IGFBP7 Binds to the IGF-1 Receptor and Blocks Its Activation by Insulin-Like Growth Factors
Abstract
By inactivating the insulin-like growth factor receptor, IGFBP7 suppresses growth and promotes cell death.
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IGFBP7 interacts with the extracellular domain of IGF1R in the absence of IGF1/2, resulting in inhibition of the IRS1-PI3K-AKT signaling cascade and consequently maintaining normal activity of p21 and p27 within the nucleoplasm by avoiding their cytoplasmic retention mediated by AKT-triggered phosphorylation.
“IGFBP7 interacts with the extracellular domain of IGF1R in the absence of IGF1/2, resulting in the inhibition of the IRS1-PI3K-AKT signaling cascade [20] and consequently maintaining the normal activity of p21 and p27 within the nucleoplasm by avoiding their cytoplasmic retention mediated by AKT-triggered phosphorylation [21].”
From Ensemble of Time-Evolving SASP Gene Sets Identifies IGFBP7 and CDKN1A as a Potential Marker Pair for Senescent Fibroblast Subpopulations Across Tissues (2026) · cites this paper as [20]
Cites
Wajapeyee, N., Serra, R. W., Zhu, X., Mahalingam, M., & Green, M. R. (2008) · Cell · doi:10.1016/j.cell.2007.12.032 · Cited by 903 · see citing works
She, Q.-B., Halilovic, E., Ye, Q., Zhen, W., Shirasawa, S., Sasazuki, T., Solit, D. B., & Rosen, N. (2010) · Cancer Cell · doi:10.1016/j.ccr.2010.05.023 · Cited by 400 · see citing works
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Lindbohm, J. V., Mars, N., Walker, K. A., Singh‐Manoux, A., Livingston, G., Brunner, E. J., Sipilä, P. N., Saksela, K., Ferrie, J. E., Lovering, R. C., et al. (2022) · Alzheimer's & Dementia · doi:10.1002/alz.12419 · Cited by 70 · see citing works
Cutano, V., Di Giorgio, E., Minisini, M., Picco, R., Dalla, E., & Brancolini, C. (2019) · Molecular Oncology · doi:10.1002/1878-0261.12503 · Cited by 44 · see citing works
Fitzgerald, G. S., Chuchta, T. G., & McNay, E. C. (2023) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14160 · Cited by 22 · see citing works
Kim, H., Kummerfeld, E., Niedernhofer, L. J., Aliferis, C., Robbins, P. D., & Wang, J. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27073012 · Cited by 1 · see citing works
“IGFBP7 interacts with the extracellular domain of IGF1R in the absence of IGF1/2, resulting in the inhibition of the IRS1-PI3K-AKT signaling cascade [20] and consequently maintaining the normal activity of p21 and p27 within the nucleoplasm by avoiding their cytoplasmic retention mediated by…”
- Authors
- Evdokimova, V., Tognon, C. E., Benatar, T., Yang, W., Krutikov, K., Pollak, M., Sorensen, P. H. B., & Seth, A.
- Affiliations
- University of Toronto (CA)
- BC Cancer Agency (CA)
- Biological Sciences Platform, Sunnybrook Research Institute and Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario M4N 3M5, Canada.
- Departments of Medicine and Oncology, McGill University and Jewish General Hospital, Montreal, Quebec H3T 1E2, Canada.
- Corresponding author
- Seth, Arun
- Venue
- Science Signaling
- Published
- 2012-12-18
- Volume
- 5
- Issue
- 255
- Pages
- ra92-ra92
- ISSN
- 1937-9145 (ISSN-L)
- 1945-0877
- OpenAlex
- W2035846842
- Cited by
- 176
- References
- 2
- Citations by year
- 2026: 17 · 2025: 14 · 2024: 18 · 2023: 13 · 2022: 13 · 2021: 17 · 2020: 13 · 2019: 14 · 2018: 10 · 2017: 7 · 2016: 9 · 2015: 11 · 2014: 14 · 2013: 6
- FWCI
- 7.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science Signaling (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research (97996_1, MOP119599)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- IGFBP7, IGF-1 receptor, insulin-like growth factor I, insulin-like growth factor II, receptor internalization, PI3K/Akt signaling, 4E-BP1, protein synthesis inhibition, apoptosis, breast cancer, tumor suppression, receptor binding
- MeSH terms
- Animals, Breast Neoplasms, Carrier Proteins, Cell Survival, Female, Humans, Insulin-Like Growth Factor I, Insulin-Like Growth Factor II, Neoplasm Proteins, Phosphoproteins, Protein Binding, Protein Biosynthesis, Signal Transduction, Mice, SCID, Mice, Inbred NOD, Apoptosis, Receptor, IGF Type 1, Mice, Knockout, Cell Cycle Proteins, Insulin-Like Growth Factor Binding Proteins, Eukaryotic Initiation Factors, Cell Line, Tumor, Adaptor Proteins, Signal Transducing, Mice
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