mProX™ Human MTNR1A Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 Exploring the impact of MTNR1A gene suppression and the addition of Melatonin on the temporal dynamics of progesterone, estradiol, Inhibin β, and Activin B secretion.
The varying levels of progesterone, estradiol, Inhibin β, and Activin B were assessed at 24, 48, and 72 hours within conditioned media originating from GCs subjected to pshRNA-3 transfection and/or Melatonin treatment. Distinct letters indicate notable dissimilarity (p<0.05, determined through one-way analysis of variance).
Ref: Wang, Shu-Juan, et al. "The role of Melatonin receptor MTNR1A in the action of Melatonin on bovine granulosa cells." Molecular Reproduction and Development 84.11 (2017): 1140-1154.
Pubmed: 28805353
DOI: 10.1002/mrd.22877
Research Highlights
Liao Y, et al. "Melatonin suppresses tumor proliferation and metastasis by targeting GATA2 in ." Journal of pineal research, 2023.
Endometrial cancer (EC) is a reproductive system disease that primarily affects perimenopausal and postmenopausal women. However, the underlying cause of this cancer is not fully understood. Previous studies have identified melatonin (MT) as a potential therapeutic agent for EC, yet its precise mechanism of action remains unclear. In a recent study, it was discovered that GATA-binding protein 2 (GATA2) is expressed at low levels in EC and is regulated by MT. The study further revealed that MT can increase the expression of GATA2 through its receptor, MT receptor 1A (MTNR1A), while GATA2 can also promote the expression of MTNR1A by binding to its promoter region. Furthermore, both in vivo and in vitro experiments demonstrated that MT inhibits EC cell proliferation and metastasis by increasing the expression of GATA2. It was also observed that the protein kinase B (AKT) pathway is impacted by MT treatment. These findings highlight the significant role of MT and GATA2 in the development of EC.
Pubmed:
37814536
DOI:
10.1111/jpi.12918
Skubis-Sikora A, et al. "Regulation of Adipose-Derived Stem Cell Activity by Melatonin Receptors in Terms ." Pharmaceuticals (Basel, Switzerland), 2023.
Melatonin, a hormone secreted by the pineal gland, can significantly increase bone formation during regeneration through its receptors Mel1A and Mel1B. While human adipose-derived mesenchymal stem cells (ADSCs) have the ability to differentiate into bone cells, their culturing process is hindered by loss of properties or low survival rates on scaffolds. A study was conducted to evaluate the impact of melatonin on ADSCs and their osteogenic potential. Results showed that a low concentration of melatonin (100 microM) improved cell viability without affecting their potential for bone tissue healing. These findings suggest that melatonin can be safely used in regenerative medicine for ADSC expansion.
Pubmed:
37765045
DOI:
10.3390/ph16091236