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Study · Not a test of the peptide alone · 2001

2 results

Effect of IGFBP-3 on IGF- and IGF-analogue-induced insulin-like growth factor-I receptor (IGFIR) signalling.

Devi GR, Graham DL, Oh Y, Rosenfeld RG

Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society1 Aug 2001Cited by 7 (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 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 receptor-signalling assays, IGFBP-3 dose-dependently inhibited Des(1‑3)IGF-I-induced IGFIR phosphorylation at concentrations similar to those inhibiting other IGFs.

    In plain wordsIn cells, IGFBP-3 reduced Des(1‑3)IGF-I-induced receptor phosphorylation compared with stimulation alone.

    Outcome
    DecreaseIGFIR phosphorylation inhibition by IGFBP-3
    Study

    n: not reported in source

    Comparator
    Des(1-3)IGF-I stimulation without IGFBP-3
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    IGFBP-3 inhibited IGF-I-, IGF-II-, Des(1-3)IGF-I- and Long(R3)IGF-I-induced IGFIR phosphorylation in a dose-dependent manner at similar concentration range but not QAYL-induced IGFIR-P.
    1 context sentence
    Summary · context
    In the present study, we examined the effects of IGFBP-3 and its proteolytic fragments on the initial events of the IGFIR signalling pathway.

    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 receptor-signalling assays, the (1-97)IGFBP-3 fragment did not inhibit Des(1‑3)IGF-I-induced IGFIR phosphorylation, inhibiting only the IGF-I response.

    In plain wordsIn cells, the IGFBP-3 fragment did not reduce Des(1‑3)IGF-I-induced receptor phosphorylation compared with stimulation alone.

    Outcome
    No significant changeIGFIR phosphorylation response to IGFBP-3 fragment
    Study

    n: not reported in source

    Comparator
    Des(1-3)IGF-I stimulation without fragment
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    The((1-97))IGFBP-3 fragment was able to inhibit only IGF-I-induced IGFIR-P.
    2 context sentences
    Summary · context
    IGFBP-3 inhibited IGF-I-, IGF-II-, Des(1-3)IGF-I- and Long(R3)IGF-I-induced IGFIR phosphorylation in a dose-dependent manner at similar concentration range but not QAYL-induced IGFIR-P.
    Summary · context
    In the present study, we examined the effects of IGFBP-3 and its proteolytic fragments on the initial events of the IGFIR signalling pathway.

    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 4Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Versions 2 to 3

    21 Oct 2026, 13:52 UTC

    The same notice was added 2 times, first on 21 Oct 2026, 12:50 UTC. The status did not change between them.

    Study data updated · source update from Europe PMC

  3. 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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