Abstract
AKT, also known as protein kinase B and RAC-PK, was first discovered as an oncogene transduced by the acute transforming retrovirus (AKT-8), which is known to cause leukemia in mice. AKT is the major downstream target of phosphatidylinositol 3-kinase (PI3K), which can be activated by receptor tyrosine kinases in response to various growth factors. AKT is a serine/threonine kinase located at the apex of a cascade of signaling pathways. Deregulated AKT signaling is implicated in cancer cell growth, proliferation, and survival. Novel antitumor strategies have now been developed to target AKTand key downstream targets in the clinic.
Original language | English (US) |
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Title of host publication | Cancer Therapeutic Targets |
Publisher | Springer New York |
Pages | 3-12 |
Number of pages | 10 |
Volume | 1-2 |
ISBN (Electronic) | 9781441907172 |
ISBN (Print) | 9781441907165 |
DOIs | |
State | Published - Jan 1 2017 |
Externally published | Yes |
Keywords
- A-443654
- AKT
- Assessment
- AT13148
- AT7867
- CCT128930
- Fluorescence in situ hybridization (FISH)
- GSK690693
- Phosphatidylinositol 3-kinase (PI3K)
- Predictive biomarkers
- Protein kinase B. See AKT
- Therapeutics
ASJC Scopus subject areas
- General Medicine
- General Biochemistry, Genetics and Molecular Biology
- Pharmacology, Toxicology and Pharmaceutics(all)