MTNR1B Membrane Protein Introduction

Introduction of MTNR1B

MTNR1B, also known as melatonin receptor 1B, melatonin receptor 1B variant B, melatonin receptor MEL1B, FGQTL2 or MT2, is an integral membrane protein with 362 amino acids and has a molecular mass of approximately 40 kDa. In humans, it is encoded by the MTNR1B gene localized at the chromosome 11q14.3. MTNR1B is one of two high-affinity forms of a receptor for melatonin, which is a major hormone secreted by the pineal gland. Melatonin receptors are split into two subtypes including MTNR1A and MTNR1B. And MTNR1B is a member of the G protein-coupled receptor (GPCR) family and has seven transmembrane domains, intracellular C-terminal domain, as well as an extracellular N-terminal domain. Comparative real-time PCR displayed that this protein is expressed in the retina and, to a lesser extent, in the brain.

Function of MTNR1B Membrane Protein

It is believed that the membrane protein MTNR1B is involved in light-dependent functions in the retina and is likely to participate in the neurobiological effects of melatonin. Melatonin is a hormone released by the brain pineal gland when it is dark, whose signals contribute to sleep and help to coordinate many essential physiological processes during sleep, such as metabolism, appetite regulation, heart rate and blood pressure. It has been identified to play a critical role in the etiology of AIS and scoliosis development. MTNR1B has several related pathways including circadian rhythm-related genes and peptide ligand-binding receptors. A number of diseases associated with this gene are diabetes mellitus and noninsulin-dependent and idiopathic scoliosis. The recent study has confirmed that MTNR1B mutations are correlated with the elevated average blood glucose level and around 20% increased the risk of developing type 2 diabetes. Additionally, MTNR1B shares a high degree of sequence homology with GPR50, which heterodimerizes with MTNR1A or MTNR1B in vitro and in intact cells.

Fig.1 The regulation of uterine contractions mediated through the circadian clock and hMNTR1B. (Beesley, 2015)

Application of MTNR1B Membrane Protein in Literature

1. Li Y., et al. Melatonin exerts an inhibitory effect on insulin gene transcription via MTNR1B and the downstream Raf‑1/ERK signaling pathway. Int J Mol Med. 2018, 41(2), 955-961. PubMed ID: 29207116
   
   

   The study found that the MAPK signaling pathway was inhibited in MIN6 cells by treatment with melatonin or overexpressed MTNR1B. The knockdown of MTNR1B attenuated the modulating effect of melatonin on insulin expression totally. That may show that melatonin inhibited the insulin transcription by MTNR1B and downstream MAPK signaling pathway.

2. Goni L., et al. Macron utrient-specific effect of the MTNR1B genotype on lipid levels in response to 2 year weight-loss diets. J Lipid Res. 2018, 59(1), 155-161. PubMed ID: 29089366
   
   

   The paper analyzed whether the rs10830963 genetic variant of MTNR1B was associated with changes in lipid levels when responded to dietary interventions with diverse macronutrient distribution in 722 overweight subjects from the POUNDS Lost trial.

3. Patel R., et al. Association of melatonin &MTNR1B variants with type 2 diabetes in Gujarat population. Biomed Pharmacother. 2018, 103, 429-434. PubMed ID: 29674279
   
   

   This study suggested that plasma melatonin levels in T2D patients were decreased and there was an association between MTNR1B rs10830963 GG genotype with elevated fasting blood glucose (FBG). So, the reduced titer of melatonin and altered FBG due to MTNR1B genetic variant may work as a potent risk factor towards T2D in Gujarat population.

4. Lopez-Minguez J., et al. Late dinner impairs glucose tolerance in MTNR1B risk allele carriers: A randomized, cross-over study. Clin Nutr. 2018, 37(4), 1133-1140. PubMed ID: 28455106
   
   

   The interaction of dinner timing and MTNR1B facilitated a causal role of endogenous melatonin in the damage of glucose tolerance. All results from this article suggested that changing the dinner to an earlier time may lead to a better glucose tolerance, especially in MTNR1B carriers.

5. Liu W., et al. RNAi-mediated knockdown of MTNR1B without disrupting the effects of melatonin on apoptosis and cell cycle in bovine granulose cells. PeerJ. 2018, 6, e4463. PubMed ID: 29707428
   
   

   In conclusion, the evidence displayed that melatonin and MTNR1B were implicated in BCL2 family and CASP3-dependent apoptotic pathway in bovine GCs. MTNR1A and MTNR1B possibly coordinated the action of medicating the appropriate melatonin response to GCs.

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Reference

1. Beesley S, et al. (2015). Circadian clock regulation of melatonin MTNR1B receptor expression in human myometrial smooth muscle cells. Mol Hum Reprod. 21(8), 662-671.

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