PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
12547833-8	2003	In non-neuronal and neuronal cells overexpressing a human Swedish variant of amyloid precursor protein, 22R-hydroxycholesterol and 9-cis-retinoic acid induced ABCA1 expression and increased apoA-I-mediated cholesterol efflux consequently decreasing cellular cholesterol content.	Alitretinoin	131-150	ATP binding cassette subfamily A member 1	Homo sapiens	159-164	
18594022-4	2008	The cell-based high-throughput screen is conducted in a 96-well format using the human hepatoma HepG2 cells stably transfected with ABCA1 promoter-luciferase construct and calibrated with reference ABCA1 upregulators (oxysterols, 9-cis-retinoic acid, thiazolidinediones, cyclic adenosine monophosphate, verapamil, fenofibrate, and oncostatin M).	Alitretinoin	230-249	ATP binding cassette subfamily A member 1	Homo sapiens	198-203	
15777536-3	2005	Both natural (22R-hydroxycholesterol/9-cis-retinoic acid) and synthetic (T0901317 and RO264456) LXR/RXR ligands increased ABCA1 and ABCG1 mRNAs in native macrophages and in cells loaded with acetylated LDL (acLDL).	Alitretinoin	37-56	ATP binding cassette subfamily A member 1	Homo sapiens	122-127	
14660648-1	2004	The dynamics of ABCA1-mediated apoA-I lipidation were investigated in intact human fibroblasts induced with 22(R)-hydroxycholesterol and 9-cis-retinoic acid (stimulated cells).	Alitretinoin	137-156	ATP binding cassette subfamily A member 1	Homo sapiens	16-21	
16289478-3	2005	ABCA1 upregulation by 8-(4-chlorophenylthio)adenosine 3":5"-cyclic monophosphate (cpt-cAMP) or 22 (R)-hydroxycholesterol (22-OH) and 9-cis retinoic acid (9cRA) increased the efflux to apo-AI of cellular sterols derived from AcLDL, but not of those from OxLDL.	Alitretinoin	133-152	ATP binding cassette subfamily A member 1	Homo sapiens	0-5	
16289478-3	2005	ABCA1 upregulation by 8-(4-chlorophenylthio)adenosine 3":5"-cyclic monophosphate (cpt-cAMP) or 22 (R)-hydroxycholesterol (22-OH) and 9-cis retinoic acid (9cRA) increased the efflux to apo-AI of cellular sterols derived from AcLDL, but not of those from OxLDL.	Alitretinoin	154-158	ATP binding cassette subfamily A member 1	Homo sapiens	0-5	
12909583-2	2003	ABCA1 mRNA and protein expression in primary cultures of rodent type II cells was sensitive to upregulation with 5 microM 9-cis-retinoic acid (9cRA) and 6.2 microM 22-hydroxycholesterol (22-OH).	Alitretinoin	122-141	ATP binding cassette subfamily A member 1	Homo sapiens	0-5	
12909583-2	2003	ABCA1 mRNA and protein expression in primary cultures of rodent type II cells was sensitive to upregulation with 5 microM 9-cis-retinoic acid (9cRA) and 6.2 microM 22-hydroxycholesterol (22-OH).	Alitretinoin	143-147	ATP binding cassette subfamily A member 1	Homo sapiens	0-5	
11279031-8	2001	Overexpression of ZNF202m1 in RAW264.7 macrophages prevented the induction of ABCA1 gene expression by 20(S)OH-cholesterol and 9-cis-retinoic acid, further substantiating the interference of ZNF202 in critical elements of transcriptional activation.	Alitretinoin	127-146	ATP binding cassette subfamily A member 1	Homo sapiens	78-83	
12401893-0	2002	Truncation mutations in ABCA1 suppress normal upregulation of full-length ABCA1 by 9-cis-retinoic acid and 22-R-hydroxycholesterol.	Alitretinoin	83-102	ATP binding cassette subfamily A member 1	Homo sapiens	24-29	
12401893-0	2002	Truncation mutations in ABCA1 suppress normal upregulation of full-length ABCA1 by 9-cis-retinoic acid and 22-R-hydroxycholesterol.	Alitretinoin	83-102	ATP binding cassette subfamily A member 1	Homo sapiens	74-79	
12401893-3	2002	To specifically test this hypothesis, we examined ABCA1 protein expression in response to 9-cis-retinoic acid (9-cis-RA) and 22-R-hydroxycholesterol (22-R-OH-Chol) in a collection of human fibroblasts representing eight different mutations and observed that truncation mutations blunted the response to oxysterol stimulation and dominantly suppressed induction of the remaining full-length allele to 5-10% of wild-type levels.	Alitretinoin	90-109	ATP binding cassette subfamily A member 1	Homo sapiens	50-55	
12401893-3	2002	To specifically test this hypothesis, we examined ABCA1 protein expression in response to 9-cis-retinoic acid (9-cis-RA) and 22-R-hydroxycholesterol (22-R-OH-Chol) in a collection of human fibroblasts representing eight different mutations and observed that truncation mutations blunted the response to oxysterol stimulation and dominantly suppressed induction of the remaining full-length allele to 5-10% of wild-type levels.	Alitretinoin	111-119	ATP binding cassette subfamily A member 1	Homo sapiens	50-55	
12176027-6	2002	The expression of ABCA1 was up-regulated during the differentiation and under the stimulation of LXR/RXR by the addition of 9-cis-retinoic acid (9-cis-RA) and 22-R-hydroxycholesterol (22-OH).	Alitretinoin	124-143	ATP binding cassette subfamily A member 1	Homo sapiens	18-23	
12176027-6	2002	The expression of ABCA1 was up-regulated during the differentiation and under the stimulation of LXR/RXR by the addition of 9-cis-retinoic acid (9-cis-RA) and 22-R-hydroxycholesterol (22-OH).	Alitretinoin	145-153	ATP binding cassette subfamily A member 1	Homo sapiens	18-23	
11785958-4	2002	In the fibroblasts homozygous for G1158A/A255T, the immunoreactive mass of ABCA1 could not be detected, even when stimulated by 9-cis-retinoic acid and 22-R-hydroxycholesterol.	Alitretinoin	128-147	ATP binding cassette subfamily A member 1	Homo sapiens	75-80	
10858438-2	2000	In cultured macrophages, ABC1 mRNA was induced in an additive fashion by 22(R)-hydroxycholesterol and 9-cis-retinoic acid (9CRA), suggesting induction by nuclear hormone receptors of the liver X receptor (LXR) and retinoid X receptor (RXR) family.	Alitretinoin	102-121	ATP binding cassette subfamily A member 1	Homo sapiens	25-29