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Study · In vitro (cells) · 2004

4 results

Humanin, a newly identified neuroprotective factor, uses the G protein-coupled formylpeptide receptor-like-1 as a functional receptor.

Ying G, Iribarren P, Zhou Y, Gong W, Zhang N, Yu ZX, Le Y, Cui Y, Wang JM

Journal of immunology (Baltimore, Md. : 1950)1 Jun 2004Cited by 170 (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 study4

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

  1. 01LabIn vitro (cells)Activity measurement

    In cell tests, synthetic humanin induced chemotaxis of mononuclear phagocytes through human FPRL1 and its murine counterpart FPR2.

    In plain wordsIn cells, humanin made immune cells called mononuclear phagocytes move toward it by using the FPRL1 receptor.

    Peptide
    Humanin
    Outcome
    IncreaseChemotaxis of mononuclear phagocytes
    Study

    n: not reported in source

    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    found that Humanin induced chemotaxis of mononuclear phagocytes by using a human G protein-coupled formylpeptide receptor-like-1 (FPRL1) and its murine counterpart FPR2.
  2. 02LabIn vitro (cells)Efficacy outcome

    In cell tests, humanin reduced aggregation and fibrillary formation by suppressing the effect of Abeta42 on mononuclear phagocytes.

    In plain wordsIn cells, humanin reduced clumping and fibre formation linked to the Alzheimer's peptide Abeta42.

    Peptide
    Humanin
    Outcome
    DecreaseAbeta42-induced aggregation and fibrillary formation
    Study

    n: not reported in source

    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Humanin reduced the aggregation and fibrillary formation by suppressing the effect of Abeta(42) on mononuclear phagocytes.
  3. 03LabIn vitro (cells)Mechanism

    In neuroblast cells, humanin activated FPRL1.

    In plain wordsIn nerve-type cells, humanin switched on the FPRL1 receptor.

    Peptide
    Humanin
    Outcome
    IncreaseFPRL1 activation in neuroblast cells
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In neuroblast cells, Humanin and Abeta(42) both activated FPRL1
  4. 04LabIn vitro (cells)Efficacy outcome

    In neuroblast cells, humanin blocked the cytopathic effect of Abeta42, which caused apoptotic death of the cells.

    In plain wordsIn nerve-type cells, humanin blocked the cell damage and death caused by Abeta42.

    Peptide
    Humanin
    Outcome
    DecreaseAbeta42-induced apoptotic death of neuroblast cells
    Study

    n: not reported in source

    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In neuroblast cells, Humanin and Abeta(42) both activated FPRL1; however, only Abeta(42) caused apoptotic death of the cells, and its cytopathic effect was blocked by 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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