indicate that RESV combined with AFP I does not improve embryo cryotolerance, while RESV pretreatment may help reduce oxidative stress before cryopreservation. - Source: PubMed
Publication date: 2026/05/15
Guimarães Mariana P POliveira Thaís ALeal Gabriela RCupello Ana Paula SBrandão Felipe ZBatista Ribrio Ivan T PCorreia Lucas F LSouza-Fabjan Joanna M G - Ischemic stroke is a highly destructive disease with extremely high mortality and disability rates. So far, there have been few available neuroprotective drugs. Rutin, a natural plant alkaloid derived from the flavonoid class of natural compounds, has been proven to have protective effects against ischemic stroke-induced brain injury via its antioxidant and anti-inflammatory pharmacological effects. However, the mechanisms of rutin's antioxidative and anti-inflammatory effects remain largely unknown. The results showed that rutin alleviated ischemia/reperfusion-induced brain injury, including reduced infarct volume, improved neurological deficits, and decreased glial scar thickness. Rutin also alleviated oxygen-glucose deprivation/reoxygenation (OGD/Re)-induced oxidative stress-related indicators, such as reactive oxygen species, lipid peroxidation levels, 4-hydroxynonenal, and malondialdehyde, as well as pro-inflammatory factors such as interleukin-6, interleukin-1β, and tumor necrosis factor-α in astrocytes, thereby ultimately reducing astrocytic injury and inhibiting the activation of reactive astrocytes. The underlying mechanism is that rutin enhances the enzymatic activity of peroxiredoxin-1 (PRDX1). Knockdown of PRDX1 weakened the pharmacological effects of rutin in inhibiting oxidative stress and inflammatory responses. Finally, rutin could indirectly protect neurons by reducing OGD/Re-induced astrocytic damage and directly reduce OGD/Re-induced damage to primary neurons. Therefore, rutin alleviates ischemic stroke-induced oxidative stress and inflammatory responses in astrocytes, at least partially, by activating PRDX1, thereby inhibiting glial scar formation and exerting neuroprotective effects. - Source: PubMed
Said AliLiu ShuaiCao RuiqiZhou XianyongZhang Huiling - 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