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Study · Not a test of the peptide alone · 2002

3 results

Insulin-like growth factor-binding protein-3 activates a phosphotyrosine phosphatase. Effects on the insulin-like growth factor signaling pathway.

Ricort JM, Binoux M

The Journal of biological chemistry8 Apr 2002Cited by 47 (Europe PMC)

PMID11940579 (opens in a new tab)DOI10.1074/jbc.m200439200 (opens in a new tab)PepBankPUB-11940579
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Summary

The proliferative action of insulin-like growth factors (IGF-I and -II) is mediated via the type I IGF receptor (IGF-IR) and is modulated by their association with high affinity binding proteins, IGFBP-1 to -6. We recently found that, in addition to its ability to bind IGFs, IGFBP-3 also inhibits IGF-IR activation independently of IGF binding and without interacting directly with IGF-IR. Here, we show that IGFBP-3 is capable of blocking the signal triggered by IGFs. Breast carcinoma-derived cells (MCF-7) were stimulated by des(1-3)IGF-I or [Gln(3),Ala(4),Tyr(15),Leu(16)]IGF-I, two IGF analogues with intact affinity for IGF-IR, but with weak or virtually no affinity for IGFBPs, then incubated with IGFBP-3. The activated IGF-IR was desensitized through reversal of its autophosphorylation, following which both phosphatidylinositol 3-kinase and p42(MAPK) activities were depressed. Direct measurement of phosphotyrosine phosphatase activity and reconstitution experiments using tyrosine-phosphorylated insulin receptor substrate-1 (IRS-1) indicated that IGFBP-3 activated a phosphotyrosine phosphatase (PTPase). This action appeared to be peculiar to IGFBP-3 among the IGFBPs, since neither IGFBP-1 nor IGFBP-5 (structurally the closest to IGFBP-3), had any such effect. Several cell lines derived from normal or tumor cells responsive to IGF-I were used to show that IGFBP-3-stimulated PTPase is cell type-specific. Although the precise nature of the phosphatase remains to be determined, the results of this study demonstrate that IGFBP-3 stimulates a phosphotyrosine phosphatase activity that down-regulates the IGF-I signaling pathway, suggesting a major role for IGFBP-3 in regulating cell proliferation.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

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

Studies that did not test the peptide alone3

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 MCF-7 cells stimulated with IGF analogues including des(1‑3)IGF-I, IGFBP-3 reversed IGF-IR autophosphorylation.

    In plain wordsIn cells stimulated with analogues including des(1‑3)IGF-I, IGF receptor autophosphorylation decreased after IGFBP-3, compared with before IGFBP-3.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    DecreaseIGF-IR autophosphorylation
    Study

    n: not reported in source

    MCF-7 breast carcinoma cells
    Comparator
    IGF analogue stimulation before IGFBP-3
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    The activated IGF-IR was desensitized through reversal of its autophosphorylation, following which both phosphatidylinositol 3-kinase and p42(MAPK) activities were depressed.
    1 context sentence
    Summary · context
    Breast carcinoma-derived cells (MCF-7) were stimulated by des(1-3)IGF-I or [Gln(3),Ala(4),Tyr(15),Leu(16)]IGF-I, two IGF analogues with intact affinity for IGF-IR, but with weak or virtually no affinity for IGFBPs, then incubated with IGFBP-3.

    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 MCF-7 cells stimulated with IGF analogues including des(1‑3)IGF-I, IGFBP-3 depressed phosphatidylinositol 3-kinase activity.

    In plain wordsIn cells stimulated with analogues including des(1‑3)IGF-I, phosphatidylinositol 3-kinase activity decreased after IGFBP-3, compared with before IGFBP-3.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    DecreasePhosphatidylinositol 3-kinase activity
    Study

    n: not reported in source

    MCF-7 breast carcinoma cells
    Comparator
    IGF analogue stimulation before IGFBP-3
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    The activated IGF-IR was desensitized through reversal of its autophosphorylation, following which both phosphatidylinositol 3-kinase and p42(MAPK) activities were depressed.
    1 context sentence
    Summary · context
    Breast carcinoma-derived cells (MCF-7) were stimulated by des(1-3)IGF-I or [Gln(3),Ala(4),Tyr(15),Leu(16)]IGF-I, two IGF analogues with intact affinity for IGF-IR, but with weak or virtually no affinity for IGFBPs, then incubated with IGFBP-3.

    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).

  3. 03LabNot a test of IGF-1 DES (des(1-3)IGF-I) aloneIn vitro (cells)Mechanism

    In MCF-7 cells stimulated with IGF analogues including des(1‑3)IGF-I, IGFBP-3 depressed p42 MAPK activity.

    In plain wordsIn cells stimulated with analogues including des(1‑3)IGF-I, p42 MAPK activity decreased after IGFBP-3, compared with before IGFBP-3.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    Decreasep42 MAPK activity
    Study

    n: not reported in source

    MCF-7 breast carcinoma cells
    Comparator
    IGF analogue stimulation before IGFBP-3
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    The activated IGF-IR was desensitized through reversal of its autophosphorylation, following which both phosphatidylinositol 3-kinase and p42(MAPK) activities were depressed.
    1 context sentence
    Summary · context
    Breast carcinoma-derived cells (MCF-7) were stimulated by des(1-3)IGF-I or [Gln(3),Ala(4),Tyr(15),Leu(16)]IGF-I, two IGF analogues with intact affinity for IGF-IR, but with weak or virtually no affinity for IGFBPs, then incubated with IGFBP-3.

    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

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