Mouse monoamine oxidase A,MAOA ELISA kit
- Known as:
- Mouse monoamine oxidase A,MAOA Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- E0600Mo
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- Sunlog
- Gene target:
- Mouse monoamine oxidase MAOA ELISA kit
Related genes to: Mouse monoamine oxidase A,MAOA ELISA kit
- Gene:
- MAOA NIH gene
- Name:
- monoamine oxidase A
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- Xp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: Mouse monoamine oxidase A,MAOA ELISA kit
Related articles to: Mouse monoamine oxidase A,MAOA ELISA kit
- Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy, yet their efficacy remains limited by tumor resistance, immune-related adverse events, and poor response in microsatellite stable colorectal cancer (CRC). To address these challenges, dual monoamine oxidase A (MAO-A) and heat shock protein 90 (HSP90) inhibitors, MPT1B098 and MPT1B099, were developed and evaluated for their therapeutic potential and immune-modulatory efficacy in CRC. - Source: PubMed
Publication date: 2026/08/24
Tseng Hui-JuWu Yueh-LinChen Yan-LingWang Chien-HuaBanerjee SuddhasatwaLiou Jing-Ping - Ketamine may have antidepressant and anti-suicidal effects. However, the mechanism underlying ketamine-mediated improvement in cognitive impairment in patients with depression remains unclear. To improve patient cognition in depression using molecular docking and network pharmacology, we examined ketamine's key targets and identified its molecular mechanisms. - Source: PubMed
Publication date: 2026/08/06
Yang LeiZhang QiuyuZhang YingYao KaifangChen XimingTian HongjunZhuo Chuanjun - Mitochondrial calcium(mtCa~(2+)) overload constitutes a core pathological process in the initiation and progression of heart failure(HF) following myocardial infarction(MI). Abnormal accumulation of the lipid peroxide 4-hydroxynonenal(4-HNE) mediated by monoamine oxidase A(MAOA), as well as dysfunction of the mtCa~(2+) uniporter(MCU), can both induce mtCa~(2+) overload. Linggui Zhugan Decoction(LGZGD), a classical traditional Chinese medicine prescription for the treatment of cardiovascular diseases, is extensively used to manage post-MI HF. However, its regulatory effects on mtCa~(2+) homeostasis and the underlying molecular mechanisms remain unclear. In the present study, a rat model of post-MI HF and a H_2O_2-induced oxidative stress model in H9C2 cardiomyocytes were established, combined with MAOA overexpression and knockdown validation experiments, to systematically investigate the cardioprotective mechanisms of LGZGD. The results revealed that LGZGD significantly improved cardiac systolic function in MI rats(P<0.01), reduced creatine kinase(CK) and lactate dehydrogenase(LDH) activities(P<0.05), alleviated myocardial pathological injury, and significantly decreased the level of the oxidative stress marker 4-HNE while restoring the content of the antioxidant glutathione(GSH)(P<0.05). In vitro experiments further demonstrated that LGZGD-medicated serum effectively suppressed apoptosis in H9C2 cardiomyocytes, restored mitochondrial membrane potential(P<0.01), and promoted mitophagy to eliminate damaged mitochondria. Moreover, LGZGD markedly inhibited MAOA expression and activation, reduced 4-HNE accumulation, subsequently downregulated MCU-mediated mtCa~(2+) overload, and effectively maintained mtCa~(2+) homeostasis(P<0.01). MAOA functional modulation experiments further demonstrated that MAOA knockdown mimicked the protective effects of LGZGD, whereas MAOA overexpression exacerbated cardiomyocyte injury, and LGZGD partially reversed this adverse effect(P<0.05). Collectively, this study confirms that LGZGD significantly ameliorates post-MI HF and oxidative stress-induced cardiomyocyte injury, with the underlying mechanism closely associated with modulation of the MAOA/4-HNE/MCU pathway, clearance of damaged mitochondria, and maintenance of mtCa~(2+) homeostasis. - Source: PubMed
Wang RongHuang Sheng-YiWang FangHuang Jin-Ling - Depression is a complex disorder involving multiple pathological processes, and the identification of bioactive candidates from traditional Chinese medicine (TCM) remains challenging. This study established an integrated network pharmacology (NP)-cell membrane chromatography (CMC)-high-performance liquid chromatography (HPLC) strategy (NP-CMC-HPLC) for activity-guided screening of potential bioactive compounds and activity-associated quality characterization of the dried tuberous root of Curcuma wenyujin Y. H. Chen & C. Ling (WYJ). The chemical profile of WYJ was comprehensively characterized using ultra-performance liquid chromatography coupled with quadrupole Orbitrap mass spectrometry (UPLC-Q-Orbitrap-MS), combined with headspace solid-phase microextraction gas chromatography-mass spectrometry (HS-SPME-GC-MS) and headspace gas chromatography-ion mobility spectrometry (HS-GC-IMS). A total of 184 compounds were identified, and potential bioactive compounds were prioritized through network pharmacology analysis. Multi-target cell membrane chromatography (CMC) systems based on 5-hydroxytryptamine 1 A receptor (5-HT), 5-hydroxytryptamine 2 A receptor (5-HT), dopamine D1 receptor (DRD1), dopamine D2 receptor (DRD2), and monoamine oxidase A (MAO-A) were subsequently established, enabling the identification of six compounds exhibiting target-associated retention behavior. Molecular docking and a corticosterone-induced PC12 cell injury model provided complementary computational and cellular evidence supporting compound selection. Finally, a parallel reaction monitoring (PRM)-based method was developed for the quantitative analysis of four non-volatile CMC-prioritized compounds. The proposed strategy integrates chemical profiling, target affinity screening, cellular evaluation, and quantitative analysis to facilitate the discovery of bioactive candidates and activity-associated quality characterization of complex herbal medicines. - Source: PubMed
Publication date: 2026/08/26
Song MengleiLiu HairuiWang WanjiaoZhang YutingShen XinjieWang YuHan ShengliHe LangchongShi LeiBao YanyuLi ZhengYin JiaxinYu Heshui - The part played by synaptic plasticity in natural learning can be reassessed owing to the discovery of dormant neurons in the cortical layer-2 of large-brained mammals. Here, the recruitment of that contain these quiescent cells is argued to underlie the lifelong building of long-term memories, albeit only during periods when cortical regions are segregated, while perception, cognition and motor skills are at their lowest level. As records of online experience are replayed by the hippocampus, about half of every sleep cycle would harbour the relevant outgrowth between in-use and free cortical columns. This translation of labile traces into steady imprints is simulated on computer, in an attempt to link experimental findings to specific functions and possibly generate predictions. Rapid eyes movement observed at the end of every sleep cycle is notably interpreted as a side effect of the necessary priming of peripheral effectors whereby cortical replay can induce activation in the hippocampus and thus allow new connections between paths that are thus concurrently activated. Architectural and functional data highlight a topological matching between key components of the underlying model and those of structures. Several factors are considered for the experience-driven development of these structures, including slow-wave activity whereby the guided growth of axons may occur from layer-2 of their host column towards the layer-4 of free columns, possibly steered in parallel by distinct calcium waves. In addition to this main prediction, this theory supports the central role of sleep in the development of autistic symptoms. Rooted in an epigenetic downregulation of the MAOA brain enzyme, the resulting offline over-activity would entail aberrant branching between . Whereas most features of the condition have already been interpreted through this systemic approach, the evolution of autism prevalence across four human generations is derived here from the masking effects of genetic variants and X chromosome inactivation, while a host of risk factors is liable to promote MAOA. Accordingly, pregnancy should be prevented from excess MAOA activity by being subjected to prior blood testing, which may lead to the individualized prescription of MAOA inhibitors. - Source: PubMed
Publication date: 2026/08/14
Béroule Dominique G