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APOE — JUN

Text-mined interactions from Literome

Singh et al., Arterioscler Thromb Vasc Biol 2006 : Using THP-1 cell line as a model system, with key findings confirmed in primary cultures, we show that TGF-beta induces the expression of apoE , and this is prevented by pharmacological inhibitors of c-Jun N-terminal kinase (JNK) , p38 kinase, and casein kinase 2 ( CK2 ) ... TGF-beta also increases the phosphorylation and expression of c-Jun, a downstream target for JNK action and a component of activator protein-1 (AP-1), and DN c-Jun inhibits the induction of apoE expression in response to the cytokine ... These studies reveal a novel role for JNK, p38 kinase, CK2, and c-Jun/AP-1 in the TGF-beta induced expression of apoE
Gafencu et al., J Biol Chem 2007 (Inflammation) : The activity of the apoE promoter was repressed by c-Jun , whereas small interference RNA mediated inhibition of endogenous c-Jun expression reversed the inhibitory effect of Tpl-2 on the apoE promoter
Huwait et al., Cell Signal 2011 : The expression of ApoE and ABCA1 induced by synthetic or natural LXR ligands [ TO901317, GW3965, and 22- ( R ) -hydroxycholesterol ( 22- ( R ) -HC ), respectively ] was attenuated by inhibitors of c-Jun N-terminal kinase (JNK) ( curcumin and SP600125 ) and phosphoinositide 3-kinase (PI3K) ( LY294002 )