nNOS N_Terminal Peptide Control
- Known as:
- nNOS N_Terminal Peptide Control
- Catalog number:
- 24447
- Product Quantity:
- 25 µg
- Category:
- Peptides
- Supplier:
- Immunostar
- Gene target:
- nNOS N_Terminal Peptide Control
Related genes to: nNOS N_Terminal Peptide Control
- Gene:
- NOS1 NIH gene
- Name:
- nitric oxide synthase 1
- Previous symbol:
- NOS
- Synonyms:
- nNOS
- Chromosome:
- 12q24.22
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-09
- Date modifiied:
- 2017-07-12
Related products to: nNOS N_Terminal Peptide Control
Related articles to: nNOS N_Terminal Peptide Control
- Osteoarthritis (OA) is a degenerative joint disease involving multiple cell types, yet the role of osteoblast (OB)-immune cell interactions remains poorly understood. - Source: PubMed
Publication date: 2026/04/11
Liu KunLi Jia-LiChen YanLi Yu-XinDeng Jeffrey DGong YunCao ChongZeng QinXiao Zheng-WuWen Kai-ZhiQu Xiao-ChaoChen Xiang-DingDeng YunDeng Hong-WenTan Li-Jun - Erectile dysfunction (ED) is a multifactorial condition influenced by vascular, neuroendocrine, metabolic, and psychological factors. Growing evidence suggests that genetic variation may contribute to individual susceptibility, severity, and therapeutic response, particularly regarding nitric oxide (NO) signaling and vascular pathways. To systematically synthesize evidence on genetic biomarkers associated with the risk, severity, or therapeutic response of ED in adult men. - Source: PubMed
Publication date: 2026/03/24
Ferezin Letícia PerticarraraKayzuka CezarPaiva de Alcântara E Silva MaurielyTavares Peixeiro Cecilia NogueiraRondon-Pereira Vitória CarolinaTanus-Santos Jose EduardoLacchini Riccardo - Fabry disease (FD) is an X-linked lysosomal disorder caused by a deficiency in α-galactosidase A, leading to the accumulation of globotriaosylceramide (Gb3) and lysoGb3. While this accumulation was long seen as the leading cause of symptoms, FD pathogenesis now involves complex mechanisms like autophagy dysregulation, inflammation, oxidative stress, and inter-organelle communication. Cardiovascular diseases (CVD) remain a significant reason for premature death in FD. Gaining a better understanding of cardiac pathophysiology and developing new biomarkers for early detection and monitoring in FD are still essential. In this study, we proposed an FD-CVD protein signature by analyzing the plasma proteome of 55 FD patients, including 18 with CVD and 37 without (woCVD), and 30 non-FD controls. We found 141 altered proteins in FD-CVD compared to FD-woCVD. Among them, 38 differential proteins are related to cardiometabolism. Moreover, ten proteins were identified as potential biomarkers for differentiating FD-CVD from FD-woCVD. The 10-protein signature performed well in RF and partial least squares discriminant analysis models but had limited predictive ability in support vector machine and logistic regression. Importantly, this biosignature demonstrated an ability to classify FD and non-FD controls, regardless of CVD complications, with AUCs greater than 0.90. Using a local interpretable model-agnostic explanation, the RF model interpretation revealed the classification rule for FD-woCVD and highlighted the significance of GDF15, NOS1, CCN5, CTSF, and NAAA. Our findings suggest an early indication of combined cardiac involvement in FD, paving the way for future validation studies that may ultimately inform personalized treatment before irreversible heart damage develops. KEY MESSAGES: Cardiovascular diseases (CVD) remain the leading cause of premature death in Fabry. A ten-protein signature was identified to differentiate Fabry with and without CVD. The protein signature could classify Fabry with controls regardless of CVD status. - Source: PubMed
Publication date: 2026/03/29
Nguyen Thi Hai YenNguyen Quang ThuDucatez FranklinTebani AbdellahNguyen Phuoc LongBekri Soumeya - Valproic acid (VPA) is a well - known teratogen and neuro-teratogen affecting many animals including humans. In rodents, prenatal VPA may induce a wide range of malformations and/or neurodevelopmental disorders depending on the time of administration and dose. We previously found that early postnatal administration of VPA in mice induced autistic like behaviour, and in the brain changes in gene expression and increased oxidative stress. S-adenosylmethionine (SAMe) normalized these deviations. We now assessed the possible alleviation by SAMe of the injuries caused by VPA administration during days 8.5, 9.5 of gestation on brain oxidative and nitrosative stress. ICR mice received intraperitoneally 300 mg/Kg VPA with or without 30 mg/kg SAMe, or a mixture of VPA and SAMe in the same ration. Fetuses were studied on Embryonic day 15.5. VPA induced fetal growth retardation, 32.5% of exencephaly, high resorption rate and, in the brain, increased Malondialdehyde (MDA) concentrations, increased antioxidant enzyme activity and elevated expression of antioxidant genes with increased expression of NOS1 and NOS2 genes, implying increased nitrosative stress. SAMe alone did not cause changes in the parameters tested. The addition of SAMe to VPA, abolished the VPA-induced damage. Administration of the mixture of VPA and SAMe did not induce any embryonic damage or changes in the redox potential of the brain, except for an unexplained up regulation of SOD1 and SOD2 genes. It is concluded that SAMe, an epigenetic modulator, neutralizes VPA's neuro-teratogenic effects when administered together with VPA during neurulation, like its postnatal effects. - Source: PubMed
Publication date: 2026/03/25
Echefu BonifaceBecker MariaBazylevich AndriiOrnoy Asher - Neonicotinoid insecticides and fluoroquinolone antibiotics frequently co-occur in aquatic and terrestrial environments, posing a threat to human health, yet their combined neurotoxic potential remains poorly characterized. This study aimed to assess the cytotoxicity of typical neonicotinoids and fluoroquinolones as well as their mixtures in human neuroblastoma SK-N-SH cells and identify affected pathways. SK-N-SH cells were exposed to clothianidin (CLO), imidacloprid (IMI), enrofloxacin (ENR), and ofloxacin (OFX) individually and in fixed-ratio mixtures (50% of each compound's IC) for 24 h and 48 h, and cell viability was quantified using the alamarBlue method. Single-compound dose-response testing showed time-dependent cytotoxicity, with higher potency for fluoroquinolones (24 h IC: ENR 1.446 mM, OFX 2.742 mM; 48 h IC: ENR 0.826 mM, OFX 2.005 mM) than neonicotinoids (24 h IC: IMI 4.754 mM, CLO 5.356 mM; 48 h IC: IMI 3.631 mM, CLO 4.029 mM). Concentration-addition analysis indicated that most mixtures produced synergistic interaction in reduction in cell viability, with ENR+OFX showing the strongest effect at 48 h (Observed viability 7.138% vs. Predicated viability 82.368%). RNA-seq (24 h) revealed that binary mixtures generally induced more differentially expressed genes than single exposures, and ENR-containing mixtures showed the largest transcriptomic shifts, enriching pathways related to cellular stress and injury as well as neuronal signaling and connectivity. RT-qPCR validated the changes in expressions of five key neurobiology-relevant genes (, , , and ). These findings highlight the importance of assessing insecticide-antibiotic mixtures when evaluating their hazards in environment. - Source: PubMed
Publication date: 2026/02/25
Yeerkenbieke GulijiaziWang TaoYang YunShi ShuaiLu Xiaoxia