PIKE (Phosphatidylinositol 3-Kinase Enhancer)-A GTPase Stimulates Akt Activity and Mediates Cellular Invasion

Jee Yin Ahn, Rong Rong, Todd G. Kroll, Erwin G. Van Meir, Solomon H. Snyder, Keqiang Ye*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

80 Citations (Scopus)


Akt/PKB is a crucial regulator of diverse cellular processes and contributes to cancer progression. Activation of Akt is essentially dependent on phosphatidylinositol (PI) 3-kinase signaling. Here, we describe a novel mediator of Akt that is independent of PI 3-kinase. This mediator, PIKE-A, is a PIKE isoform and contains GTPase, pleckstrin homology, ArfGAP, and ankyrin repeats domains. PIKE-A directly binds to activated Akt but not PI 3-kinase in a guanine nucleotide-dependent way and stimulates the kinase activity of Akt. Overexpression of PIKE-A enhances Akt activity and promotes cancer cell invasion, whereas dominant-negative PIKE-A and PIKE-A knockdown markedly inhibit these processes. Our results demonstrate that PIKE-A is a physiologic regulator of Akt and an oncogenic effector of cell invasion.

Original languageEnglish
Pages (from-to)16441-16451
Number of pages11
JournalJournal of Biological Chemistry
Issue number16
Publication statusPublished - 16 Apr 2004
Externally publishedYes


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