| Using these cells , we show that : a ) LDL receptor induction was reduced in reporter constructs containing mutation in either Sp 1 or sterol regulatory element 1 ( SRE 1 ) sites , whereas inactivation of both sites abolished the induction ; b ) E1A , which inhibits CREB binding protein ( CBP ) , a common activator of SRE 1 binding protein and Sp 1 , strongly repressed the induction ; c ) intracellular inhibition of the 90 kDa ribosomal S 6 kinase ( pp90RSK ) cascade reduced LDL receptor induction ; d ) highly selective protein kinase C ( PKC ) inhibitors effectively abrogated the induction without affecting activation of pp90RSK ; and e ) overexpression of PKC beta significantly induced LDL receptor promoter activity . ^^^ Taken together , these results demonstrate that pp90RSK and PKC beta are downstream effectors and Sp 1 , SRE 1 binding protein , and CBP are part of the transcriptional complex resulting in induction of LDL receptor expression in response to activation of the Raf / MEK / p42 / 44MAPK cascade . ^^^ |