PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34107900-14	2021	Induction of other regulatory factors by A1542-A1543 including EGR1, AP1 (FOS + JUN) LDLR, IER2 and others may cooperate with SREBP1/2 to induce cholesterol genes.	Cholesterol	145-156	jun proto-oncogene	Mus musculus	69-72	
34107900-15	2021	Indeed, pharmacological inhibition of AP1 significantly inhibited cholesterol gene expression induced by A1542.	Cholesterol	66-77	jun proto-oncogene	Mus musculus	38-41	
24675662-0	2014	Coenzyme Q10 promotes macrophage cholesterol efflux by regulation of the activator protein-1/miR-378/ATP-binding cassette transporter G1-signaling pathway.	Cholesterol	33-44	jun proto-oncogene	Mus musculus	73-92	
24675662-3	2014	APPROACH AND RESULTS: CoQ10 treatment suppressed oxidized low-density lipoprotein-induced macrophage foam cell formation by ameliorating the binding of activator protein-1 to the putative promoter region of miR-378 primary transcript, thus decreasing the miR-378 level and enhancing the ATP-binding cassette transporter G1-mediated macrophage cholesterol efflux to high-density lipoprotein.	Cholesterol	343-354	jun proto-oncogene	Mus musculus	152-171	
24675662-4	2014	Subsequently, the axis of activator protein-1/miR-378/ATP-binding cassette transporter G1 cholesterol efflux was confirmed in peritoneal macrophages isolated from CoQ10-treated apolipoprotein E-deficient mice.	Cholesterol	90-101	jun proto-oncogene	Mus musculus	26-45	
24675662-6	2014	CONCLUSIONS: This study identified activator protein-1/miR-378/ATP-binding cassette transporter G1 as a novel cascade for CoQ10 in facilitating macrophage cholesterol efflux in vitro and in vivo.	Cholesterol	155-166	jun proto-oncogene	Mus musculus	35-54	
17456467-2	2007	We show that adenovirus-mediated gene transfer of the dominant negative form of c-Jun (dn-c-Jun) in C57BL/6 mice increased greatly apoE hepatic mRNA and plasma levels, increased plasma cholesterol, triglyceride, and very low density lipoprotein levels, and resulted in the accumulation of discoidal high density lipoprotein particles.	Cholesterol	185-196	jun proto-oncogene	Mus musculus	80-85	
17456467-2	2007	We show that adenovirus-mediated gene transfer of the dominant negative form of c-Jun (dn-c-Jun) in C57BL/6 mice increased greatly apoE hepatic mRNA and plasma levels, increased plasma cholesterol, triglyceride, and very low density lipoprotein levels, and resulted in the accumulation of discoidal high density lipoprotein particles.	Cholesterol	185-196	jun proto-oncogene	Mus musculus	87-95	
17456467-4	2007	Unexpectedly, infection of apoE(-/-) mice with adenovirus expressing dn-c-Jun reduced plasma cholesterol by 70%, suggesting that dn-c-Jun affected other genes that control plasma cholesterol levels.	Cholesterol	93-104	jun proto-oncogene	Mus musculus	69-77	
17456467-4	2007	Unexpectedly, infection of apoE(-/-) mice with adenovirus expressing dn-c-Jun reduced plasma cholesterol by 70%, suggesting that dn-c-Jun affected other genes that control plasma cholesterol levels.	Cholesterol	179-190	jun proto-oncogene	Mus musculus	69-77	
17456467-4	2007	Unexpectedly, infection of apoE(-/-) mice with adenovirus expressing dn-c-Jun reduced plasma cholesterol by 70%, suggesting that dn-c-Jun affected other genes that control plasma cholesterol levels.	Cholesterol	179-190	jun proto-oncogene	Mus musculus	129-137	
17456467-7	2007	The involvement of Scd-1 in lowering plasma cholesterol was confirmed by restoration of high cholesterol levels of apoE(-/-) mice following coinfection with adenoviruses expressing dn-c-Jun and Scd-1.	Cholesterol	44-55	jun proto-oncogene	Mus musculus	181-189	
17456467-8	2007	In conclusion, dn-c-Jun appears to trigger two opposing events in mice that affect plasma cholesterol and triglyceride levels as follows: one results in apoE overexpression and triggers dyslipidemia and the other results in inhibition of Scd-1 and offsets dyslipidemia.	Cholesterol	90-101	jun proto-oncogene	Mus musculus	15-23