The DOI matches its Crossref record; 83 of the 83 references it cites were found in a registry or an index.
Phosphatidylinositol 3‐kinase
Abstract
Currently, a central question in biology is how signals from the cell surface modulate intracellular processes. In recent years phosphoinositides have been shown to play a key role in signal transduction. Two phosphoinositide pathways have been characterized, to date. In the canonical phosphoinositide turnover pathway, activation of phosphatidylinositol‐specific phospholipase C results in the hydrolysis of phosphatidylinositol 4,5‐bisphospate and the generation of two second messengers, inositol 1,4,5‐trisphosphate and diacylglycerol. The 3‐phosphoinositide pathway involves protein‐tyrosine kinase‐mediated recruitment and activation of phosphatidylinositol 3‐kinase, resulting in the production of phosphatidylinositol 3,4‐bisphosphate and phosphatidylinositol 3,4,5‐trisphosphate. The 3‐phosphoinositides are not substrates of any known phospholipase C, are not components of the canonical phosphoinositide turnover pathway, and may themselves act as intracellular mediators. The 3‐phosphoinositide pathway has been implicated in growth factor‐dependent mitogenesis, membrane ruffling and glucose uptake. Furthermore the homology of the yeast vps34 with the mammalian phosphatidylinositol 3‐kinase has suggested a role for this pathway in vesicular trafficking. In this review the different mechanisms employed by protein‐tyrosine kinases to activate phosphatidylinositol 3‐kinase, and its involvement in the signaling cascade initiated by tyrosine phosphorylation, are examined.
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Cites
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Self-citationSH2 domains recognize specific phosphopeptide sequences
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Structure of the insulin receptor substrate IRS-1 defines a unique signal transduction protein
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The trk proto-oncogene encodes a receptor for nerve growth factor
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Self-citationPhosphatidylinositol 3′-kinase is activated by association with IRS-1 during insulin stimulation.
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Cited by
A Single Ataxia Telangiectasia Gene with a Product Similar to PI-3 Kinase
Savitsky, K., Bar-Shira, A., Gilad, S., Rotman, G., Ziv, Y., Vanagaite, L., Tagle, D. A., Smith, S., Uziel, T., Sfez, S., et al. (1995) · Science · doi:10.1126/science.7792600 · Cited by 2,785
Hunter, T. (2000) · Cell · doi:10.1016/s0092-8674(00)81688-8 · Cited by 2,586
The IL-4 receptor: signaling mechanisms and biologic functions
Nelms, K., Keegan, A. D., Zamorano, J., Ryan, J. J., & Paul, W. E. (1999) · Annual Review of Immunology · doi:10.1146/annurev.immunol.17.1.701 · Cited by 1,545
PIK3CA is implicated as an oncogene in ovarian cancer
Shayesteh, L., Lu, Y., Kuo, W.-L., Baldocchi, R., Godfrey, T., Collins, C., Pinkel, D., Powell, B., Mills, G. B., & Gray, J. W. (1999) · Nature Genetics · doi:10.1038/5042 · Cited by 1,155
The PI 3-kinase/Akt signaling pathway delivers an anti-apoptotic signal.
Kennedy, S. G., Wagner, A. J., Conzen, S. D., Jordán, J., Bellacosa, A., Tsichlis, P. N., & Hay, N. (1997) · Genes & Development · doi:10.1101/gad.11.6.701 · Cited by 1,074
Metadata
- Authors
- Kapeller, R., & Cantley, L. C.
- Venue
- BioEssays
- Publisher
- Wiley
- Published
- 1994-08
- Volume
- 16
- Issue
- 8
- Pages
- 565-576
- ISSN
- 0265-9247 (ISSN-L)
- 1521-1878
- OpenAlex
- W2156475226
- Cited by
- 638
- References
- 83
- FWCI
- 7.07
- Type
- journal article
- Language
- en
- Open access
- closed
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