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BAX — PTGS2

Text-mined interactions from Literome

Dandekar et al., Clin Cancer Res 2004 (Neoplasms, Hormone-Dependent...) : Suppression of COX-2 increased Bax protein and decreased Bcl-x ( L ) protein in vitro
Tari et al., Lab Invest 2005 (Breast Neoplasms) : However, we did not observe any changes in Bcl-2, Bcl-XL, or Bax expression induced by COX-2 or PGE2
Kim et al., Arch Pharm Res 2009 (Colonic Neoplasms) : NF-kappaB target gene expression of apoptotic cell death proteins ( Bax , caspase-3, caspase-9 ) was significantly enhanced, but the expression of anti-apoptotic genes and cell proliferation marker genes ( Bcl-2, inhibitor of apoptosis protein ( IAP-1 ) and X chromosome IAP (XIAP), Cox-2 , c-Fos, c-Jun and cyclin D1 ) was significantly inhibited by the combined treatment compared to Rg3 or docetaxel alone
Oh et al., Carcinogenesis 2010 (Carcinoma, Squamous Cell...) : The E5-induced decrease in Bax expression was inhibited by a cyclooxygenase-2 (COX-2) inhibitor, prostaglandin E2 ( PGE ( 2 ) ) receptor antagonists and cyclic adenosine monophosphate dependent protein kinase (PKA) inhibitor
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