Ask about this productRelated genes to: nNOS antibody
- 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 antibody
Related articles to: nNOS antibody
- Skeletal muscle fiber composition plays a critical role in determining muscle growth and meat quality in livestock species. However, the molecular mechanisms underlying muscle fiber-type transformation in meat rabbits remain poorly understood. - Source: PubMed
Publication date: 2026/05/07
Jia ChengQianwen WuZhengwei JiZhongqiang YaoLing WangHongzhao LuWenxian Zeng - Interleukin-1β (IL-1β) plays a central role in driving vascular inflammation and endothelial dysfunction, key processes in the development of atherosclerosis. While biologic therapies targeting IL-1β have shown clinical benefit, their high cost, injectable nature, and potential side effects limit their broader use. Therefore, there is a need to explore more accessible alternatives. In this study, we aimed to identify repurposed small-molecule inhibitors that can effectively modulate IL-1β signaling and protect endothelial function. - Source: PubMed
Publication date: 2026/05/01
Solanki KundanRaja Sk RameejSamanta SunandaShishira P SRoy AnjaliKar ParimalBiswas SwatiRamkumar K MBaig Mirza S - Illustration depicts a mechanistic pathway where metformin affects Desulfovibrio bacteria, leading to increased hydrogen sulfide production. This crosses the intestinal barrier, activates NOS1, induces 3-NT formation, and increases oxidative stress in the gastrocnemius muscle. - Source: PubMed
Publication date: 2026/04/13
Wang HejieCao ZhigangYousaf WafaHaseeb AbdulWang ZiyangZheng Jiangang - Colorectal cancer (CRC) is a leading cause of cancer-related deaths worldwide. Although epigenetic alterations are common in CRC, the epigenetic changes that occur during colorectal carcinogenesis remain unclear. Thus, we sought to elucidate the role of methylation in colorectal carcinogenesis, which is essential for understanding disease pathology. We used the UCSC Xena database to comparatively analyze expression and methylation status between tumour and adjacent normal tissues across 33 cancer types. Low expression and hypermethylation of have been identified in 12 cancer types, with CRC demonstrating this characteristic epigenetic regulation. promoter methylation status was examined using genomic DNA extraction and MassARRAY EpiTYPER methylation analysis. hypermethylation was confirmed among CRCs in in-house dataset 1 ( < 0.001), and among CRCs and advanced adenomas in in-house dataset 2 ( < 0.001). An upward trend in methylation changes was identified from non-advanced adenoma to advanced adenoma to CRC ( for trend < 0.001). Quantitative real-time PCR was used to analyze expression in in-house Dataset 3, and significantly low expression was also identified in CRCs ( < 0.001). Kaplan-Meier estimator and Cox proportional hazard models were used to assess the prognostic and predictive roles of . hypermethylation was significantly associated with better disease-specific survival (DSS) in CRC patients. hypermethylation is an epigenetic driver of colorectal tumorigenesis and is associated with better survival. - Source: PubMed
Publication date: 2026/04/28
Zhang ZhaohuiYeerken AibutaShao XinyaoQian SangniLin ShujuanGu SimengYing XiaojiangLi ZhenjunFei XinglinYang JinhuaTang MenglingWang JianbingJin MingjuanChen Kun - Gastrointestinal (GI) dysmotility is a highly prevalent and clinically significant feature of Rett syndrome (RTT), yet its underlying mechanisms remain poorly defined. Here, we investigated these mechanisms of GI dysmotility in a mouse model of RTT. First, we observed that MeCP2 was expressed in murine myenteric ganglia, including in enteric neurons and that males developed maturation-associated functional regression in their GI motility. In dysmotile mice, longitudinal muscle-myenteric plexus tissue showed marked reductions in enteric soforms and , whereas expression of the BDNF receptor isoforms TrkB.FL and TrkB.T1 was not significantly altered, consistent with reduced enteric BDNF-TrkB signaling. Despite impaired GI motility, mice showed no significant changes in total enteric neuronal density, nitrergic neuronal abundance, or expression of , and In contrast, expression was significantly reduced, while expression of VIP receptor genes: and was increased, indicating disrupted VIPergic signaling. Integration with publicly available enteric single-cell/nucleus datasets and targeted qRT-PCR further suggested altered inhibitory neuronal subtype composition, with reduced signatures and increased expression, suggesting that MeCP2 loss differentially affects distinct inhibitory neuronal subpopulations. Finally, conditional loss of TrkB.FL in neural crest-derived cells reduced expression without recapitulating the full VIPergic phenotype, indicating that impaired BDNF-TrkB signaling contributes to, but does not completely explain, the GI dysmotility in this model of RTT. Together, these findings identify enteric BDNF-TrkB and VIPergic dysfunction as key mechanisms underlying GI dysmotility in RTT. - Source: PubMed
Publication date: 2026/04/15
Puttapaka Srinivas NAdmasu Israel AScott AinsleighSonmez GamzeSeika PhilippaRajkumar MahalakshmiValencia XavierConsorti AlanHong Su MinSlosberg JaredFagiolini MichelaKulkarni Subhash