The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Cross-talk between the insulin and angiotensin signaling systems.
Open accessAbstract
Angiotensin II (AII), acting via its G-protein linked receptor, is an important regulator of cardiac, vascular, and renal function. Following injection of AII into rats, we find that there is also a rapid tyrosine phosphorylation of the major insulin receptor substrates 1 and 2 (IRS-1 and IRS-2) in the heart. This phenomenon appears to involve JAK2 tyrosine kinase, which associates with the AT1 receptor and IRS-1/IRS-2 after AII stimulation. AII-induced phosphorylation leads to binding of phosphatidylinositol 3-kinase (PI 3-kinase) to IRS-1 and IRS-2; however, in contrast to other ligands, AII injection results in an acute inhibition of both basal and insulin-stimulated PI 3-kinase activity. The latter occurs without any reduction in insulin receptor or IRS phosphorylation or in the interaction of the p85 and p110 subunits of PI 3-kinase with each other or with IRS-1/IRS-2. These effects of AII are inhibited by AT1 receptor antagonists. Thus, there is direct cross-talk between insulin and AII signaling pathways at the level of both tyrosine phosphorylation and PI 3-kinase activation. These interactions may play an important role in the association of insulin resistance, hypertension, and cardiovascular disease.
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Cites
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Self-citationIdentification of JAK2 as a growth hormone receptor-associated tyrosine kinase
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Role of IRS-2 in insulin and cytokine signalling
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Direct stimulation of Jak/STAT pathway by the angiotensin II AT1 receptor
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PDGF- and insulin-dependent pp70S6k activation mediated by phosphatidylinositol-3-OH kinase
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Cited by
The JAK/STAT signaling pathway: from bench to clinic
Hu, X., li, J., Fu, M., Zhao, X., & Wang, W. (2021) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-021-00791-1 · Cited by 2,633
Diabetes and Vascular Disease: Pathophysiology, Clinical Consequences, and Medical Therapy: Part I
Creager, M. A., Lüscher, T. F., of, P. W. T. A., Cosentino, F., & Beckman, J. A. (2003) · Circulation · doi:10.1161/01.cir.0000091257.27563.32 · Cited by 1,650
Kim, J.-A., Montagnani, M., Koh, K. K., & Quon, M. J. (2006) · Circulation · doi:10.1161/circulationaha.105.563213 · Cited by 1,652
Phosphoinositide 3-kinase: the key switch mechanism in insulin signalling
SHEPHERD, P. R., WITHERS, D. J., & SIDDLE, K. (1998) · Biochemical Journal · doi:10.1042/bj3330471 · Cited by 953
Cross-talk between Epidermal Growth Factor Receptor and c-Met Signal Pathways in Transformed Cells*
Jo, M., Stolz, D. B., Esplen, J. E., Dorko, K., Michalopoulos, G. K., & Strom, S. C. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.275.12.8806 · Cited by 347
Metadata
- Authors
- Velloso, L. A., Folli, F., Sun, X. J., White, M. F., Saad, M. J., & Kahn, C. R.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1996-10-29
- Volume
- 93
- Issue
- 22
- Pages
- 12490-12495
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2030338284
- Cited by
- 403
- References
- 42
- FWCI
- 10.70
- Type
- journal article
- Language
- en
- Open access
- green
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- Velloso, L. A., Folli, F., Sun, X. J., White, M. F., Saad, M. J., & Kahn, C. R. (1996). Cross-talk between the insulin and angiotensin signaling systems. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.93.22.12490
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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