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Study · Not a test of the peptide alone · 2001

6 results

Cysteine residues are involved in structure and function of melanocortin 1 receptor: Substitution of a cysteine residue in transmembrane segment two converts an agonist to antagonist.

Frändberg PA, Doufexis M, Kapas S, Chhajlani V

Biochemical and biophysical research communications1 Mar 2001Cited by 37 (Europe PMC)

PMID11237737 (opens in a new tab)DOI10.1006/bbrc.2001.4429 (opens in a new tab)PepBankPUB-11237737
Publisher pagePubMedAsk about this study
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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 study6

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone6

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).

  1. 01LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Mechanism

    In cells with hMC1R, increasing DTT concentrations decreased the binding of [125I]-NDP-MSH in a biphasic manner.

    In plain wordsIn lab tests, breaking the receptor's disulfide bonds with DTT reduced NDP-MSH binding to the MC1R receptor.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    Decrease[125I]-NDP-MSH binding after DTT reduction of hMC1R
    Study

    n: not reported in source

    wild-type and mutant human MC1R
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    Reduction of disulfide bonds in human melanocortin 1 receptor (hMC1R) with increasing concentrations of DTT (dithiothreitol) resulted in a decrease in the binding of [125I]-ACTH (adrenocorticotropic hormone, L-isomer) in an uniphasic manner and a decrease in [125I]-NDP-MSH ([Nle(4),D-Phe(7)]-alpha-m…
    1 context sentence
    Summary · context
    To characterize the role of individual cysteine residues, we employed site-directed mutagenesis to substitute cysteine by glycine at all fourteen positions in hMC1R and analysed wild-type and mutant receptors for ligand binding and cAMP signalling.

    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).

  2. 02LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Mechanism

    In cells with hMC1R, 10 mM DTT pretreatment did not affect the affinity of NDP-MSH, while alpha-MSH lost 36-fold affinity.

    In plain wordsIn lab tests, DTT did not change how tightly NDP-MSH bound the MC1R receptor, but alpha-MSH bound 36-fold less tightly.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    No significant changeNDP-MSH affinity after 10 mM DTT
    Study

    n: not reported in source

    wild-type and mutant human MC1R
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Measurements

    affinity loss for alpha-MSH
    36 fold
    10 mM DTT

    Source sentences

    Summary
    Pretreatment of hMC1R with 10 mM DTT resulted in a 36-fold loss of affinity for alpha-MSH (L-isomer) without affecting the affinity of NDP-MSH (D-isomer).
    1 context sentence
    Summary · context
    To characterize the role of individual cysteine residues, we employed site-directed mutagenesis to substitute cysteine by glycine at all fourteen positions in hMC1R and analysed wild-type and mutant receptors for ligand binding and cAMP signalling.

    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).

  3. 03LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Mechanism

    In hMC1R mutants, replacing any one of four extracellular loop cysteines (C35G, C267G, C273G, C275G) with glycine abolished [125I]-NDP-MSH binding.

    In plain wordsIn lab tests, changing any one of four cysteines in the receptor's outer loops stopped NDP-MSH from binding.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    Decrease[125I]-NDP-MSH binding in four extracellular loop cysteine mutants
    Study

    n: not reported in source

    wild-type and mutant human MC1R
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    Single point mutation of four cysteine residues in extracellular loops to glycine (C35G, C267G, C273G, and C275G) resulted in a complete loss of binding for [125I]-NDP-MSH.
    1 context sentence
    Summary · context
    To characterize the role of individual cysteine residues, we employed site-directed mutagenesis to substitute cysteine by glycine at all fourteen positions in hMC1R and analysed wild-type and mutant receptors for ligand binding and cAMP signalling.

    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).

  4. 04LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Mechanism

    In hMC1R mutants C191G, C215G and C315G, ligand binding was normal but alpha-MSH and NDP-MSH failed to generate a cAMP signal.

    In plain wordsIn lab tests, three mutant receptors still bound NDP-MSH but did not send a signal after it bound.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreasecAMP signal in C191G, C215G and C315G mutants
    Study

    n: not reported in source

    wild-type and mutant human MC1R
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    Moreover, mutants with normal ligand binding, at positions C191G (transmembrane segment 5), C215G (third intracellular loop), and C315G (C-terminal loop) failed to generate cAMP signal in response to both agonists alpha-MSH and NDP-MSH.
    1 context sentence
    Summary · context
    To characterize the role of individual cysteine residues, we employed site-directed mutagenesis to substitute cysteine by glycine at all fourteen positions in hMC1R and analysed wild-type and mutant receptors for ligand binding and cAMP signalling.

    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).

  5. 05LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Mechanism

    At the hMC1R C78G mutant, NDP-MSH could not stimulate a cAMP signal, while alpha-MSH generated a signal identical to wild-type.

    In plain wordsIn lab tests, a single receptor change stopped NDP-MSH from triggering a signal, while alpha-MSH still worked normally.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreasecAMP signal of NDP-MSH at the C78G mutant
    Study

    n: not reported in source

    wild-type and mutant human MC1R
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    Mutant at position C78G (with wild-type binding to alpha-MSH as well as NDP-MSH) generated a cAMP signal in response to alpha-MSH (identical to wild-type hMC1R) but interestingly could not be stimulated by NDP-MSH.
    1 context sentence
    Summary · context
    To characterize the role of individual cysteine residues, we employed site-directed mutagenesis to substitute cysteine by glycine at all fourteen positions in hMC1R and analysed wild-type and mutant receptors for ligand binding and cAMP signalling.

    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).

  6. 06LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Mechanism

    At the hMC1R C78G mutant, NDP-MSH acted as an antagonist instead of an agonist.

    In plain wordsIn lab tests, NDP-MSH blocked the receptor instead of activating it when one amino acid in the receptor was changed.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    Not applicableNDP-MSH agonist-to-antagonist conversion at C78G
    Study

    n: not reported in source

    wild-type and mutant human MC1R
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    Moreover, this single amino acid substitution converted NDP-MSH from being an agonist to antagonist at the C78G mutant receptor.
    1 context sentence
    Summary · context
    To characterize the role of individual cysteine residues, we employed site-directed mutagenesis to substitute cysteine by glycine at all fourteen positions in hMC1R and analysed wild-type and mutant receptors for ligand binding and cAMP signalling.

    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).

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.

  1. Version 2Current

    13 Oct 2026, 21:44 UTC

    Study results updated

  2. 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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