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MMP2 — PI3

Text-mined interactions from Literome

Kurata et al., Exp Cell Res 2000 : Taken together, these results strongly suggest that MEK-MAP kinase signaling, but not PI3 kinase signaling, plays a critical role in the activation of MMP-2 secretion and, subsequently, in the invasiveness of v-src transformed cells
Zhang et al., J Biol Chem 2004 (Carcinoma, Lewis Lung) : MMP-2 induction was blocked by the PI 3-kinase inhibitors LY294002 and wortmannin, by overexpression of a dominant negative Akt or wild-type PTEN ( phosphatase and tensin homologue deleted on chromosome 10 ), and by rapamycin
Choi et al., J Biol Chem 2004 (MAP Kinase Signaling System) : The involvement of phosphatidylinositol 3-kinase (PI3K) and Akt in the regulation of MMP-2 activity was further suggested by the findings that PI3K and Akt were phosphorylated by sPLA ( 2 )
Stawowy et al., Biochem Biophys Res Commun 2004 : Induction of MMP-2 by IGF-1 was inhibited by the PI3-kinase inhibitor wortmannin, but not by the MEK-inhibitor PD98059
Morozevich et al., Biochemistry (Mosc) 2008 (Breast Neoplasms...) : These data suggest that alpha5beta1 controls invasion ability of these cells by regulating expression of MMP-2 , which involves PI-3K and Erk1/2 protein kinase signaling
Furundzija et al., Biochem Biophys Res Commun 2010 (Atherosclerosis) : This involves activation of integrins and focal adhesion formation via inside-out PI3-kinase/PKC/p38 dependent signaling, but does not require MMP activation