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Study · Not a test of the peptide alone · 2001

5 results

Insulin-like growth factor (IGF) binding protein-3 inhibits type 1 IGF receptor activation independently of its IGF binding affinity.

Ricort JM, Binoux M

Endocrinology1 Jan 2001Cited by 44 (Europe PMC)

PMID11145572 (opens in a new tab)DOI10.1210/endo.142.1.7915 (opens in a new tab)PepBankPUB-11145572
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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 study5

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

Studies that did not test the peptide alone5

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, IGFBP-3 dose-dependently depressed IGF receptor autophosphorylation stimulated by IGF-I or its analogues including des(1‑3)IGF-I.

    In plain wordsIn cells, IGFBP-3 reduced IGF receptor autophosphorylation stimulated by IGF-I or analogues including des(1‑3)IGF-I, compared with stimulation alone.

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

    n: not reported in source

    MCF-7 breast carcinoma cells
    Comparator
    IGF analogue stimulation without IGFBP-3
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Stimulation of autophosphorylation of the receptor and its tyrosine kinase activity was dose-dependently depressed.
    1 context sentence
    Summary · context
    MCF-7 breast carcinoma cells were preincubated with increasing concentrations of IGFBP-3 and then stimulated with IGF-I, des(1-3)IGF-I, or [Q(3)A(4)Y(15)L(16)]-IGF-I, the latter two being IGF-I analogs with intact affinity for the type 1 IGF receptor, but weak or virtually no affinity for IGFBPs.

    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, IGFBP-3 dose-dependently depressed receptor tyrosine kinase activity stimulated by IGF-I or its analogues including des(1‑3)IGF-I.

    In plain wordsIn cells, IGFBP-3 reduced receptor tyrosine kinase activity stimulated by IGF-I or analogues including des(1‑3)IGF-I, compared with stimulation alone.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    DecreaseIGF receptor tyrosine kinase activity
    Study

    n: not reported in source

    MCF-7 breast carcinoma cells
    Comparator
    IGF analogue stimulation without IGFBP-3
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Stimulation of autophosphorylation of the receptor and its tyrosine kinase activity was dose-dependently depressed.
    1 context sentence
    Summary · context
    MCF-7 breast carcinoma cells were preincubated with increasing concentrations of IGFBP-3 and then stimulated with IGF-I, des(1-3)IGF-I, or [Q(3)A(4)Y(15)L(16)]-IGF-I, the latter two being IGF-I analogs with intact affinity for the type 1 IGF receptor, but weak or virtually no affinity for IGFBPs.

    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, IGFBP-3 at 2.5 nM inhibited stimulation induced by 3 nM des(1‑3)IGF-1 by more than 50%.

    In plain wordsIn cells, IGFBP-3 at 2.5 nM inhibited des(1‑3)IGF-1 stimulation by more than 50% compared with stimulation alone.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    DecreaseInhibition of des(1-3)IGF-I stimulation at low IGFBP-3 concentration
    Study

    n: not reported in source

    MCF-7 breast carcinoma cells
    Comparator
    IGF analogue stimulation without IGFBP-3
    Outcome group
    Receptor activity and mechanism · Cancer

    Measurements

    inhibition
    > 50%
    2.5 nM IGFBP-3 with 3 nM des(1-3)IGF-1

    Source sentences

    Summary
    At 2.5 nM, IGFBP-3 provoked more than 50% inhibition of the stimulation induced by 3 nM des(1-3)IGF-1 and, at 10 nM, more than 80% inhibition.
    1 context sentence
    Summary · context
    MCF-7 breast carcinoma cells were preincubated with increasing concentrations of IGFBP-3 and then stimulated with IGF-I, des(1-3)IGF-I, or [Q(3)A(4)Y(15)L(16)]-IGF-I, the latter two being IGF-I analogs with intact affinity for the type 1 IGF receptor, but weak or virtually no affinity for IGFBPs.

    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).

  4. 04LabNot a test of IGF-1 DES (des(1-3)IGF-I) aloneIn vitro (cells)Mechanism

    In MCF-7 cells, IGFBP-3 at 10 nM inhibited des(1‑3)IGF-1-induced stimulation by more than 80%.

    In plain wordsIn cells, IGFBP-3 at 10 nM inhibited des(1‑3)IGF-1 stimulation by more than 80% compared with stimulation alone.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    DecreaseInhibition of des(1-3)IGF-I stimulation at high IGFBP-3 concentration
    Study

    n: not reported in source

    MCF-7 breast carcinoma cells
    Comparator
    IGF analogue stimulation without IGFBP-3
    Outcome group
    Receptor activity and mechanism · Cancer

    Measurements

    inhibition
    > 80%
    10 nM IGFBP-3

    Source sentences

    Summary
    At 2.5 nM, IGFBP-3 provoked more than 50% inhibition of the stimulation induced by 3 nM des(1-3)IGF-1 and, at 10 nM, more than 80% inhibition.
    1 context sentence
    Summary · context
    MCF-7 breast carcinoma cells were preincubated with increasing concentrations of IGFBP-3 and then stimulated with IGF-I, des(1-3)IGF-I, or [Q(3)A(4)Y(15)L(16)]-IGF-I, the latter two being IGF-I analogs with intact affinity for the type 1 IGF receptor, but weak or virtually no affinity for IGFBPs.

    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).

  5. 05LabNot a test of IGF-1 DES (des(1-3)IGF-I) aloneIn vitro (cells)Mechanism

    In MCF-7 cells stimulated with IGF-I or analogues including des(1‑3)IGF-I, IGFBP-1 and IGFBP-5 at 10 nM had no significant effect.

    In plain wordsIn cells stimulated with IGF-I or analogues including des(1‑3)IGF-I, IGFBP-1 and IGFBP-5 did not significantly change receptor stimulation versus stimulation alone.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    No significant changeEffect of IGFBP-1 and IGFBP-5 on IGF receptor stimulation
    Study

    n: not reported in source

    MCF-7 breast carcinoma cells
    Comparator
    IGF receptor stimulation without the binding proteins
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    The inhibition appeared to be specific to IGFBP-3, because IGFBP-1 and IGFBP-5 at 10 nM had no significant effect.
    1 context sentence
    Summary · context
    MCF-7 breast carcinoma cells were preincubated with increasing concentrations of IGFBP-3 and then stimulated with IGF-I, des(1-3)IGF-I, or [Q(3)A(4)Y(15)L(16)]-IGF-I, the latter two being IGF-I analogs with intact affinity for the type 1 IGF receptor, but weak or virtually no affinity for IGFBPs.

    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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