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Study · Not a test of the peptide alone · 2000

2 results

Insulin-like growth factor (IGF)-binding protein-related protein-1: an autocrine/paracrine factor that inhibits skeletal myoblast differentiation but permits proliferation in response to IGF.

Haugk KL, Wilson HM, Swisshelm K, Quinn LS

Endocrinology1 Jan 2000Cited by 27 (Europe PMC)

PMID10614628 (opens in a new tab)DOI10.1210/endo.141.1.7235 (opens in a new tab)PepBankPUB-10614628
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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 study2

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone2

In this study, IGF-1 DES (des(1-3)IGF-I) 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 IGF-1 DES (des(1-3)IGF-I).

  1. 01LabNot a test of IGF-1 DES (des(1-3)IGF-I) aloneIn vitro (cells)Mechanism

    In C2 myoblasts, IGFBP-rP1 overexpression reduced differentiation responses to des(1‑3)IGF-I and other IGFs versus control-vector cells.

    In plain wordsIn cells, IGFBP-rP1 overexpression reduced the differentiation response to des(1‑3)IGF-I compared with control-vector cells.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    DecreaseDifferentiation response
    Study

    n: not reported in source

    C2-rP1 and C2-LX skeletal myoblasts
    Comparator
    Control-vector C2-LX myoblasts
    Outcome group
    Muscle injury and repair · Musculoskeletal

    Source sentences

    Summary
    Compared with C2-LX myoblasts, the differentiation responses of C2-rP1 myoblasts to IGF-I, IGF-II, insulin, and des(1-3)IGF-I were significantly reduced (P < 0.05).
    1 context sentence
    Summary · context
    To determine the role of IGFBP-rP1 in myogenesis, IGFBP-rP1 was overexpressed in C2 myoblasts using a retroviral vector.

    In this study, IGF-1 DES (des(1-3)IGF-I) 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 IGF-1 DES (des(1-3)IGF-I).

  2. 02LabNot a test of IGF-1 DES (des(1-3)IGF-I) aloneIn vitro (cells)Mechanism

    In C2 myoblasts, IGFBP-rP1 overexpression did not significantly alter proliferation responses to des(1‑3)IGF-I and other factors versus control-vector cells.

    In plain wordsIn cells, proliferation responses to des(1‑3)IGF-I did not differ significantly between IGFBP-rP1-overexpressing cells and control-vector cells.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    No significant changeProliferation response
    Study

    n: not reported in source

    C2-rP1 and C2-LX skeletal myoblasts
    Comparator
    Control-vector C2-LX myoblasts
    Outcome group
    Muscle injury and repair · Musculoskeletal

    Source sentences

    Summary
    However, proliferation responses of C2-rP1 and C2-LX myoblasts to these same factors were not significantly different.
    2 context sentences
    Summary · context
    Compared with C2-LX myoblasts, the differentiation responses of C2-rP1 myoblasts to IGF-I, IGF-II, insulin, and des(1-3)IGF-I were significantly reduced (P < 0.05).
    Summary · context
    To determine the role of IGFBP-rP1 in myogenesis, IGFBP-rP1 was overexpressed in C2 myoblasts using a retroviral vector.

    In this study, IGF-1 DES (des(1-3)IGF-I) 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 IGF-1 DES (des(1-3)IGF-I).

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 3Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 2

    21 Oct 2026, 13:52 UTC

    Study data updated · source update from Europe PMC

  3. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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