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Study · In vitro (cells) · 2018

3 results

The structure-function relationships of insulin-like growth factor 1 Ec in C2C12 cells.

Yi Q, Feng J, He L, Wan R, Zeng H, Yang L, Wu S, Tang L

Cell adhesion & migration12 May 2017Cited by 8 (Europe PMC)

PMID28471324 (opens in a new tab)PMCIDPMC5810762 (opens in a new tab)DOI10.1080/19336918.2017.1318240 (opens in a new tab)PepBankPUB-28471324
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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 study3

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

  1. 01LabIn vitro (cells)Mechanism

    In C2C12 muscle cells, the C-terminal sequence of IGF1Ec, which is identical to MGF E, promoted differentiation.

    In plain wordsIn muscle cells in a dish, the MGF E sequence helped the cells to mature.

    Peptide
    MGF / PEG-MGF
    Outcome
    IncreaseC2C12 differentiation with MGF E
    Study

    n: not reported in source

    C2C12 muscle cells
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    the C-terminal sequence of IGF1Ec, which is identical to MGF E, promotes differentiation and migration of C2C12 cells.
    1 context sentence
    Summary · context
    In this study, we systematically investigated physiologic responses of C2C12 muscle cells to IGF1Ec, IGF1 and MGF E peptide.
  2. 02LabIn vitro (cells)Mechanism

    In C2C12 muscle cells, the C-terminal sequence of IGF1Ec, which is identical to MGF E, promoted migration.

    In plain wordsIn muscle cells in a dish, the MGF E sequence helped the cells to move.

    Peptide
    MGF / PEG-MGF
    Outcome
    IncreaseC2C12 migration with MGF E
    Study

    n: not reported in source

    C2C12 muscle cells
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    the C-terminal sequence of IGF1Ec, which is identical to MGF E, promotes differentiation and migration of C2C12 cells.
    1 context sentence
    Summary · context
    In this study, we systematically investigated physiologic responses of C2C12 muscle cells to IGF1Ec, IGF1 and MGF E peptide.

Studies that did not test the peptide alone1

In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.

  1. 03LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism

    In C2C12 muscle cells, the N-terminal sequence of IGF1Ec, which is homolog in part with IGF1, promoted proliferation.

    In plain wordsIn muscle cells in a dish, the IGF1-like part of IGF1Ec helped the cells to multiply.

    Peptide
    MGF / PEG-MGF
    Outcome
    IncreaseC2C12 proliferation with IGF1Ec N-terminal sequence
    Study

    n: not reported in source

    C2C12 muscle cells
    Outcome group
    Muscle injury and repair · Musculoskeletal

    Source sentences

    Summary
    the N-terminal sequence of IGF1Ec, which is homolog in part with IGF1, promotes proliferation
    1 context sentence
    Summary · context
    In this study, we systematically investigated physiologic responses of C2C12 muscle cells to IGF1Ec, IGF1 and MGF E peptide.

    In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.

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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