nNOS Rabbit pAb
- Known as:
- nNOS Rabbit pAb
- Catalog number:
- ASAKAP-NO030F
- Product Quantity:
- 200 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- nNOS Rabbit pAb
Related genes to: nNOS Rabbit pAb
- 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 Rabbit pAb
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host Rabbit, Extraction-free, CE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host RabbitExtraction-freeCE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host: Rabbit, Extraction-free, CE-marked Related articles to: nNOS Rabbit pAb
- The global burden of respiratory disorders is significant and affecting humans socially, physically and economically, therefore, effective multi-target therapeutic strategies have been required. Indian medicinal plants have long been employed for control of respiratory diseases. However, their molecular mechanisms are not fully characterized. This study employed a network pharmacology strategy for testing the multi-target therapeutic activity of a series of medicinal plants, including , , , and . Phytoconstituents were selected from the literature and compared to those with established respiratory disease-associated targets from the GeneCards database. Compound-protein interaction networks, protein-protein interaction (PPI) analysis, GO enrichment, and disease association studies were conducted by Cytoscape, STRING, Metascape and DisGeNET. The major bioactive compounds detected by the results included quercetin, kaempferol, glycyrrhizin and emodin that interacted with critical targets like NOS1 or NOS3 and AKT1 and CASP3 and were included in the target list. Functional enrichment characterization showed considerable engagement as an integral part of these pathways in the control of inflammation, vasodilation, immune response and metabolic pathways. Patterns of PPI network analysis indicated prominent connection and clustering with target proteins to highlight synergistic effects in therapy. The combined conclusions have reinforced the multifactorial and synergistic actions of Indian medicinal plants in the treatment of respiratory diseases. This study offers a systems-level perspective on their pharmacological actions, and also validates their ability to act in a system as a complementary therapy agent. These results should be confirmed by further experimental validation. - Source: PubMed
Publication date: 2026/06/02
Kumar SantoshYadav Dinesh KumarSingh MhaveerSalar SapnaSingh AnjaliSingh Manju - The coordinated transit of intestinal contents is crucial for digestion and host defense, and is regulated by cross-talk between neural circuits, the muscular gut wall and luminal factors. Here we show that androgen signaling to Nos1 enteric neurons and Scn10a spinal afferent neurons is required for normal intestinal transit in mice and is microbiome dependent. Microbial depletion with antibiotics abolished androgen receptor expression in enteric neurons, diminished serum testosterone and caused dysmotility. Androgens were necessary for antibiotics to affect transit and partly sufficient to rescue dysmotility. Nos1 neurons upregulate androgen receptor upon puberty in parallel with shifts in fecal bacterial beta-glucuronidase (GUS) enzymes that can deconjugate steroid glucuronides in mice and humans. Intracolonic administration of a GUS enzyme found to metabolize androgen glucuronides was sufficient to restore neuronal androgen signaling in microbe-depleted mice. Thus, gut microbial reactivation of host-excreted androgens via GUS enzymes represents a dynamic microbe-host interaction that is essential for peripheral nervous system function in homeostasis. - Source: PubMed
Publication date: 2026/06/02
Lagomarsino Valentina NRobinson ArielMitchell Perry EJiang MiraHutchinson Lauren ESekela Josh JohnCaron PatrickGehris McKenzie KNavas Kathleen IDuarte-Silva MurilloNetherland MichaelHasan Nur AGuillemette ChantalRedinbo Matthew RRao Meenakshi - The vagus nerve connects the brain and pancreas and enhances postprandial endocrine secretion from the pancreas through cholinergic signaling, such as increasing insulin release immediately after food intake in the cephalic-phase insulin response (CPIR). Here, we investigated how obesity affects vagal regulation of pancreatic endocrine function using designer receptors exclusively activated by designer drugs (DREADDs) to manipulate vagal activity. As expected, the plasma concentration of insulin was increased by vagal activation in mice expressing the excitatory DREADD hM3Dq (M3 mice) and decreased by vagal inactivation in mice expressing inhibitory DREADD hM4Di (M4 mice). However, vagal activation in M3 mice with diet-induced obesity did not elicit an early increase in insulin and instead produced a delayed insulin decrease. Mathematical modeling showed that plasma insulin dynamics in these mice were best explained by a model incorporating both the insulin-increasing and insulin-decreasing effects of the vagus nerve. Furthermore, the insulin-decreasing effect was mediated by nitric oxide (NO)-dependent, noncholinergic signaling and was enhanced in obesity. In obese M3 mice, vagal deficiency of neuronal NO synthase (nNOS) abolished the insulin-decreasing effect and restored insulin release after vagal activation. Vagal nNOS deficiency also enhanced insulin release after voluntary feeding, consistent with the CPIR. These findings suggest that vagal NO action inhibits postprandial insulin release, particularly in obesity. - Source: PubMed
Publication date: 2026/05/26
Hashiuchi EmiInaba YukaSugimoto HikaruKimura KumiWatanabe HitoshiKajino MayuAsahara Shun-IchiroKobayashi MasakiKikuchi OsamuHayashi YoshitakaHorike Shin-IchiDaikoku TakikoMieda MichihiroSakurai TakeshiSakai MashitoMatsumoto MichihiroKitamura TadahiroSato MakotoRavnskjaer KimKasuga MasatoTanida MamoruKuroda ShinyaInoue Hiroshi - Fabry disease is an X-linked lysosomal storage disorder caused by α-galactosidase A deficiency, leading to progressive accumulation of Gb3 and lyso-Gb3 and a complex multisystem phenotype extending beyond substrate storage. Cardiovascular involvement remains the leading cause of morbidity and mortality, yet early detection and risk stratification remain challenging. In this context, a new proteomic study leveraging high-throughput proximity extension assays and machine learning has defined a cardiovascular risk signature in Fabry disease. Differential expression analysis identified widespread proteomic remodeling involving inflammatory signaling, extracellular matrix organization, angiogenesis, and metabolic pathways, supporting a systems-level view of disease pathogenesis. A 10-protein biosignature integrating markers of mitochondrial stress, lysosomal function, vascular remodeling, and immune activation demonstrated the ability to discriminate patients with cardiovascular involvement. Notably, proteins such as GDF15, NT-proBNP, NOS1, CTSF, and TNFRSF11B highlight the interplay between mitochondrial dysfunction, lysosomal impairment, and vascular inflammation. These findings suggest that Fabry cardiomyopathy reflects coordinated dysregulation across metabolic and inflammatory networks and that multi-protein signatures may improve precision phenotyping and cardiovascular risk prediction beyond conventional biomarkers. - Source: PubMed
Publication date: 2026/05/22
Santulli GaetanoPande ShivangiVarzideh Fahimeh - 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