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BAX — MMP2

Text-mined interactions from Literome

Boya et al., Oncogene 2003 : The data reported herein indicate that LMP does not suffice to trigger caspase activation and that Bax/Bak dependent MMP is a critical step of LMP induced cell death
Shen et al., Biochem Biophys Res Commun 2006 : Moreover, MMP-2 inhibition reduced Bax expression and caspase3 activity, as well as increasing Bcl2 expression
Zhang et al., Curr Mol Med 2012 (Breast Neoplasms...) : Addition of sera obtained from patients treated with combination of radiotherapy and EGCG feeding for 2-8 weeks to in vitro cultures of highly-metastatic human MDA-MB-231 breast cancer cells resulted in the following significant changes : ( 1 ) suppression of cell proliferation and invasion ; ( 2 ) arrest of cell cycles at the G0/G1 phase ; ( 3 ) reduction of activation of MMP9/MMP2 , expressions of Bcl-2/Bax , c-Met receptor, NF-?B, and the phosphorylation of Akt
Lecoeur et al., Cell death & disease 2012 : Pharmacologic inhibitors of the permeability transition pore, Bax/Bak inhibitors, and recombinant Bcl-2 and Bcl-XL proteins do not reduce Tat induced MMP
Khoufache et al., PloS one 2012 (Endometriosis...) : Actually, mice treatment with ISO-1 significantly reduced the expression of cell adhesion receptors av and ß3 integrins ( P < 0.05 ), matrix metalloproteinases (MMP) 2 and 9 ( P < 0.05 ), vascular endothelial cell growth factor ( VEGF ) ( P < 0.01 ), interleukin 8 (IL8) ( P < 0.05 ), cyclooxygenease (COX)2 ( P < 0.001 ) and the anti-apoptotic protein Bcl2 ( P < 0.01 ), but significantly induced the expression of Bax ( P < 0.05 ), a potent pro-apoptotic protein
Seitz et al., Int J Cancer 2013 (Neuroblastoma) : In combination, BEZ235 and CQ cooperate to trigger LMP, Bax activation , loss of mitochondrial membrane potential ( MMP ) and caspase dependent apoptosis
Barlaka et al., Can J Physiol Pharmacol 2013 (Myocardial Reperfusion Injury) : These results indicate that PPAR-a activation by its selective ligand WY may confer delayed preconditioning-like protection in rat hearts subjected to I/R by modulating oxidative stress, activation of matrix metalloproteinase-2 , and expression of Bcl-2 and Bax