SOD1 Antibody
- Known as:
- SOD1 Antibody
- Catalog number:
- abx000659
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- SOD1 Antibody
Related genes to: SOD1 Antibody
- Gene:
- SOD1 NIH gene
- Name:
- superoxide dismutase 1
- Previous symbol:
- ALS, ALS1
- Synonyms:
- IPOA
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: SOD1 Antibody
Related articles to: SOD1 Antibody
- Pregnancy complications such as preeclampsia are associated with circulating cell-free mitochondrial DNA (mtDNA), a damage-associated molecular pattern capable of activating Toll-like receptor 9 (TLR9). We hypothesized that acute mtDNA exposure induces maternal inflammation and endothelial dysfunction during pregnancy via TLR9 activation. Non-pregnant and pregnant rats (gestational days 14-15) were treated intravenously with saline or purified mtDNA and euthanized 4 h after treatment. mtDNA increased cytokine mRNA expression in lung and liver of non-pregnant and pregnant rats, with magnitude varying by pregnancy status and organ. Aortas from pregnant, but not non-pregnant, rats exhibited reduced acetylcholine (ACh)-induced relaxation following mtDNA treatment (Emax, saline: 90.1 ± 3.9 % vs. mtDNA: 62.1 ± 20.7 % KClmax, p<0.05), while uterine artery function was preserved, indicating vascular bed-specific effects. Ex vivo incubation of aortic rings with mtDNA ± white blood cells did not replicate in vivo findings, implicating systemic rather than direct vascular mechanisms. Nuclear DNA did not affect ACh-induced relaxation (p>0.05), confirming that the vascular effects were mtDNA-specific. Pharmacological antagonism of TLR9 with ODN2088 partially attenuated mtDNA-induced maternal endothelial dysfunction. Although overt vascular ROS increases were not detected, aortas from pregnant rats had reduced sod-1 expression (p<0.05) and increased eNOS protein abundance (p<0.05). Acute mtDNA exposure during pregnancy induces maternal organ inflammation and impairs endothelium-dependent vasodilation, with partial TLR9 involvement. In conclusion, aortic transcriptional changes in antioxidant pathways and increased eNOS abundance were also observed, though their functional significance remains to be determined. - Source: PubMed
Publication date: 2026/08/18
Hula NataliiaOliveira da Silva Reneé de NazaréEscalera DesiraeLopez LeslieKelly GabrielleGorham Isabelle KRowe MeganLiu TaimingBlood Arlin BMata-Greenwood EugeniaHu Xiang-QunZhang LuboPhillips Nicole RGoulopoulou Styliani - Parkinson's disease (PD) results primarily from the loss of midbrain dopaminergic neurons. Mitochondrial dysfunction may contribute to PD pathogenesis and depletion of vacuolar protein sorting 13 homolog C (VPS13C) leads to mitochondrial dysfunction. Traditional Chinese medicine (TCM) extracts , , and were reported to have anti-PD effects. This study aimed to examine these three extracts for enhancing VPS13C expression and mechanisms of neuroprotection. Using FCCP-mediated oxidative phosphorylation uncoupling or RNA interference-directed knockdown, reduced cell viability and mitochondrial membrane potential (MMP) accompanied with increased mitochondrial superoxide in human neuroblastoma SH-SY5Y cells were established. Treatment of cells with these extracts increased cell viability, MMP, and reduced the mitochondrial superoxide. In differentiated SH-SY5Y cells with knockdown, these extracts reduced lactate dehydrogenase release, caspase-3 activity, reactive oxygen species production, and promoted neurite outgrowth. The extracts increased VPS13C, superoxide dismutase (SOD) 1 and 2, nuclear respiratory factor 2 (NRF2), PPARG coactivator 1 alpha (PGC-1α), and B-cell lymphoma 2 (BCL2) expression in these cells, accompanied by increases in MMP, mitochondrial mass, and reduction in mitochondrial superoxide. In conclusion, treatments with these three TCM compounds reduced mitochondrial dysfunction and oxidative stress in -knockdown cells, making them potential drug candidates for PD. - Source: PubMed
Publication date: 2026/08/13
Wu Yih-RuLin Chih-HsinHuang Pei-SyuanChao Chih-YingLin Te-HsienChen Wan-LingChen Chiung-MeiChang Kuo-HsuanLee Ming-ChungChen I-ChengLee-Chen Guey-Jen - The SOD1 gene encodes superoxide dismutase 1, an antioxidant enzyme in which pathogenic variants cause a subset of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Although the clinical and molecular consequences of SOD1 variants are well established, its locus-wide population genetic architecture has not been systematically characterized across global populations. - Source: PubMed
Publication date: 2026/08/17
Flores Sergio VLillo PatriciaBriceño-Moya Jorge - Maternal Western diet (WD) consumption during pregnancy is linked to adverse gestational and offspring metabolic outcomes. Dimethyl fumarate (DMF), a Nrf2 activator with antioxidant and anti-inflammatory properties, is a proposed therapeutic candidate, but its safety and efficacy during pregnancy remain unexplored. This pilot study aimed to establish a guinea pig model of gestational WD consumption and evaluate the feasibility of DMF treatment on maternal, placental, and fetal outcomes. - Source: PubMed
Publication date: 2026/08/12
Hasan DaniellaKutzler MichellePatton Kristin MBionaz Massimo - To determine whether radiation directly compromises AT2 cell stemness through oxidative and DNA damage, and to evaluate whether Compound Kushen Injection (CKI) protects AT2 cells, restores alveolar regeneration, and mitigates radiation-induced pulmonary fibrosis. - Source: PubMed
Publication date: 2026/08/15
Liu Yan-LiXu Cheng-YanWang YongLiang Xiao-YanChen Yun