mProX™ Human MC3R Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 NFκB activity is effectively curbed via MC3R modulation.
HBE cells underwent co-transfection with siRNA targeting the MC3R receptor alongside the NFκB luciferase reporter, followed by RSV (rhino syncitial virus) treatment. Notably, the application of siRNA effectively nullified the α and γ MSH-induced suppression of NFκB (*P<0.05, n=4).
Ref: Land, Stephen C. "Inhibition of cellular and systemic inflammation cues in human bronchial epithelial cells by melanocortin-related peptides: mechanism of KPV action and a role for MC3R agonists." International journal of physiology, pathophysiology and pharmacology 4.2 (2012): 59.
Pubmed: 22837805
DOI: NA
Research Highlights
Sandbaumhuter FA, et al. "Label-Free Quantitative Thermal Proteome Profiling Reveals Target Transcription ." Analytical chemistry, 2023.
The study focused on identifying the signaling pathways and transcription factors involved in the cellular response to ligand treatment of ACTH, alpha-MSH, and gamma-MSH. A workflow was used to analyze and identify differentially expressed proteins and their thermal stability upon MC3R activation. A total of 298 proteins were found to have altered thermal stability, with several being identified as transcription factors in the MC3R signaling cascade. These transcription factors, including CCAR2, DDX21, HMGB2, SRSF7, and TET2, were also found to play essential roles in immune responses. Bayesian statistics and label-free quantitative LC-MS were used to infer and validate the activities of these transcription factors, highlighting the role of post-translational modifications. The multidimensional data analysis workflow used in this study provides a comprehensive understanding of the downstream processes triggered by MC3R activation. All proteomic data generated in this study can be accessed at DOI: 10.6019/PXD039945.
Pubmed:
37804223
DOI:
10.1021/acs.analchem.3c03643
Gui Y, et al. "Melanocortin-3 receptor expression in AgRP neurons is required for normal ." Cell reports, 2023.
The melanocortin-3 receptor (MC3R) plays a key role in regulating the central melanocortin circuitry by negatively impacting the expression of agouti-related protein (AgRP) nerve terminals. These terminals influence GABA release onto secondary neurons expressing MC4R. Although MC3R knockout (KO) mice display dysfunctional behavioral and neuroendocrine responses to fasting, it remains unclear how these mice respond to other energy-related signals. Through experiments using MC3R KO mice, it was discovered that the activation of AgRP neurons in response to fasting, cold exposure, or ghrelin was impaired, while normal inhibition was observed in the presence of food in ad libitum-fed mice. Furthermore, using a conditional MC3R KO model, it was found that the presence of MC3R specifically within AgRP neurons is necessary for the regulation of AgRP neuron activation in response to fasting and ghrelin. These findings highlight the critical role of MC3R in modulating the responsiveness of AgRP neurons to hormonal and neuronal signals related to energy need.
Pubmed:
37792535
DOI:
10.1016/j.celrep.2023.113188
