Gene interactions and pathways from curated databases and text-mining

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BAX — JUN

Text-mined interactions from Literome

Mandal et al., Gastroenterology 2001 (Colorectal Neoplasms) : BA-induced enhancement of DNA fragmentation and stimulation of Bax promoter activity were blocked by the expression of dominant negative mutants of JNK1 or AP1 but not NF-kappaB
Papadakis et al., FEBS Lett 2006 : The regulation of Bax by c-Jun N-terminal protein kinase (JNK) is a prerequisite to the mitochondrial induced apoptotic pathway
Zhang et al., J Neurochem 2006 (Brain Ischemia...) : Subsequently, inhibition of c-Jun N-terminal kinase 3 ( JNK3 ) results in decreased serine phosphorylation of 14-3-3, a cytoplasmic anchor of Bax, and prevents ischemia induced mitochondrial translocation of Bax , release of cytochrome c and activation of caspase 3
Keramaris et al., J Biol Chem 2008 : Moreover, Bax deficiency does not affect c-Jun phosphorylation
Kim et al., FEBS J 2008 (Uterine Cervical Neoplasms) : In addition, dominant negative form of c-Jun inhibited radiation induced Fas expression and Bax and Bak activation
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
Byun et al., Mol Pharmacol 2009 (Uterine Cervical Neoplasms) : We also showed that c-Jun N-terminal kinase (JNK) is involved in ROS dependent Bax activation
Liu et al., Biomaterials 2010 (Necrosis) : Silica nanoparticles also activated c-Jun N-terminal kinase (JNK), c-Jun , p53, caspase-3 and NF-kappaB, increased Bax expression and suppressed Bcl-2 protein
Bergeron et al., Curr Opin Neurobiol 1998 (Nervous System Diseases) : When neurons are deprived of trophic factors, a sequence of events is initiated, which includes a reduction in macromolecule synthesis, elevation of c-Jun and cyclin D1, and activation of BAX