The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
Protein kinase B (PKB/Akt) activity is elevated in glioblastoma cells due to mutation of the tumor suppressor PTEN/MMAC
Open accessAbstract
Glioblastomas are highly malignant tumors of the central nervous system that are resistant to radiation and chemotherapy [1]. We explored the role of the phosphatidylinositol (PI) 3-kinase signal transduction pathway in glioblastomas, as this pathway has been shown to inhibit apoptosis induced by cytokine withdrawal and the detachment of cells from the extracellular matrix [2]. Components of this pathway have been implicated in tumor development [3-6]. We show that glioblastoma cells, in contrast to primary human astrocytes, contain high endogenous protein kinase B (PKB/Akt) activity and high levels of PI 3,4,5-triphosphate (PI(3,4,5)P3) and PI(3,4)P2, the lipid products of PI 3-kinase. These glioblastoma cells express mutant forms of the putative 3' phospholipid phosphatase PTEN, also known as MMAC. Expression of wild-type PTEN derived from primary astrocytes, but not of mutant forms of PTEN, reduced the levels of 3' phosphoinositides and inhibited PKB/Akt activity. PTEN antagonized the activation of PKB/Akt by growth factors, by activated PI 3-kinase and by PI-dependent protein kinase-1 (PDK1), but did not antagonize the phospholipid-independent activation of PKB/Akt lacking the pleckstrin homology (PH) domain. These results suggest a role for PTEN in regulating the activity of the PI 3-kinase pathway in malignant human cells.
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Phosphatidylinositol-3-OH kinase direct target of Ras
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PI3K: Downstream AKTion Blocks Apoptosis
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Mechanisms and consequences of activation of protein kinase B/Akt
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Dual Role of Phosphatidylinositol-3,4,5-trisphosphate in the Activation of Protein Kinase B
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Self-citationMolecular alterations of the AKT 2 oncogene in ovarian and breast carcinomas
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Cited by
DeBerardinis, R. J., Mancuso, A., Daikhin, E., Nissim, I., Yudkoff, M., Wehrli, S., & Thompson, C. B. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0709747104 · Cited by 2,622
The PI3K‒PDK1 connection: more than just a road to PKB
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Synthesis and Function of 3-Phosphorylated Inositol Lipids
Vanhaesebroeck, B., Leevers, S. J., Ahmadi, K., Timms, J., Katso, R., Driscoll, P. C., Woscholski, R., Parker, P. J., & Waterfield, M. D. (2001) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.70.1.535 · Cited by 1,535
Ten years of protein kinase B signalling: a hard Akt to follow
Brazil, D. P., & Hemmings, B. A. (2001) · Trends in Biochemical Sciences · doi:10.1016/s0968-0004(01)01958-2 · Cited by 1,177
Regulation of PTEN Transcription by p53
Stambolic, V., MacPherson, D., Sas, D., Lin, Y., Snow, B., Jang, Y., Benchimol, S., & Mak, T. W. (2001) · Molecular Cell · doi:10.1016/s1097-2765(01)00323-9 · Cited by 912
Metadata
- Authors
- Haas-Kogan, D., Shalev, N., Wong, M., Mills, G., Yount, G., & Stokoe, D.
- Venue
- Current Biology
- Publisher
- Elsevier BV
- Published
- 1998-10
- Volume
- 8
- Issue
- 21
- Pages
- 1195-S1
- ISSN
- 0960-9822 (ISSN-L)
- OpenAlex
- W2029219396
- Cited by
- 477
- References
- 19
- FWCI
- 14.18
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Protein kinase B (PKB/Akt) activity is elevated in glioblastoma cells due to mutation of the tumor suppressor PTEN/MMAC. https://app.cochat.ai/papers/10.1016/s0960-9822(07)00493-9
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- Haas-Kogan, D., Shalev, N., Wong, M., Mills, G., Yount, G., & Stokoe, D. (1998). Protein kinase B (PKB/Akt) activity is elevated in glioblastoma cells due to mutation of the tumor suppressor PTEN/MMAC. Current Biology. https://doi.org/10.1016/s0960-9822(07)00493-9
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
