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Study · In vitro (cells) · 2004

4 results

Activation of MAP kinase by MC4-R through PI3 kinase.

Vongs A, Lynn NM, Rosenblum CI

Regulatory peptides1 Aug 2004Cited by 66 (Europe PMC)

PMID15177928 (opens in a new tab)DOI10.1016/j.regpep.2004.02.018 (opens in a new tab)PepBankPUB-15177928
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 study4

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

  1. 01LabIn vitro (cells)Mechanism

    In stably transfected CHO-K1 cells, the MC4-R agonist NDP-alpha-MSH activated the MAP kinases p42 (ERK2) and p44 (ERK1) in a time- and dose-dependent manner.

    In plain wordsIn cells carrying the MC4-R receptor, NDP-alpha-MSH switched on the MAP kinases ERK1 and ERK2, and the response depended on time and dose.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    Increasep42/p44 (ERK2/ERK1) MAPK activation
    Study

    n: not reported in source

    Stably transfected CHO-K1 cells expressing MC4-R
    Outcome group
    Receptor activity and mechanism · Pharmacology
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We demonstrate that the mitogen-activated protein kinases p42 (ERK2) and p44 (ERK1) are also activated by MC4-R following treatment with the MC4-R agonist NDP-alpha-MSH in stably transfected CHO-K1 cells.
    1 context sentence
    Summary · context
    This time- and dose-dependent response is abolished by the MC4-R antagonist SHU-9119

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).

  1. 02LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Mechanism

    In stably transfected CHO-K1 cells, the MC4-R antagonist SHU-9119 abolished the MAPK response to NDP-alpha-MSH.

    In plain wordsIn cells, the blocker SHU-9119 stopped the MAPK response that NDP-alpha-MSH caused.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseMAPK activation after MC4-R antagonist SHU-9119
    Study

    n: not reported in source

    Stably transfected CHO-K1 cells expressing MC4-R
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    This time- and dose-dependent response is abolished by the MC4-R antagonist SHU-9119
    1 context sentence
    Summary · context
    We demonstrate that the mitogen-activated protein kinases p42 (ERK2) and p44 (ERK1) are also activated by MC4-R following treatment with the MC4-R agonist NDP-alpha-MSH in stably transfected CHO-K1 cells.

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

    In stably transfected CHO-K1 cells, the PI3K inhibitors wortmannin and LY294002 blocked p42/p44 MAPK activation by NDP-alpha-MSH.

    In plain wordsIn cells, drugs that block PI3K stopped the MAPK activation that NDP-alpha-MSH caused.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    Decreasep42/p44 MAPK activation after PI3K inhibitors
    Study

    n: not reported in source

    Stably transfected CHO-K1 cells expressing MC4-R
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    p42/p44 MAPK activation is blocked by the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002
    1 context sentence
    Summary · context
    We demonstrate that the mitogen-activated protein kinases p42 (ERK2) and p44 (ERK1) are also activated by MC4-R following treatment with the MC4-R agonist NDP-alpha-MSH in stably transfected CHO-K1 cells.

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

    In stably transfected CHO-K1 cells, the PKA inhibitor Rp-cAMPS did not block p42/p44 MAPK activation by NDP-alpha-MSH.

    In plain wordsIn cells, the PKA blocker Rp-cAMPS did not stop the MAPK activation that NDP-alpha-MSH caused.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    No significant changep42/p44 MAPK activation after PKA inhibitor Rp-cAMPS
    Study

    n: not reported in source

    Stably transfected CHO-K1 cells expressing MC4-R
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    but not by the protein kinase A (PKA) inhibitor Rp-cAMPS
    1 context sentence
    Summary · context
    We demonstrate that the mitogen-activated protein kinases p42 (ERK2) and p44 (ERK1) are also activated by MC4-R following treatment with the MC4-R agonist NDP-alpha-MSH in stably transfected CHO-K1 cells.

    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.

Publication types

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