In cells expressing hMC4R, deleting the distal 25, 22, 18, 17, 16 or 15 amino acids of the C terminus caused complete loss of NDP-MSH binding.
In plain wordsIn cells, removing the end of the MC4 receptor tail stopped NDP-MSH from binding to it.
- Peptide
- Melanotan I (afamelanotide)
- Outcome
- DecreaseNDP-MSH binding after large C-terminal deletions
- Study
n: not reported in source
cells expressing mutant hMC4R- Outcome group
- Receptor activity and mechanism · Pharmacology
Source sentences
Our results indicate that deletions of the distal 25 (the entire C terminus), 22, 18, 17, 16, and 15 amino acids of the C terminus result in the complete loss of both [Nle(4)-d-Phe(7)]-alpha-melanocyte stimulating hormone (NDP-MSH) binding and NDP-MSH-mediated cAMP production.
1 context sentence(design, population, supporting numbers)
In this study, we utilized deletions and mutations of specific portions of the hMC4R to determine the molecular mechanism of both the C terminus and the third intracellular loop in receptor signaling.
In this study, Melanotan I (afamelanotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Melanotan I (afamelanotide).