The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Class I PI3K in oncogenic cellular transformation
Open accessAbstract
Class I phosphoinositide 3-kinase (PI3K) is a dimeric enzyme, consisting of a catalytic and a regulatory subunit. The catalytic subunit occurs in four isoforms designated as p110α, p110β, p110γ and p110δ. These isoforms combine with several regulatory subunits; for p110α, β and δ, the standard regulatory subunit is p85, for p110γ, it is p101. PI3Ks play important roles in human cancer. PIK3CA, the gene encoding p110α, is mutated frequently in common cancers, including carcinoma of the breast, prostate, colon and endometrium. Eighty percent of these mutations are represented by one of the three amino-acid substitutions in the helical or kinase domains of the enzyme. The mutant p110α shows a gain of function in enzymatic and signaling activity and is oncogenic in cell culture and in animal model systems. Structural and genetic data suggest that the mutations affect regulatory inter- and intramolecular interactions and support the conclusion that there are at least two molecular mechanisms for the gain of function in p110α. One of these mechanisms operates largely independently of binding to p85, the other abolishes the requirement for an interaction with Ras. The non-α isoforms of p110 do not show cancer-specific mutations. However, they are often differentially expressed in cancer and, in contrast to p110α, wild-type non-α isoforms of p110 are oncogenic when overexpressed in cell culture. The isoforms of p110 have become promising drug targets. Isoform-selective inhibitors have been identified. Inhibitors that target exclusively the cancer-specific mutants of p110α constitute an important goal and challenge for current drug development.
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Cited by
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Metadata
- Authors
- Zhao, L., & Vogt, P. K.
- Venue
- Oncogene
- Published
- 2008-09-15
- Volume
- 27
- Issue
- 41
- Pages
- 5486-5496
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2030899725
- Cited by
- 594
- References
- 11
- FWCI
- 15.88
- Type
- journal article
- Language
- en
- Open access
- green
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