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Study · In vitro (cell-free) · 2009

5 results

Humanin inhibits neuronal cell death by interacting with a cytokine receptor complex or complexes involving CNTF receptor alpha/WSX-1/gp130.

Hashimoto Y, Kurita M, Aiso S, Nishimoto I, Matsuoka M

Molecular biology of the cell22 Apr 2009Cited by 169 (Europe PMC)

PMID19386761 (opens in a new tab)DOI10.1091/mbc.e09-02-0168 (opens in a new tab)PepBankPUB-19386761
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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 study5

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

  1. 01LabIn vitro (cell-free)Mechanism

    In an in vitro-reconstituted binding assay, HN, but not a control peptide, induced hetero-oligomerization of CNTFR, WSX-1 and gp130.

    In plain wordsIn lab tests, humanin, but not a control peptide, pulled the CNTFR, WSX-1 and gp130 receptor parts together.

    Peptide
    Humanin
    Outcome
    IncreaseHetero-oligomerization of CNTFR, WSX-1 and gp130
    Study

    n: not reported in source

    In vitro-reconstituted binding assay
    Comparator
    Control peptide
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro-reconstituted binding assays showed that HN, but not the other control peptide, induced the hetero-oligomerization of CNTFR, WSX-1, and gp130.

Studies that did not test the peptide alone4

In this study, Humanin 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 Humanin.

  1. 02LabNot a test of Humanin aloneIn vitro (cells)Mechanism

    Loss-of-function tests indicated that gp130, the common subunit of IL-6 family receptors, was essential for HN-induced neuroprotection.

    In plain wordsIn cells, tests that removed gp130 showed that humanin's protection of nerve cells needs gp130.

    Peptide
    Humanin
    Outcome
    Not applicablegp130 requirement for HN-induced neuroprotection
    Study

    n: not reported in source

    Neuronal cells
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition

    Source sentences

    Summary
    In this study, a series of loss-of-function tests indicated that gp130, the common subunit of receptors belonging to the IL-6 receptor family, was essential for HN-induced neuroprotection.

    In this study, Humanin 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 Humanin.

  2. 03LabNot a test of Humanin aloneIn vitro (cells)Mechanism

    Overexpression of CNTFR and/or WSX-1, but not of other tested gp130-related subunits, up-regulated HN binding to neuronal cells.

    In plain wordsIn cells, adding more CNTFR or WSX-1 receptors increased humanin binding to nerve cells.

    Peptide
    Humanin
    Outcome
    IncreaseHN binding after CNTFR or WSX-1 overexpression
    Study

    n: not reported in source

    Neuronal cells
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition

    Source sentences

    Summary
    Overexpression of ciliary neurotrophic factor receptor alpha (CNTFR) and/or the IL-27 receptor subunit, WSX-1, but not that of any other tested gp130-related receptor subunit, up-regulated HN binding to neuronal cells

    In this study, Humanin 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 Humanin.

  3. 04LabNot a test of Humanin aloneIn vitro (cells)Mechanism

    siRNA-mediated knockdown of endogenous CNTFR and/or WSX-1 reduced HN binding to neuronal cells.

    In plain wordsIn cells, removing CNTFR or WSX-1 receptors reduced humanin binding to nerve cells.

    Peptide
    Humanin
    Outcome
    DecreaseHN binding after CNTFR or WSX-1 knockdown
    Study

    n: not reported in source

    Neuronal cells
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition

    Source sentences

    Summary
    whereas siRNA-mediated knockdown of endogenous CNTFR and/or WSX-1 reduced it.

    In this study, Humanin 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 Humanin.

  4. 05LabNot a test of Humanin aloneIn vitro (cells)Mechanism

    Loss of function of CNTFR or WSX-1 in neuronal cells nullified their responsiveness to HN-mediated protection.

    In plain wordsIn cells, nerve cells without CNTFR or WSX-1 no longer responded to humanin's protection.

    Peptide
    Humanin
    Outcome
    DecreaseHN-mediated protection after loss of CNTFR or WSX-1
    Study

    n: not reported in source

    Neuronal cells
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition

    Source sentences

    Summary
    Consistent with these results, loss-of-functions of CNTFR or WSX-1 in neuronal cells nullified their responsiveness to HN-mediated protection.

    In this study, Humanin 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 Humanin.

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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