Skip to content

Study · In vitro (cells) · 2006

7 results

Melanocortin-4 receptor-mediated inhibition of apoptosis in immortalized hypothalamic neurons via mitogen-activated protein kinase.

Chai B, Li JY, Zhang W, Newman E, Ammori J, Mulholland MW

Peptides27 Jun 2006Cited by 70 (Europe PMC)

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 study7

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

  1. 01LabIn vitro (cells)Activity measurement

    In GT1-1 cells, NDP-MSH showed specific binding and stimulated cAMP production, implying functional melanocortin receptor expression.

    In plain wordsIn cells, NDP-MSH bound specifically and raised cAMP, which suggests working melanocortin receptors.

    Outcome
    IncreaseNDP-MSH binding and cAMP production
    Study

    n: not reported in source

    GT1-1 hypothalamic cell line
    Outcome group
    Receptor activity and mechanism · Pharmacology
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Functional melanocortin receptor expression was implied by specific binding of NDP-MSH and cAMP production.
    1 context sentence
    Summary · context
    In this study, GT1-1 cells were used to study MC4R signaling pathways and to examine the effects of melanocortin receptor agonist NDP-MSH on apoptosis.
  2. 02LabIn vitro (cells)Activity measurement

    In GT1-1 cells, NDP-MSH stimulated GnRH release in a dose-dependent manner.

    In plain wordsIn cells, NDP-MSH increased GnRH release in a dose-dependent way.

    Outcome
    IncreaseGnRH release
    Study

    n: not reported in source

    GT1-1 hypothalamic cell line
    Outcome group
    Sex hormones and fertility · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NDP-MSH-stimulated GnRH release in a dose-dependent manner.
    1 context sentence
    Summary · context
    In this study, GT1-1 cells were used to study MC4R signaling pathways and to examine the effects of melanocortin receptor agonist NDP-MSH on apoptosis.
  3. 03LabIn vitro (cells)Efficacy outcome

    In GT1-1 cells with serum deprivation-induced apoptosis, NDP-MSH inhibited the apoptosis.

    In plain wordsIn cells, NDP-MSH reduced cell death caused by serum deprivation.

    Outcome
    DecreaseSerum deprivation-induced apoptosis
    Study

    n: not reported in source

    GT1-1 hypothalamic cell line
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Serum deprivation-induced apoptosis in GT1-1 cells, and the NDP-MSH inhibited this effect.
    1 context sentence
    Summary · context
    In this study, GT1-1 cells were used to study MC4R signaling pathways and to examine the effects of melanocortin receptor agonist NDP-MSH on apoptosis.
  4. 04LabIn vitro (cells)Mechanism

    In GT1-1 cells, NDP-MSH stimulated ERK1/2 phosphorylation in a dose-dependent manner.

    In plain wordsIn cells, NDP-MSH increased ERK1/2 phosphorylation in a dose-dependent way.

    Outcome
    IncreaseERK1/2 phosphorylation
    Study

    n: not reported in source

    GT1-1 hypothalamic cell line
    Outcome group
    Receptor activity and mechanism · Pharmacology
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NDP-MSH-stimulated ERK1/2 phosphorylation in a dose-dependent manner.
    1 context sentence
    Summary · context
    In this study, GT1-1 cells were used to study MC4R signaling pathways and to examine the effects of melanocortin receptor agonist NDP-MSH on apoptosis.

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

    In GT1-1 cells, the antagonist SHU9119 blocked the antiapoptotic action of NDP-MSH.

    In plain wordsIn cells, the blocker SHU9119 stopped the anti-cell-death action of NDP-MSH.

    Outcome
    DecreaseAntiapoptotic effect of NDP-MSH with SHU9119
    Study

    n: not reported in source

    GT1-1 hypothalamic cell line
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    The melanocortin receptor antagonist SHU9119 blocked the antiapoptotic actions of NDP-MSH
    1 context sentence
    Summary · context
    In this study, GT1-1 cells were used to study MC4R signaling pathways and to examine the effects of melanocortin receptor agonist NDP-MSH on apoptosis.

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

    In GT1-1 cells, the MAP kinase inhibitor PD98059 significantly attenuated the antiapoptotic effect of NDP-MSH.

    In plain wordsIn cells, the MAP kinase blocker PD98059 reduced the anti-cell-death effect of NDP-MSH.

    Outcome
    DecreaseAntiapoptotic effect of NDP-MSH with PD98059
    Study

    n: not reported in source

    GT1-1 hypothalamic cell line
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    and the MAP kinase inhibitor PD98059 significantly attenuated the antiapoptotic effect.
    2 context sentences
    Summary · context
    Serum deprivation-induced apoptosis in GT1-1 cells, and the NDP-MSH inhibited this effect.
    Summary · context
    In this study, GT1-1 cells were used to study MC4R signaling pathways and to examine the effects of melanocortin receptor agonist NDP-MSH on apoptosis.

    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. 07LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Mechanism

    In GT1-1 cells, SHU9119 abolished NDP-MSH-stimulated ERK1/2 phosphorylation.

    In plain wordsIn cells, SHU9119 removed the ERK1/2 phosphorylation caused by NDP-MSH.

    Outcome
    DecreaseNDP-MSH-induced ERK1/2 phosphorylation with SHU9119
    Study

    n: not reported in source

    GT1-1 hypothalamic cell line
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    ERK1/2 phosphorylation could be abolished by SHU9119.
    2 context sentences
    Summary · context
    NDP-MSH-stimulated ERK1/2 phosphorylation in a dose-dependent manner.
    Summary · context
    In this study, GT1-1 cells were used to study MC4R signaling pathways and to examine the effects of melanocortin receptor agonist NDP-MSH on apoptosis.

    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.

PepBank is a research reference. Talk to a doctor before you use any peptide.