Nos1
- Known as:
- Nos1
- Catalog number:
- 000165A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Nos1
Related genes to: Nos1
- 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: Nos1
Anti-Nitric Oxide Synthase, Brain(1-181) NOS1 Antibody (monoclonal, NOS-B1)anti-nNOS NOS1anti-nNOS / NOS1anti-nNOS / NOS1 (C-Terminus)anti-NOS1anti-NOS1 (N1)anti-NOS1 (N1)anti-NOS1 (N1) type: Primary antibodies host: Mouseanti-NOS1 (N1), Mouse monoclonal to NOS1, Isotype IgG1, Host MouseAnti-NOS1, Rabbit Polyclonal to NOS1, Isotype , Host Rabbitanti-NOS1, Rabbit polyclonal to NOS1, Isotype IgG, Host RabbitAntibodies: NOS1 Epitope:C TerminusAntibodies: NOS1 HOST: Goat Clonality: pAbAntibody to Nitric Oxide Synthase 1, Neuronal (NOS1) Organism: Mus musculus (Mouse) Type: Polyclonal Source: RabbitAntibody to Nitric Oxide Synthase 1, Neuronal (NOS1) Organism: Mus musculus (Mouse) Type: Polyclonal Source: Rabbit Related articles to: Nos1
- To systematically investigate the molecular mechanisms linking perfluorooctanoic acid (PFOA) to male reproductive health outcomes within a network toxicology framework, and to compare shared pathways across erectile dysfunction (ED), male infertility, and testicular dysfunction. - Source: PubMed
Publication date: 2026/09/28
Zhou TaoZhang XinyuYang JinghongWang Juan - NOS1AP (CAPON) is a signaling adaptor implicated in glioblastoma (GBM) proliferation, but its chemical tractability remains largely unexplored. Here, affinity selection-mass spectrometry screening of 10,000 drug-like compounds identified , a small molecule scaffold that directly binds NOS1AP. Binding was confirmed by microscale thermophoresis (MST), yielding a dissociation constant of 11.9 ± 7.0 μM. Focused structure-activity analysis and molecular modeling identified structural features associated with NOS1AP recognition and provided a framework for compound optimization. In living cells, produced a concentration-dependent reduction in the NanoBRET signal generated by the NOS1AP-NOS1 reporter pair, consistent with perturbation of the complex. reduced viability in U87 and U251 GBM cells, with IC values of 12.7 ± 0.91 and 17.3 ± 1.04 μM, respectively, while normal human astrocyte viability remained above 50% at 150 μM. Mechanistic studies in U87 cells demonstrated reduced DNA synthesis, G/G cell-cycle accumulation, and induction of apoptosis, accompanied by increased p53 and CDKN1A and decreased CDK6. Collectively, these findings establish the initial chemical tractability of NOS1AP and identify as a chemical scaffold for investigating NOS1AP-associated signaling in GBM. The findings also provide a foundation for optimizing NOS1AP-directed compounds. - Source: PubMed
Publication date: 2026/09/11
Abdo Ashraf NCho SungwooGabr Moustafa - DCPMU, a major demethylated metabolite of diuron, is an environmentally persistent contaminant with potential endocrine-disrupting and carcinogenic relevance, yet its mechanistic association with prostate cancer remains unclear. This study investigated DCPMU-related mechanisms in prostate cancer by integrating network toxicology, molecular modeling, bulk transcriptomics, single-cell and spatial transcriptomics, and virtual perturbation analysis. Differentially expressed genes from TCGA-PRAD were intersected with DCPMU-associated and prostate cancer-related targets. Functional enrichment, machine learning screening, and external GEO validation identified seven candidate hub genes: APOBEC3G, SCGB1A1, PTGS1, CA12, CES1, FOLH1, and NOS1. Molecular docking showed favorable DCPMU binding to these proteins, and molecular dynamics simulations further supported stable interactions with PTGS1, CA12, CES1, and FOLH1. Single-cell analysis of GSE141445 revealed cell-type-specific expression, with FOLH1 and CA12 enriched in epithelial cells, CES1 in fibroblasts, and PTGS1 in mast cells. Spatial transcriptomics from GSE181294 showed tumor-enriched FOLH1 expression and increased Core4 module activity in malignant regions. Virtual knockout analysis suggested that FOLH1 perturbation was associated with predicted downstream transcriptional changes, with PTGS1 showing marked perturbation responsiveness. Overall, our integrative analyses suggest that DCPMU exposure is associated with epithelial malignancy, inflammatory metabolism, xenobiotic handling, and tumor-microenvironment remodeling, particularly within malignant epithelial niches. These hypothesis-generating findings require experimental validation to establish any causal role in prostate cancer progression. - Source: PubMed
Publication date: 2026/09/13
Lin JianhaoFang DajunDing LiSu Deqi - Sleep-wake disturbances are among the most prevalent and persistent consequences of traumatic brain injury (TBI), yet the circuit mechanisms underlying post-traumatic alterations in rapid eye movement sleep (REM) and associated cortical oscillations remain incompletely understood. Previous work has shown that REM-associated theta oscillations are determined by a Supramammillary (SuM) - hippocampal vesicular glutamate transporter 2 (Vglut2) circuit. First, we examined whether severe focal penetrating TBI (pTBI) suppresses REM and REM-associated theta power. Secondly, we examined whether these changes are associated with alterations in hypothalamic neuropeptide systems and SuM-hippocampal glutamatergic signaling. Adult male Sprague-Dawley rats (pTBI, n = 7; Sham, n = 6) were exposed to pTBI or sham procedures. After sham/TBI surgeries, EEG/EMG data was continuously sampled for 14 days by using telemetric implants, enabling analyses of sleep-wake states and cortical oscillations. At 14 days post injury, animals were sacrificed and brain tissue was sampled for immunohistochemical and in situ hybridization analyses. We analyzed orexin A (OXA) and melanin-concentrating hormone (MCH) in the lateral hypothalamus (LHA), Vglut2 in the SuM and hippocampus (CA2 and dentate gyrus), and nitric oxide synthase 1 (NOS1) in the SuM. pTBI resulted in reduced wakefulness during the light phase, increased non-REM sleep (NREM), and reduced REM. Power spectral density analyses of EEG data showed reduced theta (4-8 Hz) power during wake, REM, and NREM. Also, alpha (8-12 Hz) and sigma (12-16 Hz) reduced, in contrast to delta (1-4 Hz) power which increased across all vigilance states. Histological analyses showed reduced OXA and MCH in the LHA in pTBI animals. Similarly, Vglut2 transcript levels were reduced in the lateral SuM, and Vglut2 immunoreactivity was decreased in hippocampal CA2 and dentate gyrus. NOS1 expression in the SuM was not altered. Correlation analyses showed an association between the Vglut2 reduction in the SuM-hippocampal circuit and REM-theta oscillations. For the first time, we show that severe focal pTBI produces a sustained suppression of REM and REM associated theta oscillations, associated with decreased Vglut2 within the SuM-hippocampal circuit. These findings provide a framework linking SuM-hippocampal circuit dysfunction to post-traumatic REM sleep disturbances. Further research is needed to study potential causal effects of TBI on suppression of the SuM-hippocampal circuit and effects on hippocampal dependent cognitive functions. - Source: PubMed
Publication date: 2026/09/23
Aurfan ZabihFransson AnetteDavidsson JohanRisling MårtenGünther MattiasThams Sebastian - Extra-virgin olive oil (EVOO) is a rich source of bioactive compounds, including the secoiridoids oleocanthal (OLC) and oleacein (OLE), which exhibit antioxidant, anti-inflammatory, and neuroprotective activities. However, their direct impact on neuronal hyperexcitability and seizure susceptibility has not yet been specifically investigated in vivo. A sustainable extraction approach based on natural deep eutectic solvents (NaDESs) has recently enabled the production of a novel EVOO-derived extract enriched in OLC and OLE, whose toxicological and functional properties remain uncharacterized. - Source: PubMed
Publication date: 2026/09/22
Damiano AntonellaArana Álvaro JMerola CarmineGilardini FedericaLaurenti DavideMosca LucianaPetrini AntonioBaffoni MarinaCacciola Nunzio AntonioD'Addario ClaudioSánchez LauraFrancioso AntonioAmorena Michele