Pharmacological characterization of three chicken melanocortin-3 receptor mutants.

Zhang HJ, Cui ZH, Liu M, Min TQ, Xiao X, Wang ZQ, Tao YX

Domestic animal endocrinology8 Jun 2020Cited by 4 (Europe PMC)

PMID32841887DOI10.1016/j.domaniend.2020.106507PepBankPUB-32841887

Publisher page PubMedAsk about this study

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study4

1 result from studies that gave the peptide. No result from this study comes from people.

01LabIn vitro (cells)Activity measurement
In cells expressing chicken MC3R, the G104S mutant generated 24% of the wild-type response when stimulated by NDP-MSH.
In plain wordsIn cells with a chicken MC3R mutant, NDP-MSH produced only 24% of the normal receptor response.
Peptide
Melanotan I (afamelanotide)
Outcome
DecreaseG104S response to NDP-MSH
Study
chickenn: not reported in source
chicken MC3R mutants expressed in cells
Comparator
Wild-type cMC3R
Outcome group
Receptor activity and mechanism · Pharmacology
Studied dose
Dose not stated
Measurements
response relative to wild type
24%
G104S, NDP-MSH
Source sentences
Summary
although it generated 24% WT response when stimulated by NDP-MSH
2 context sentences(design, population, supporting numbers)
Summary · context
Here, we inserted the full-length cMC3R coding sequence into pcDNA3.1(+) and generated the 3 mutations by site-directed mutagenesis.
Summary · context
We analyzed the pharmacological characteristics, including binding and cyclic adenosine monophosphate (cAMP) and mitogen-activated protein kinase (MAPK) signaling, using 6 ligands ([Nle⁴, D-Phe⁷]-α-melanocyte stimulating hormone (MSH), α-, β-, γ-, and D-Trp⁸-γ-MSHs,…
Report a problemFND-3284188701

Studies that did not test the peptide alone3

In this study, Melanotan I (afamelanotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Melanotan I (afamelanotide).

02LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Activity measurement
In cells expressing chicken MC3R, the M54L mutant had pharmacological properties similar to the wild type across the tested ligands.
In plain wordsIn cells, the chicken MC3R mutant M54L behaved like the normal receptor across the tested ligands.
Peptide
Melanotan I (afamelanotide)
Outcome
No significant changeM54L pharmacological properties across ligands
Study
chickenn: not reported in source
chicken MC3R mutants expressed in cells
Comparator
Wild-type cMC3R
Outcome group
Receptor activity and mechanism · Pharmacology
Source sentences
Summary
M54L had similar pharmacological properties as the WT cMC3R.
2 context sentences(design, population, supporting numbers)
Summary · context
Here, we inserted the full-length cMC3R coding sequence into pcDNA3.1(+) and generated the 3 mutations by site-directed mutagenesis.
Summary · context
We analyzed the pharmacological characteristics, including binding and cyclic adenosine monophosphate (cAMP) and mitogen-activated protein kinase (MAPK) signaling, using 6 ligands ([Nle⁴, D-Phe⁷]-α-melanocyte stimulating hormone (MSH), α-, β-, γ-, and D-Trp⁸-γ-MSHs,…
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).
Report a problemFND-3284188702
03LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Activity measurement
In cells expressing chicken MC3R, the L151R mutant had normal binding but agonist responses reduced to approximately 25% of the wild type.
In plain wordsIn cells, the chicken MC3R mutant L151R bound ligands normally but responded at about 25% of the normal receptor.
Peptide
Melanotan I (afamelanotide)
Outcome
DecreaseL151R agonist response across ligands
Study
chickenn: not reported in source
chicken MC3R mutants expressed in cells
Comparator
Wild-type cMC3R
Outcome group
Receptor activity and mechanism · Pharmacology
Measurements
response relative to wild type
≈ 25%
L151R, agonists
Source sentences
Summary
Although L151R had normal binding, the responses to agonists were reduced to approximately 25% of that of the WT.
2 context sentences(design, population, supporting numbers)
Summary · context
Here, we inserted the full-length cMC3R coding sequence into pcDNA3.1(+) and generated the 3 mutations by site-directed mutagenesis.
Summary · context
We analyzed the pharmacological characteristics, including binding and cyclic adenosine monophosphate (cAMP) and mitogen-activated protein kinase (MAPK) signaling, using 6 ligands ([Nle⁴, D-Phe⁷]-α-melanocyte stimulating hormone (MSH), α-, β-, γ-, and D-Trp⁸-γ-MSHs,…
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).
Report a problemFND-3284188703
04LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Activity measurement
In cells expressing chicken MC3R, all 3 mutants showed significantly increased agonist-stimulated ERK1/2 phosphorylation, which indicates biased signaling at G104S and L151R.
In plain wordsIn cells, all 3 chicken MC3R mutants showed more agonist-stimulated ERK signaling than the normal receptor.
Peptide
Melanotan I (afamelanotide)
Outcome
IncreaseAgonist-stimulated ERK1/2 phosphorylation in mutants
Study
chickenn: not reported in source
chicken MC3R mutants expressed in cells
Comparator
Wild-type cMC3R
Outcome group
Receptor activity and mechanism · Pharmacology
Source sentences
Summary
In MAPK signaling, all 3 mutants showed significantly increased agonist-stimulated phosphorylation of extracellular signal-regulated protein kinases 1/2, indicating the existence of biased signaling at G104S and L151R.
2 context sentences(design, population, supporting numbers)
Summary · context
Here, we inserted the full-length cMC3R coding sequence into pcDNA3.1(+) and generated the 3 mutations by site-directed mutagenesis.
Summary · context
We analyzed the pharmacological characteristics, including binding and cyclic adenosine monophosphate (cAMP) and mitogen-activated protein kinase (MAPK) signaling, using 6 ligands ([Nle⁴, D-Phe⁷]-α-melanocyte stimulating hormone (MSH), α-, β-, γ-, and D-Trp⁸-γ-MSHs,…
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).
Report a problemFND-3284188704

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
13 Oct 2026, 21:44 UTC
Study results updated
Version 1
13 Oct 2026, 16:31 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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