The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
AKT/PKB signaling mechanisms in cancer and chemoresistance
Open accessAbstract
During the past decade, Akt (also known as protein kinase B, PKB) has been extensively studied. It regulates a variety of cellular processes by mediating extracellular (mitogenic growth factor, insulin and stress) and intracellular (altered tyrosine receptor kinases, Ras and Src) signals. Activation of Akt by these signals is via its pleckstrin homology (PH) domain binding to products of phosphatidylinositol 3-kinase (PI3K). This process is negatively regulated by a dual phosphatase PTEN tumor suppressor. Today, more than 30 Akt substrates have been identified. These phosphorylation events mediate the effects of Akt on cell survival, growth, differentiation, angiogenesis, migration and metabolism. Further, PI3K/PTEN/Akt pathway is frequently altered in many human malignancies and overexpression of Akt induces malignant transformation and chemoresistance. Thus, the Akt pathway is a major target for anti-cancer drug development. This review focuses on Akt signaling mechanism in oncogenesis and chemoresistance, and ongoing translational efforts to therapeutically target Akt.
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Cites
Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation
Dimmeler, S., Fleming, I., Fisslthaler, B., Hermann, C., Busse, R., & Zeiher, A. M. (1999) · Nature · doi:10.1038/21224 · Cited by 3,591
TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling
Inoki, K., Li, Y., Zhu, T., Wu, J., & Guan, K.-L. (2002) · Nature Cell Biology · doi:10.1038/ncb839 · Cited by 3,083
Rheb GTPase is a direct target of TSC2 GAP activity and regulates mTOR signaling
Inoki, K., Li, Y., Xu, T., & Guan, K.-L. (2003) · Genes & Development · doi:10.1101/gad.1110003 · Cited by 1,911
Laughner, E., Taghavi, P., Chiles, K., Mahon, P. C., & Semenza, G. L. (2001) · Molecular and Cellular Biology · doi:10.1128/mcb.21.12.3995-4004.2001 · Cited by 1,256 · cited 1×
“(140) of HIF1α through regulation of mTOR pathway.”
Basu, S., Totty, N. F., Irwin, M. S., Sudol, M., & Downward, J. (2003) · Molecular Cell · doi:10.1016/s1097-2765(02)00776-1 · Cited by 843
Akt Enhances Mdm2-mediated Ubiquitination and Degradation of p53
Ogawara, Y., Kishishita, S., Obata, T., Isazawa, Y., Suzuki, T., Tanaka, K., Masuyama, N., & Gotoh, Y. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m109745200 · Cited by 617 · cited 5×
“Akt targets several key cell cycle regulators including p21cip1/waf1, p27kip1, and MDM2.”
InfluentialSkorski, T., Bellacosa, A., Nieborowska‐Skorska, M., Majewski, M., Martinez, R., Choi, J. K., Trotta, R., Wlodarski, P., Perrotti, D., Chan, T. O., et al. (1997) · The EMBO Journal · doi:10.1093/emboj/16.20.6151 · Cited by 567
Castro, A. F., Rebhun, J. F., Clark, G. J., & Quilliam, L. A. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.c300226200 · Cited by 381
Mitogenic Activation, Phosphorylation, and Nuclear Translocation of Protein Kinase Bβ
Meier, R., Alessi, D. R., Cron, P., Andjelković, M., & Hemmings, B. A. (1997) · Journal of Biological Chemistry · doi:10.1074/jbc.272.48.30491 · Cited by 378
Cited by
The Different Mechanisms of Cancer Drug Resistance: A Brief Review
Mansoori, B., Mohammadi, A., Davudian, S., Shirjang, S., & Baradaran, B. (2017) · Advanced Pharmaceutical Bulletin · doi:10.15171/apb.2017.041 · Cited by 1,883
The Akt/PKB pathway: molecular target for cancer drug discovery
Cheng, J. Q., Lindsley, C. W., Cheng, G. Z., Yang, H., & Nicosia, S. V. (2005) · Oncogene · doi:10.1038/sj.onc.1209088 · Cited by 498
Li, F., & Sethi, G. (2010) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2010.01.002 · Cited by 398
Contributions of the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways to leukemia
Steelman, L. S., Abrams, S. L., Whelan, J., Bertrand, F. E., Ludwig, D. E., Bäsecke, J., Libra, M., Stivala, F., Milella, M., Tafuri, A., et al. (2008) · Leukemia · doi:10.1038/leu.2008.26 · Cited by 385
Martelli, A. M., Nyåkern, M., Tabellini, G., Bortul, R., Tazzari, P. L., Evangelisti, C., & Cocco, L. (2006) · Leukemia · doi:10.1038/sj.leu.2404245 · Cited by 342
Metadata
- Authors
- Kim, D.
- Venue
- Frontiers in Bioscience
- Publisher
- IMR Press
- Published
- 2005
- Volume
- 10
- Issue
- 1-3
- Pages
- 975
- ISSN
- 1093-4715 (ISSN-L)
- 1093-9946
- DOI
- 10.2741/1592
- OpenAlex
- W2104461354
- Cited by
- 204
- References
- 9
- FWCI
- 6.34
- Type
- journal article
- Language
- en
- Open access
- bronze
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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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