Signalling by insulin and IGF receptors: supporting acts and new players
Open accessAbstract
The signalling pathways utilised by insulin receptor (IR) and IGF receptor to transduce their diverse effects on cellular metabolism, growth and survival are well established in broad outline, but many details remain to be elucidated. Tyrosine phosphorylation of IR substrates and Shc initiates signalling via canonical phosphoinositide 3-kinase/Akt and Ras/MAP kinase pathways, which together mediate many of the actions of insulin and IGFs. However, a variety of additional substrates and scaffolds have been described that may play roles in modulating the canonical pathways or in specific biological responses. This review will focus on recent studies that have extended our understanding of insulin/IGF signalling pathways, and the elements that may contribute to specificity.
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Cross-talk between the Wnt and insulin signaling pathways has been demonstrated in different disorders such as diabetes and cancer.
“Cross-talk between the Wnt and insulin signaling pathways has been demonstrated in different disorders such as diabetes and cancer49-53.”
From Altered proliferation and networks in neural cells derived from idiopathic autistic individuals (2017) · cites this paper as [53]
IGF-1 has been shown to stimulate the β-catenin pathway through signaling cascades involving the activation of phosphatidylinositol 3-kinase (PI 3-K)/Akt and the inhibition of glycogen synthase kinase-3 (GSK-3).
“IGF-1 has been shown to stimulate the β-catenin pathway through signaling cascades involving the activation of phosphatidylinositol 3-kinase (PI 3-K)/Akt and the inhibition of glycogen synthase kinase-3 (GSK-3)53.”
From Altered proliferation and networks in neural cells derived from idiopathic autistic individuals (2017) · cites this paper as [53]
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Mechanisms of Insulin Action and Insulin Resistance
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- Authors
- Siddle, K.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Siddle, Kenneth
- Venue
- Journal of Molecular Endocrinology
- Publisher
- Bioscientifica
- Published
- 2011-04-15
- Volume
- 47
- Issue
- 1
- Pages
- R1-R10
- ISSN
- 0952-5041 (ISSN-L)
- 1479-6813
- OpenAlex
- W2137521058
- Cited by
- 456
- References
- 135
- Citations by year
- 2026: 9 · 2025: 9 · 2024: 17 · 2023: 31 · 2022: 35 · 2021: 31 · 2020: 38 · 2019: 27 · 2018: 43 · 2017: 46 · 2016: 36 · 2015: 40 · 2014: 38 · 2013: 30 · 2012: 21
- FWCI
- 4.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Molecular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Diabetes UK
- Biotechnology and Biological Sciences Research Council (BB/F-15364/1)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- insulin receptor, IGF receptors, insulin signaling, IGF signalling, tyrosine phosphorylation, Shc, phosphoinositide 3-kinase/Akt pathway, RAS/MAPK pathway, cellular metabolism, cell growth and survival
- MeSH terms
- Animals, Glucose, Humans, Insulin, Phosphorylation, Protein Conformation, Receptor, Insulin, Signal Transduction, Proto-Oncogene Proteins p21(ras), Receptors, Somatomedin, Phosphatidylinositol 3-Kinases, Mitogen-Activated Protein Kinases, Protein Transport, Intracellular Signaling Peptides and Proteins, Proto-Oncogene Proteins c-akt
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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