GSNO | Nitroso_L.glutathione
- Known as:
- GSNO | Nitroso_L.GSH
- Catalog number:
- AS08361
- Product Quantity:
- 100 ul
- Category:
- -
- Supplier:
- Agris
- Gene target:
- GSNO | Nitroso_L.glutathione
Related genes to: GSNO | Nitroso_L.glutathione
- Gene:
- ADH5 NIH gene
- Name:
- alcohol dehydrogenase 5 (class III), chi polypeptide
- Previous symbol:
- FDH
- Synonyms:
- ADH-3, ADHX, GSNOR
- Chromosome:
- 4q23
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-01-18
Related products to: GSNO | Nitroso_L.glutathione
(4R)- N-Nitroso Thiazolidine-4-carboxylic Acid C4H6N2O3S CAS: 86594-16-3 (4R)- N-Nitroso Thiazolidine-4-carboxylic Acid CAS: 86594-16-3 Formula: C4H6N2O3S (Des-Gly)-Glutathione (reduced)
H-γ-Glu-Cys-OH 98% C8H14N2O5S CAS: 636-58-8(R)-N-Nitroso Anatabine C10H11N3O CAS:(R)-N-Nitroso Anatabine CAS: Formula: C10H11N3O(R,S)-N-Nitroso Anabasine C10H13N3O CAS: 37620-20-5 (R,S)-N-Nitroso Anabasine CAS: 37620-20-5 Formula: C10H13N3O(R,S)-N-Nitroso Anabasine D-Glucoside Chloride C16H24ClN3O6 CAS:(R,S)-N-Nitroso Anabasine D-Glucoside Chloride CAS: Formula: C16H24ClN3O6(R,S)-N-Nitroso Anabasine-d4 (0.1 mg/mL in Methanol) CAS: 1020719-68-9 Formula: C10H9D4N3O(R,S)-N-Nitroso Anabasine-d4 C10H9D4N3O CAS: 1020719-68-9(R,S)-N-Nitroso Anabasine-d4 CAS: 1020719-68-9 Formula: C10H9D4N3O(R,S)-N-Nitroso Anatabine C10H11N3O CAS: 887407-16-1 (R,S)-N-Nitroso Anatabine CAS: 887407-16-1 Formula: C10H11N3O(R,S)-N-Nitroso Anatabine N-β-D-Glucuronide
(Mixture of Diastereomers) C16H19N3O7 CAS: Related articles to: GSNO | Nitroso_L.glutathione
- B cell-activating factor (BAFF) is a key mediator of B cell-driven autoimmune pathology. In mice with experimental autoimmune encephalomyelitis (EAE), a widely used model of multiple sclerosis (MS), we observed a pronounced accumulation of B cells within the spinal cord, alongside elevated BAFF expression, particularly in GFAP activated astrocytes located in the subpial-region. This upregulation of BAFF coincided with the infiltration of CD4 T cells, notably Th1 cells producing IFNγ, a cytokine critical for inducing BAFF gene expression in astrocytes. Concurrently, elevated BAFF levels in the spinal cords of EAE mice were associated with increased expression of S-nitrosoglutathione (GSNO) reductase (GSNOR), the enzyme that degrades GSNO, a molecule known for its anti-inflammatory properties. Pharmacological inhibition of GSNOR using N6022, a reversible inhibitor, significantly reduced BAFF expression and decreased B cell accumulation in the CNS. In vitro, both GSNO and N6022 suppressed IFNγ- and TNFα-induced BAFF expression in cultured astrocytes by inhibiting STAT1 and NF-κB activation. Furthermore, co-culture of B cells with IFNγ/TNFα-stimulated astrocytes, or exposure to their conditioned media, resulted in an increased number of B cells and enhanced IL-6 production. These effects were attenuated either by pretreating astrocytes with GSNO or by applying BAFF-neutralizing antibodies to B cells. Collectively, these findings suggest that GSNOR modulates astrocytic BAFF expression, thereby influencing B cell activation and their IL-6-mediated functions in EAE. Modulation of this pathway may represent a promising avenue for future investigation into immune regulation in MS and related autoimmune conditions. - Source: PubMed
Publication date: 2025/12/25
Won JeseongKim JudongIslam S M TouhidulQiao FeiSingh Avtar KSingh Inderjit - Although the aroma profile of has been extensively studied in fruiting bodies, the mycelial stage provides a distinct context for elucidating the fundamental metabolic pathways, free from the complexities of organismal development. To elucidate the mechanism underlying aroma differences between strain 808 (the control strain) and its mutant strain ww808 (with almost no shiitake aroma), this study employed GC-IMS combined with PCA and OPLS-DA to identify key aroma biomarkers during the mycelial stage. All analyses were performed with three biological replicates. Furthermore, fatty acids composition, key enzyme activities of the LOX pathway, and their gene expression levels were systematically compared. The results indicated significant differences in the content of volatile aroma compounds in the mycelia of the two strains, primarily stemming from fundamental restructuring of gene expression and enzyme activity in the LOX pathway. The gene expression and LOX activity of 808 mycelium were relatively high, facilitating the accumulation of key aroma compounds such as phenylethanal, benzaldehyde, and ethyl acetate, which constitute its distinctive aromatic profile. However, although the mycelium of ww808 possessed richer fatty acid precursor (C18:2), its lower gene expression restricted the flux of this pathway. The significantly increased expression of , , and genes and higher ADH activity enhanced the conversion capacity of aldehydes to alcohols and ketones. Given the generally higher odor thresholds of alcohols and ketones compared to aldehydes, distinct aroma profiles emerged between the two strains. Pearson correlation analysis further confirmed the significant correlations between the aroma biomarkers, fatty acids, key genes, and enzyme activities. This study revealed the formation mechanism of aroma differences in the mycelia of the two strains from the perspective of metabolic pathways, providing a theoretical foundation and candidate targets for the directed genetic improvement of aroma quality. - Source: PubMed
Publication date: 2025/11/28
Yu ChangxiaJiang JunZhang MengkeDong QinYang LinZha LeiGuo QianZhao Yan - -nitrosoglutathione reductase (GSNOR), a regulator of protein -nitrosylation (SNO), has been proposed as a longevity protein. GSNOR signaling has been implicated in both the alleviation and exacerbation of aging. In the context of ischemia-reperfusion injury, we previously showed a sex-dependent response to GSNOR inhibition; cardiac damage was alleviated in males and exacerbated in females. Considering sex differences in the incidence of cardiovascular disease with age, we investigated the effect of GSNOR deletion () on age-related changes in cardiac function. We performed longitudinal two-dimensional echocardiography measurements in M-mode on male and female, wild-type (WT) and mice at young (3-4 mo), middle (13-15 mo), and old age (18-20 mo). Left ventricular wall thickness and ejection fraction decreased with age in WT mice but were maintained in . Western blot and GSNOR activity assays showed GSNOR activity and expression decreased with age in WT females. Isolated cardiomyocyte force-coupling analysis showed that increasing age was inversely correlated with sarcomere shortening and Ca release kinetics in WT males but not . WT females showed slower Ca re-uptake after contraction and time to peak sarcomere shortening, but all other parameters were maintained. females exhibited slower Ca re-uptake and decreased sarcomere shortening. Proteomic analysis of SNO from females showed increased modification of pyruvate dehydrogenase, E1β, and dihydrolipoamide dehydrogenase in young WT females relative to middle-aged mice. Together, our data suggest that GSNOR deletion is beneficial in males by maintaining cardiac function; although the absence of GSNOR in females removes an age-essential SNO imbalance, which may exacerbate age-related pathology. GSNOR deficiency appears beneficial to cardiac aging in both sexes, but at the cellular level, we discovered a sex disparity and the potential for underlying cellular dysfunction in female hearts. Taken together, GSNOR deficiency may present a mechanism through which the female heart specifically is at a higher risk of age-related cardiovascular disease and may represent a potential clinical target. - Source: PubMed
Publication date: 2025/12/17
Ebenebe Obialunanma VKabir RaihanBooher AllisonGarbus HaleyCohen Charles DJani VivekLin Brian LAdamo LuigiKohr Mark J - Ischemic heart disease is a primary cause of death for men and women in the United States. Recent epidemiologic findings, however, suggest that premenopausal women have inherent protection from many cardiovascular pathologies compared to age-matched men, which is lost with menopause. We and others have documented similar protective signaling in animal models, with females exhibiting protection from ischemic injury that is lost with ovariectomy (OVX). Furthermore, in recent studies, we demonstrated that the loss of alcohol dehydrogenase 5 (ADH5) blocked sex-specific cardioprotection in females, but activation of aldehyde dehydrogenase 2 (ALDH2) provided a rescue. ADH5 and ALDH2 both metabolize formaldehyde to formate, potentially implicating formate in female-specific cardioprotection. Therefore, the objective of this study was to examine a role for formate during ischemic injury in female hearts using wild-type (WT) and ADH5 mice. We also aimed to explore estrogen-dependent effects by using ovariectomized (OVX) WT mice. To assess the protective effects of formate in intact WT and ADH5 female mice, as well as OVX WT female mice, hearts were Langendorff-perfused and subjected to ischemia/reperfusion (I/R) injury. Since formate is used in one-carbon metabolism (OCM), select OCM enzymes were also probed via western blot. Importantly, we found that formate significantly reduced infarct size in intact ADH5 female hearts subjected to I/R injury, but formate was without effect in intact WT female hearts. Additionally, formate failed to reduce I/R injury in OVX WT female hearts, despite OVX WT female hearts exhibiting reduced ADH5 and ALDH2 activity. However, we noted that the expression of certain OCM enzymes was downregulated in OVX WT female hearts versus intact WT females, which may prevent proper formate utilization by OCM in OVX WT female hearts. Furthermore, blockage of formate import into OCM in intact WT female hearts also exacerbated I/R injury. Taken together, our findings support formate utilization by OCM as a key component of cardioprotective signaling in female hearts, with estrogen acting as a potential mediator. - Source: PubMed
Publication date: 2025/12/12
Garbus-Grant HaleyEbenebe-Kasonde Obialunanma VKabir RaihanKohr Mark J - Formaldehyde (FA) is both a one-carbon (1C) metabolite and a potent genotoxin in living cells. FA plays beneficial roles in endogenous catabolic processes and cellular signaling, but its potent electrophilicity necessitates strict regulation. This dichotomy is especially important in the nucleus, where endogenously produced FA has been shown to promote toxicity and disease by generating deleterious DNA adducts. More broadly, the sources and scavenging mechanisms of FA differ across subcellular compartments, underscoring the need for imaging sensors with subcellular spatial resolution to accurately probe contributions of FA to transient, local 1C pools. Here, we report NucRFAP-2, a nuclear-targeted, activity-based ratiometric probe for FA detection, and apply it to monitor dynamic changes in the nuclear FA pool. Using this first-generation reagent for nuclear FA imaging, we demonstrate that genetic perturbation of key FA clearance pathways alters nuclear FA levels by identifying alcohol dehydrogenase 5 (ADH5) as a principal regulator of nuclear FA homeostasis. Furthermore, NucRFAP-2 reveals elevated nuclear FA pools in patient-derived T and B lymphocytes deficient in Wiskott-Aldrich syndrome protein (WASp) and Fanconi anemia group D2 protein (FANCD2), suggesting that replication-associated epigenetic rewiring may contribute to aldehyde-associated pathologies. By demonstrating the ability of NucRFAP-2 to reveal an interplay between FA metabolism, genome integrity, and 1C homeostasis, we showcase this probe as a potentially powerful chemical tool to uncover novel mechanisms of nuclear FA biology. - Source: PubMed
Publication date: 2025/12/01
Tenney LoganWen Kuo-KuangHan Seong-SuVyas Yatin MChang Christopher J