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Editorial
. 2016 Jan 5;7(1):5-6.
doi: 10.18632/oncotarget.6663.

Endosome and INPP4B

Chen Li Chew  1 , Ming Chen  1 , Pier Paolo Pandolfi  1
Affiliations
Editorial

Endosome and INPP4B

Chen Li Chew et al. Oncotarget. .
No abstract available

Keywords: INPP4B; PI3K/AKT; cancer; endosome; genetics; metastasis; thyroid.

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Figures

Figure 1
Figure 1. Regulation of PI3K/AKT signaling through phosphatases
Growth factor signaling results in the activation of PI3K, which produces PI(3,4,5)P3. PI(3,4,5)P3 can subsequently be dephosphorylated by SHIP1/2 to PI(3,4)P2. Both PI(3,4,5)P3 and PI(3,4)P2 can activate AKT, leading to cell proliferation, survival, migration and invasion. PTEN and INPP4B dephosphorylate PI(3,4,5)P3 and PI(3,4)P2 respectively, acting as tumor suppressors by antagonizing AKT signaling. Under certain circumstances, INPP4B can act as an oncogene – PI(3)P, the product of INPP4B action, can activate SGK3, which activates pathways in proliferation, cell survival, migration and invasion. Figure adapted from Gewinner C et al. Cancer Cell. 2009.
See this image and copyright information in PMC

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