MTNR1A
- Known as:
- MTNR1A
- Catalog number:
- Y214257
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- MTNR1A
Related genes to: MTNR1A
- Gene:
- MTNR1A NIH gene
- Name:
- melatonin receptor 1A
- Previous symbol:
- -
- Synonyms:
- MEL-1A-R
- Chromosome:
- 4q35.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-22
- Date modifiied:
- 2016-10-25
Related products to: MTNR1A
Related articles to: MTNR1A
- Melatonin, a signaling molecule secreted by the pineal gland, is closely associated with physiological activities, such as animal growth, development, and reproduction. Multiple studies have indicated that melatonin acts on the adenohypophysis to promote the synthesis and secretion of growth hormone (GH), but the specific mechanism of melatonin remains unclear. We have previously reported that melatonin levels in bovine serum are closely correlated with GH levels. In the present study, transcriptome sequencing was performed on primary bovine adenohypophyseal cells treated with melatonin, which identified FOXO1 as a key transcription factor that is responsive to melatonin and regulates GH synthesis and secretion. Cellular experiments revealed that melatonin binds to the MTNR1A in bovine adenohypophyseal cells, activates the cAMP/PKA signaling pathway, and promotes the expression of FOXO1 protein. Dual-luciferase reporter assays verified the binding of FOXO1 to the GH1 promoter. Treatment with Luzindole, 4P-PDOT, 2',5'-Dideoxyadenosine or H-89 elucidated the molecular mechanism through which melatonin promotes GH synthesis and secretion in adenohypophyseal cells through the cAMP/PKA/CREB/FOXO1 pathway. The present study provides critical evidence for the direct action of melatonin on adenohypophyseal cells and its targeted regulatory sites, and it offers new insights into the conserved and species-specific modes of action of melatonin across different species, providing data and theoretical support for the application of melatonin in promoting animal growth and development. - Source: PubMed
Zheng YiChen Qing-QingGuo Hai-XiangZhang Yu-XinQiu Ling-LingWang Bing-BingYu SongGao Jia-RuiZhang ZheZhang Jia-BaoLiu Guo-ShiYuan Bao - Insomnia, as one of the most common sleep problems, seriously affects the normal life and work of individuals. Aromatherapy is regarded as a promising alternative medicine for improving sleep quality. Based on network pharmacology and data mining, this study screened natural raw materials for improving insomnia. Then, we developed an aromatherapy product informed by the screening results and investigated its mechanism for improving insomnia through network pharmacology. Five core insomnia targets were identified through literature. 1600 candidate compounds and 1757 candidate herbs related to the target were matched using HERB and TCMSP databases. By comparing with the Catalogue of Used Cosmetic Materials (2021 edition), 597 kinds of usable candidate materials were selected, including 85 raw materials related to target MTNR1A, 86 raw materials related to target MTNR1B, 120 raw materials related to target HTR1A, 7 raw materials related to target GABRB2, and 582 raw materials related to target GABRA1. Then based on the screening results, we selected sandalwood, lime, angelica sinensis, yilan, sage and lavender to design Pinghe Sleep Aromatherapy Product to improve insomnia. Network pharmacological analysis revealed that the main ingredients of the Pinghe Sleep Aromatherapy Product are beta-sitosterol, stigmasterol, isorhamnetin, luteolin, tanshinone IIA, D-limonene, and linalool. It exerts improvement effects by influencing targets such as IL6, TNF, AKT1, CASP3, TP53, and VEGFA, regulating signaling pathways such as AGE-RAGE, neuroactive ligand-receptor interactions, the HIF-1 signaling pathway, and the calcium signaling pathway. This study provides an idea of raw material screening and product development, which can save product development cost and shorten product development cycle by using network pharmacology and data mining. - Source: PubMed
Yue LizhiJiao QianLi JunxiangLu YiYi MeitingHe CongfenJia Yan - Our previous studies showed that the prostates of the wild ground squirrels were capable of locally synthesizing testosterone (T), dihydrotestosterone (DHT) and estrogen. In this study, we investigated expression levels of luteinizing hormone receptor (LHR), steroidogenic factor 1 (SF-1), steroidogenic acute regulatory protein (StAR), cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), 3β-hydroxysteroid dehydrogenase (3βHSD) and 17α-hydroxylase cytochrome P450 (P450c17) in the prostates of the wild ground squirrels during the breeding and non-breeding seasons. LHR, SF-1, StAR, P450scc, 3βHSD and P450c17 were identified in the stromal cells or epithelial cells. The mRNA expression levels of LHR, SF-1, StAR, P450scc, P450c17, 3βHSD and Sterol Regulatory Element-Binding Protein 2 (Srebp2) in the prostate were remarkedly higher during the breeding period than those in the non-breeding period. In contrast, the mRNA expression levels of Melatonin Receptor 1a (Mtnr1a) and Melatonin Receptor 1b (Mtnr1b) were elevated during the non-breeding period. Consistently, the circulating LH and T as well as the prostatic T and DHT concentrations were remarkably higher in the breeding season than those of the non-breeding season, which were positively correlated with the seasonal changes of prostatic weight. Additionally, the transcriptomic study in the prostates identified that differentially expressed genes might be related to signal transduction and signaling receptor activity using GO analysis. The KEGG pathway enriched by differentially expressed genes detected to be involved in steroid biosynthesis, estrogen signaling pathway or steroidogenesis. Taken together, these findings suggested that the prostates of the wild ground squirrels potentially owned ability to synthesize steroid hormones de novo, and the steroid hormones might affect the prostatic functions of the wild ground squirrels via an autocrine or paracrine manner. - Source: PubMed
Publication date: 2025/12/31
Chen PengyuGao QingjingXie WenqianYu HuanLiu YuningZhang HaolinWeng Qiang - Type 2 diabetes mellitus (T2DM) poses a significant global health challenge. Genome-wide Association Studies have linked T2DM to genetic variants in the melatonin receptor 1a ( and 1b () genes, which encode the MT1 and MT2 receptors, respectively. Our results found that the rs2119882 MT1 mutation was associated with higher blood glucose levels and increased body mass index (BMI) in humans. Metabolomic analysis showed elevated levels of palmitic acid (a saturated fatty acid) and reduced levels of oleic acid (an unsaturated fatty acid) in individuals with this mutation. In contrast, the rs10830963 MT2 mutation did not show the significant differences in blood glucose level or BMI compared to normal control individuals. Inhibition of and expression led to lower GLUT-4 mRNA and insulin receptor protein levels in human liver cells, resulting in decreased glycogen synthesis and metabolic disruptions. We used CRISPR/Cas9 to create and knockout (KO) mice, which also exhibited reduced GLUT-4 and INSR mRNA levels, decreased glucose tolerance, and increased insulin resistance. These mice also developed obesity, liver lipid deposition, increased abdominal white adipose tissue, and lower androgen levels. Metabolomic and proteomic analyses of the KO mice revealed increased triglycerides and phospholipids, and decreased unsaturated fatty acids. Proteomic studies showed reduced levels of insulin receptor tyrosine kinase, lipid droplet-associated hydrolase, and glucose-6-phosphate dehydrogenase, disrupting fatty acid metabolism and increasing liver lipid deposition. Additionally, a high-fat diet challenge in and KO male mice accelerate the INSR protein expression suppression, hepatic triglyceride accumulation, blood glucose elevation and weight gain. Finally, we generated AANAT over-expressing sheep, which showed improved glucose tolerance and higher insulin levels after glucose injection compared to WT sheep. These findings underscore the importance of melatonin and its receptors in glucose and lipid metabolism, suggesting their deficiencies may contribute to T2DM. - Source: PubMed
Publication date: 2025/12/05
Yan LaiqingLv DongyingZhang LuGao YuZhu TianqiDing MengYao YujunWu HaixinFu YaoLi GuangdongJi PengyunWang LikaiHan HuigangLiu YunjieCoto-Montes AnaHardeland RüdigerLiu Guoshi - Parkinson's disease (PD) is a neurodegenerative disease characterized by dopaminergic neuron loss and Lewy bodies in the substantia nigra. Abnormal mitochondrial function and accumulated α-synuclein (α-syn) are key etiological factors of PD. Melatonin type 1 receptor (MT1) regulates sleep upon activation by melatonin and may be reduced in PD patients. However, the role of MT1 in PD pathogenesis remains elusive. In this study, we found knockdown of MT1 caused mitochondrial dysfunction, mitochondrial fission and mitophagy in SH-SY5Y cells. Expression of mitochondrial fission protein dynamin-related protein 1 (DRP1) was increased and expression of fusion proteins optic atrophy 1 (OPA1), mitofusin 1 (MFN1) and mitofusin 2 (MFN2) were decreased. This was probably attributed to decreased phosphorylation of DRP1 at S637 by protein kinase A (PKA) and increased phosphorylation at S616 by extracellular-regulated kinase 1/2 (ERK1/2). Loss of MT1 exacerbated mitochondrial fission without influencing mitophagy, TH expression and movement in an MPTP-induced mouse model. Neuronal MT1 deficiency aggravated preformed fibrils induced autophagy inhibition and α-syn aggregation. Overexpression of MT1 reduced mitochondrial fission, increased LC3II expression and decreased P62 accumulation to promote autophagy in HEK293T cells, thus mitigating aggregation of α-syn. This study demonstrates the function of MT1 in mitochondria and autophagy, which sheds further light on PD prevention targeting MT1. - Source: PubMed
Publication date: 2025/11/25
Wang Xiao-BoQi Li-LiWang Jian-MinSun Yan-RuiLv Qian-KunCao Bing-ErJiang Shu-MinMa Quan-HongLiu Chun-FengLiu Jun-YiWang Fen