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Articles in PresS, published online ahead of print August 29, 2001
Physiol Genomics, 10.1152/physiolgenomics.00052.2001
Submitted on June 19, 2001
Accepted on August 19, 2001
1 Cancer Research, Genomics and Gene Therapy, and Immunology, Berlex Biosciences, Richmond, CA, USA
2 Molecular Pharmacology, Stanford Medical School, Stanford, CA, USA
* To whom correspondence should be addressed. E-mail: Irene_Kuhn{at}Berlex.com.
AKT/Protein Kinase B plays a critical role in the phosphoinositide 3-kinase (PI3-kinase) pathway regulating cell growth, differentiation and oncogenic transformation. Akt1-regulated genes were identified by c-DNA array hybridization analysis using an inducible Akt1 gene, MERAkt. Treatment of MERAkt cells with estrogen receptor ligands resulted in phosphorylative activation of MERAKT. Genes differentially expressed in MERAkt/NIH3T3 cells treated with TamoxifenTM, RaloxifeneTM, ICI 182780, and ZK955, were dentified at 3 and 20 hours. AKT-activation resulted in the repression of c-myc, EGR1, TGFßr III, and THBS1. Although c-myc induction is often associated with oncogenic transformation, the c-myc repression observed here is consistent with the anti-apoptotic function of AKT. Repression of THBS1 and EGR1 is consistent with the known pro-angiogenic functions of AKT. AKT-regulated genes were found to be largely distinct from PDGFß-regulated genes; only TDAG51 was induced in both cases. In contrast to their repression by AKT, c-myc, THBS1, and EGR1 were induced by PDGFß, indicating negative interference between elements upstream and downstream of Akt1 in the PDGFß signal transduction pathway.
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