PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
10357838-8	1999	In vitro incubation studies of plasma from apoA-II knockout mice, which contains largely apoA-I HDL particles, showed active lipolysis of HDL triglyceride, whereas similar studies of plasma from apoA-I knockout mice, which contains largely apoA-II particles, did not.	Triglycerides	142-154	apolipoprotein A-I	Mus musculus	43-49
10357838-8	1999	In vitro incubation studies of plasma from apoA-II knockout mice, which contains largely apoA-I HDL particles, showed active lipolysis of HDL triglyceride, whereas similar studies of plasma from apoA-I knockout mice, which contains largely apoA-II particles, did not.	Triglycerides	142-154	apolipoprotein A-I	Mus musculus	89-95
10357841-6	1999	In apoA-I+/+ mice, after injection of LPS, remodeling of HDL occurred: total cholesterol increased and apoA-I decreased slightly and shifted to lighter density.	Cholesterol	77-88	apolipoprotein A-I	Mus musculus	3-9
10357841-10	1999	In the apoA-I-/- mice, which normally have very low plasma lipid levels, LPS injection resulted in significantly increased total and HDL cholesterol.	Cholesterol	137-148	apolipoprotein A-I	Mus musculus	7-13
10323777-7	1999	Cholesterol efflux to sera from the A-IM carriers was only reduced slightly compared with control sera (25.0+/-4.2% versus 30.4+/-3.3%), although there was a large reduction (-45%) in the serum ApoA-I concentration in the former.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	194-200
10323777-11	1999	Therefore, the relative efflux potential reflects the relative efficiency of ApoA-I in determining cell cholesterol efflux.	Cholesterol	104-115	apolipoprotein A-I	Mus musculus	77-83
10073953-0	1999	ApoA1 reduces free cholesterol accumulation in atherosclerotic lesions of ApoE-deficient mice transplanted with ApoE-expressing macrophages.	Cholesterol	19-30	apolipoprotein A-I	Mus musculus	0-5
10073953-1	1999	Along with apolipoprotein (apo) E, which promotes cholesterol efflux from foam cells, apoA1-containing high density lipoprotein (HDL) is thought to facilitate the transport of cholesterol from lesions.	Cholesterol	176-187	apolipoprotein A-I	Mus musculus	86-91
10073953-9	1999	Therefore, apoA1 reduces free cholesterol accumulation in vivo in atherosclerotic lesions.	Cholesterol	30-41	apolipoprotein A-I	Mus musculus	11-16
10064737-1	1999	ApoA-I(R160L)Oslo and apoA-I(P165R) are naturally occurring apolipoprotein (apo) A-I variants that are associated with low HDL-cholesterol in heterozygous carriers.	Cholesterol	127-138	apolipoprotein A-I	Mus musculus	0-5
10064737-1	1999	ApoA-I(R160L)Oslo and apoA-I(P165R) are naturally occurring apolipoprotein (apo) A-I variants that are associated with low HDL-cholesterol in heterozygous carriers.	Cholesterol	127-138	apolipoprotein A-I	Mus musculus	22-28
10064737-3	1999	During cholate dialysis, normal apoA-I and both variants associated completely with dipalmitoylphosphatidylcholine (DPPC) and formed rLpA-I of identical size.	1,2-Dipalmitoylphosphatidylcholine	84-114	apolipoprotein A-I	Mus musculus	32-38
10064737-3	1999	During cholate dialysis, normal apoA-I and both variants associated completely with dipalmitoylphosphatidylcholine (DPPC) and formed rLpA-I of identical size.	1,2-Dipalmitoylphosphatidylcholine	116-120	apolipoprotein A-I	Mus musculus	32-38
10064737-4	1999	However, both apoA-I(P165R) and apoA-I(R160L)Oslo showed a reduced capacity to clear a turbid emulsion of dimyristoylphosphatidylcholine (DMPC).	Dimyristoylphosphatidylcholine	106-136	apolipoprotein A-I	Mus musculus	14-20
10064737-4	1999	However, both apoA-I(P165R) and apoA-I(R160L)Oslo showed a reduced capacity to clear a turbid emulsion of dimyristoylphosphatidylcholine (DMPC).	Dimyristoylphosphatidylcholine	106-136	apolipoprotein A-I	Mus musculus	14-19
10064737-4	1999	However, both apoA-I(P165R) and apoA-I(R160L)Oslo showed a reduced capacity to clear a turbid emulsion of dimyristoylphosphatidylcholine (DMPC).	Dimyristoylphosphatidylcholine	138-142	apolipoprotein A-I	Mus musculus	14-20
10064737-4	1999	However, both apoA-I(P165R) and apoA-I(R160L)Oslo showed a reduced capacity to clear a turbid emulsion of dimyristoylphosphatidylcholine (DMPC).	Dimyristoylphosphatidylcholine	138-142	apolipoprotein A-I	Mus musculus	14-19
10064737-6	1999	ApoA-I/DPPC complexes induced biphasic cholesterol efflux from SMCs with a fast and a slow efflux component.	1,2-Dipalmitoylphosphatidylcholine	7-11	apolipoprotein A-I	Mus musculus	0-6
10064737-6	1999	ApoA-I/DPPC complexes induced biphasic cholesterol efflux from SMCs with a fast and a slow efflux component.	Cholesterol	39-50	apolipoprotein A-I	Mus musculus	0-6
10064737-8	1999	Lipid-free apoA-I did not induce efflux of biosynthetic cholesterol from SMCs but induced hydrolysis of cholesteryl esters and cholesterol efflux from acetyl-LDL-loaded mouse peritoneal macrophages.	Cholesterol Esters	104-122	apolipoprotein A-I	Mus musculus	11-17
10064737-8	1999	Lipid-free apoA-I did not induce efflux of biosynthetic cholesterol from SMCs but induced hydrolysis of cholesteryl esters and cholesterol efflux from acetyl-LDL-loaded mouse peritoneal macrophages.	Cholesterol	127-138	apolipoprotein A-I	Mus musculus	11-17
10064737-9	1999	In the lipid-free form, both apoA-I variants promoted normal cholesterol efflux from murine peritoneal macrophages.	Cholesterol	61-72	apolipoprotein A-I	Mus musculus	29-35
10064737-10	1999	We conclude that amino acid residues arginine 160 and proline 165 of apoA-I contribute to the formation of a domain that is very important for initial lipid binding and contributes to LCAT-activation and promotion of initial cholesterol efflux but not to the stabilization of preformed rLpA-I.	Arginine	37-45	apolipoprotein A-I	Mus musculus	69-75
10064737-10	1999	We conclude that amino acid residues arginine 160 and proline 165 of apoA-I contribute to the formation of a domain that is very important for initial lipid binding and contributes to LCAT-activation and promotion of initial cholesterol efflux but not to the stabilization of preformed rLpA-I.	Proline	54-61	apolipoprotein A-I	Mus musculus	69-75
10064737-10	1999	We conclude that amino acid residues arginine 160 and proline 165 of apoA-I contribute to the formation of a domain that is very important for initial lipid binding and contributes to LCAT-activation and promotion of initial cholesterol efflux but not to the stabilization of preformed rLpA-I.	Cholesterol	225-236	apolipoprotein A-I	Mus musculus	69-75
9884386-3	1999	Administration of AV RSV apoA-I to C57BL/6 mice resulted in moderate expression of human apoA-I for 3 weeks, leading to a transient elevation (40% at day 11 after injection) of HDL cholesterol concentration.	Cholesterol	181-192	apolipoprotein A-I	Mus musculus	25-31
9830042-3	1998	On a chow diet SR-BI transgenic (SR-BI Tg) mice have decreased HDL-CE, apoA-I, and apoA-II levels; plasma triglycerides, low density lipoprotein (LDL) cholesterol, and very low density lipoprotein (VLDL) and LDL apoB were also decreased, compared with control mice.	Thioguanine	39-41	apolipoprotein A-I	Mus musculus	71-77
9795222-3	1998	Acute phase response (APR) was induced in C57BL/6J (apoA1+/+) and apoA1-knockout mice (apoA1-/-) by a subcutaneous injection of silver nitrate.	Silver Nitrate	128-142	apolipoprotein A-I	Mus musculus	66-71
9795222-3	1998	Acute phase response (APR) was induced in C57BL/6J (apoA1+/+) and apoA1-knockout mice (apoA1-/-) by a subcutaneous injection of silver nitrate.	Silver Nitrate	128-142	apolipoprotein A-I	Mus musculus	66-71
9795222-4	1998	The APR increased cholesterol concentrations in LDL of apoA1-/- mice and apoA1+/+ mice in a like manner.	Cholesterol	18-29	apolipoprotein A-I	Mus musculus	55-60
9743230-0	1998	Human apolipoproteins A-I and A-II in cell cholesterol efflux: studies with transgenic mice.	Cholesterol	43-54	apolipoprotein A-I	Mus musculus	6-34
9743230-7	1998	Regression analysis of cholesterol efflux versus the lipid/apolipoprotein concentrations of mouse serum suggested that 3 independent factors contribute to determine the cholesterol efflux potential of serum: the apolipoprotein composition of HDL, the serum concentration of HDL phospholipids, and the presence of a small fraction of particles containing apoA-I.	Cholesterol	169-180	apolipoprotein A-I	Mus musculus	354-360
9664079-2	1998	HDL cholesterol levels ranked: apo AI/apo E KO approximately apo AI-(1-189)-apo AII- (12-77)/apo E KO > > des-(190-243)-apo AI/apo E KO > apo E KO mice.	Cholesterol	4-15	apolipoprotein A-I	Mus musculus	31-37
9664079-2	1998	HDL cholesterol levels ranked: apo AI/apo E KO approximately apo AI-(1-189)-apo AII- (12-77)/apo E KO > > des-(190-243)-apo AI/apo E KO > apo E KO mice.	Cholesterol	4-15	apolipoprotein A-I	Mus musculus	61-67
9664079-2	1998	HDL cholesterol levels ranked: apo AI/apo E KO approximately apo AI-(1-189)-apo AII- (12-77)/apo E KO > > des-(190-243)-apo AI/apo E KO > apo E KO mice.	Cholesterol	4-15	apolipoprotein A-I	Mus musculus	61-67
9664079-5	1998	This study demonstrates that the tertiary structure of apo AI, e.g., the number and organization of its helices, and not its amino sequence is essential for protection against atherosclerosis because it determines HDL cholesterol levels and not cholesterol efflux.	Cholesterol	218-229	apolipoprotein A-I	Mus musculus	55-61
9664079-5	1998	This study demonstrates that the tertiary structure of apo AI, e.g., the number and organization of its helices, and not its amino sequence is essential for protection against atherosclerosis because it determines HDL cholesterol levels and not cholesterol efflux.	Cholesterol	245-256	apolipoprotein A-I	Mus musculus	55-61
10923465-4	1998	Northern blot showed that human apo AI mRNA was expressed mainly in the liver and kidneys, and the high level of h-apo AI mRNA was obtained in liver, kidneys and small intestine after Zinc(Zn) induction.	Zinc	189-191	apolipoprotein A-I	Mus musculus	115-121
9544740-2	1998	One exception to this trend is individuals with apolipoprotein A-I(Milano) (apo A-IM), a molecular variant of apo A-I, which results in very low plasma apo A-I and HDL-cholesterol levels.	Cholesterol	168-179	apolipoprotein A-I	Mus musculus	48-74
9416903-13	1997	Gene transfer of apo A-I increases HDL cholesterol and significantly reduces neointima formation, which suggests a direct vascular protective effect of HDL.	Cholesterol	39-50	apolipoprotein A-I	Mus musculus	17-24
9368040-3	1997	Up to a molar oxidant:lipoprotein ratio of approximately 30:1, apolipoprotein A-I (apoA-I), the major HDL3 apolipoprotein component, represented the preferential target for OCl- attack (consuming 35-76% of the oxidant), thereby protecting HDL3 fatty acids (consuming between 17 and 30% of the oxidant) against OCl--mediated modification.	Fatty Acids	244-255	apolipoprotein A-I	Mus musculus	63-81
9368040-3	1997	Up to a molar oxidant:lipoprotein ratio of approximately 30:1, apolipoprotein A-I (apoA-I), the major HDL3 apolipoprotein component, represented the preferential target for OCl- attack (consuming 35-76% of the oxidant), thereby protecting HDL3 fatty acids (consuming between 17 and 30% of the oxidant) against OCl--mediated modification.	Fatty Acids	244-255	apolipoprotein A-I	Mus musculus	83-89
9356497-5	1997	In heterozygous and homozygous mutants relative to wild-type controls, plasma cholesterol concentrations were increased by approximately 31% and 125%, respectively, because of the formation of large, apolipoprotein A-I (apoA-I)-containing particles, and adrenal gland cholesterol content decreased by 42% and 72%, respectively.	Cholesterol	78-89	apolipoprotein A-I	Mus musculus	200-218
9356497-5	1997	In heterozygous and homozygous mutants relative to wild-type controls, plasma cholesterol concentrations were increased by approximately 31% and 125%, respectively, because of the formation of large, apolipoprotein A-I (apoA-I)-containing particles, and adrenal gland cholesterol content decreased by 42% and 72%, respectively.	Cholesterol	78-89	apolipoprotein A-I	Mus musculus	220-226
9356497-5	1997	In heterozygous and homozygous mutants relative to wild-type controls, plasma cholesterol concentrations were increased by approximately 31% and 125%, respectively, because of the formation of large, apolipoprotein A-I (apoA-I)-containing particles, and adrenal gland cholesterol content decreased by 42% and 72%, respectively.	Cholesterol	268-279	apolipoprotein A-I	Mus musculus	220-226
9392429-1	1997	Human carriers of apolipoprotein A-I(Milano) (Arg173 --> Cys substitution in apolipoprotein A-I) are characterized by an HDL deficiency in which small, dense HDL accumulate in plasma.	Cysteine	60-63	apolipoprotein A-I	Mus musculus	18-36
9392429-1	1997	Human carriers of apolipoprotein A-I(Milano) (Arg173 --> Cys substitution in apolipoprotein A-I) are characterized by an HDL deficiency in which small, dense HDL accumulate in plasma.	Cysteine	60-63	apolipoprotein A-I	Mus musculus	80-98
9392429-2	1997	Because affected individuals are heterozygous for this mutation, the full impact of apolipoprotein A-I(Milano) (apoA-I(Milano)) on HDL-cholesterol metabolism is unknown.	Cholesterol	135-146	apolipoprotein A-I	Mus musculus	84-110
9392429-2	1997	Because affected individuals are heterozygous for this mutation, the full impact of apolipoprotein A-I(Milano) (apoA-I(Milano)) on HDL-cholesterol metabolism is unknown.	Cholesterol	135-146	apolipoprotein A-I	Mus musculus	112-126
9392429-8	1997	The unesterified cholesterol/cholesteryl ester mole ratio of HDL was elevated by 45% in apoA-IMilano/A-Iwt/A-II mice and by 90% in apoA-IMilano/A-II transgenics compared to wild-type (human apoA-I/A-II).	Cholesterol	17-28	apolipoprotein A-I	Mus musculus	88-111
9392429-8	1997	The unesterified cholesterol/cholesteryl ester mole ratio of HDL was elevated by 45% in apoA-IMilano/A-Iwt/A-II mice and by 90% in apoA-IMilano/A-II transgenics compared to wild-type (human apoA-I/A-II).	Cholesterol	17-28	apolipoprotein A-I	Mus musculus	88-94
9392429-8	1997	The unesterified cholesterol/cholesteryl ester mole ratio of HDL was elevated by 45% in apoA-IMilano/A-Iwt/A-II mice and by 90% in apoA-IMilano/A-II transgenics compared to wild-type (human apoA-I/A-II).	Cholesterol Esters	29-46	apolipoprotein A-I	Mus musculus	88-111
9392429-8	1997	The unesterified cholesterol/cholesteryl ester mole ratio of HDL was elevated by 45% in apoA-IMilano/A-Iwt/A-II mice and by 90% in apoA-IMilano/A-II transgenics compared to wild-type (human apoA-I/A-II).	Cholesterol Esters	29-46	apolipoprotein A-I	Mus musculus	88-94
9392429-10	1997	Thus, HDL particle size restriction was not the result of impaired LCAT activation; rather, dimerization of apoA-I(Milano) limited the esterification of cholesterol on endogenous HDL.	Cholesterol	153-164	apolipoprotein A-I	Mus musculus	108-122
9392429-11	1997	In the absence of wild-type apoA-I, the more extensive dimerization of apoA-I(Milano) severely limited cholesteryl ester accumulation on plasma HDL accounting for the abundance of small, 7.6-nm HDL3 particles in apoA-IMilano/A-II mice.	Cholesterol Esters	103-120	apolipoprotein A-I	Mus musculus	71-85
9341191-9	1997	Two-dimensional gel electrophoresis of plasma 5 min after injection of HDL labeled with 125I-apoA-I demonstrated increased levels of newly generated pre-beta-HDL in mice overexpressing PLTP.	Iodine-125	88-92	apolipoprotein A-I	Mus musculus	93-99
9315842-5	1997	Cellular cholesterol available for acylCoA:cholesterol acyltransferase (ACAT) was rapidly depleted by adding apoA-I to the medium, and the PKC inhibitor treatment reversed this effect.	Cholesterol	9-20	apolipoprotein A-I	Mus musculus	109-115
9351366-0	1997	Effects of genotype and diet on cholesterol efflux into plasma and lipoproteins of normal, apolipoprotein A-I-, and apolipoprotein E-deficient mice.	Cholesterol	32-43	apolipoprotein A-I	Mus musculus	91-109
9351366-5	1997	When apoA-I- and apoE-deficient mice received both chow- and fat-rich diets, their plasmas released significantly less 3H-cholesterol from radiolabeled fibroblasts than did plasma of normal mice.	Tritium	119-121	apolipoprotein A-I	Mus musculus	5-11
9351366-5	1997	When apoA-I- and apoE-deficient mice received both chow- and fat-rich diets, their plasmas released significantly less 3H-cholesterol from radiolabeled fibroblasts than did plasma of normal mice.	Cholesterol	122-133	apolipoprotein A-I	Mus musculus	5-11
9351366-6	1997	Removal of apoE from plasmas of normal and apoA-I-deficient mice by anti-apoE immunoaffinity chromatography decreased their cholesterol efflux capacities (per 1 minute/per 1 hour) by 26%/40% (P = 0.0092/0.0007) and 30%/26% (P = 0.0092/0.0003), respectively.	Cholesterol	124-135	apolipoprotein A-I	Mus musculus	43-49
9351366-7	1997	Net cholesterol efflux from fibroblasts into apoA-I-deficient plasma was 45% lower compared with plasma of normal mice.	Cholesterol	4-15	apolipoprotein A-I	Mus musculus	45-51
9351366-11	1997	Compared with normal plasma, both apoA-I-deficient and apoE-deficient plasmas were significantly decreased in their activity to esterify cell-derived 3H-cholesterol.	Cholesterol	150-164	apolipoprotein A-I	Mus musculus	34-40
9275209-4	1997	When the injected lipoprotein had been labeled with [3H]cholesterol, the t1/2 of labeled cholesterol loss from the muscle was about 4 days in controls and more than 7 days in apo A-I K-O mice.	Tritium	53-55	apolipoprotein A-I	Mus musculus	175-182
9275209-4	1997	When the injected lipoprotein had been labeled with [3H]cholesterol, the t1/2 of labeled cholesterol loss from the muscle was about 4 days in controls and more than 7 days in apo A-I K-O mice.	Cholesterol	56-67	apolipoprotein A-I	Mus musculus	175-182
9275209-4	1997	When the injected lipoprotein had been labeled with [3H]cholesterol, the t1/2 of labeled cholesterol loss from the muscle was about 4 days in controls and more than 7 days in apo A-I K-O mice.	Cholesterol	89-100	apolipoprotein A-I	Mus musculus	175-182
9275209-8	1997	A significantly lower efflux of [3H]cholesterol from macrophages was found with native and delipidated serum from apo A-I K-O mice.	Tritium	33-35	apolipoprotein A-I	Mus musculus	114-121
9275209-8	1997	A significantly lower efflux of [3H]cholesterol from macrophages was found with native and delipidated serum from apo A-I K-O mice.	Cholesterol	36-47	apolipoprotein A-I	Mus musculus	114-121
9275209-9	1997	In conclusion, these findings show that lack of apo A-I results in a delay in cholesterol loss from a localized depot in vivo and from macrophages in culture.	Cholesterol	78-89	apolipoprotein A-I	Mus musculus	48-55
9218525-1	1997	Previous studies showed that transgenic mice overexpressing either apolipoprotein AI (apoAI) or apolipoprotein AII (apoAII), the major proteins of HDL, exhibited elevated levels of HDL cholesterol, but, whereas the apoAI-transgenic mice were protected against atherosclerosis, the apoAII-transgenic mice had increased lesion development.	Cholesterol	185-196	apolipoprotein A-I	Mus musculus	67-84
9254069-5	1997	Supplementation of the cholesterol-rich diet with cholic acid inhibited the stimulatory effect of cholesterol on hepatic apoA-I mRNA expression, resulting in similar hepatic apoA-I mRNA levels compared to chow-fed mice.	Cholesterol	23-34	apolipoprotein A-I	Mus musculus	121-127
9254069-5	1997	Supplementation of the cholesterol-rich diet with cholic acid inhibited the stimulatory effect of cholesterol on hepatic apoA-I mRNA expression, resulting in similar hepatic apoA-I mRNA levels compared to chow-fed mice.	Cholic Acid	50-61	apolipoprotein A-I	Mus musculus	121-127
9254069-5	1997	Supplementation of the cholesterol-rich diet with cholic acid inhibited the stimulatory effect of cholesterol on hepatic apoA-I mRNA expression, resulting in similar hepatic apoA-I mRNA levels compared to chow-fed mice.	Cholic Acid	50-61	apolipoprotein A-I	Mus musculus	174-180
9254069-5	1997	Supplementation of the cholesterol-rich diet with cholic acid inhibited the stimulatory effect of cholesterol on hepatic apoA-I mRNA expression, resulting in similar hepatic apoA-I mRNA levels compared to chow-fed mice.	Cholesterol	98-109	apolipoprotein A-I	Mus musculus	121-127
9254069-14	1997	These data link hepatic apoA-I mRNA expression to hepatic cholesterol/bile acid metabolism.	Cholesterol	58-69	apolipoprotein A-I	Mus musculus	24-30
9254069-14	1997	These data link hepatic apoA-I mRNA expression to hepatic cholesterol/bile acid metabolism.	Bile Acids and Salts	70-79	apolipoprotein A-I	Mus musculus	24-30
9185508-1	1997	Dietary administration of probucol (0.5%, wt/wt) efficiently reduced total plasma cholesterol levels in apolipoprotein E-deficient mice (apoE-/-) by 40%, with decreases in high density lipoprotein (HDL) and apoAI by 70 and 50%, respectively.	Probucol	26-34	apolipoprotein A-I	Mus musculus	207-212
9186920-1	1997	The major high density lipoprotein (HDL) apolipoprotein, apoA-I, was knocked out by gene targeting in ES cells to provide a model for the study of HDL metabolism and its relationship to plasma and tissue cholesterol metabolism.	Cholesterol	204-215	apolipoprotein A-I	Mus musculus	57-63
9186920-2	1997	HDL and non-HDL cholesterol (HDL-C) were reduced in apoA-I-deficient mice.	Cholesterol	16-27	apolipoprotein A-I	Mus musculus	52-58
9186920-3	1997	Feeding a high fat-high cholesterol diet raised HDL-C minimally in apoA-I knockout compared to the large increase seen in control mice, suggesting an interaction between diet and apoA-I genotype.	Cholesterol	24-35	apolipoprotein A-I	Mus musculus	67-73
9186920-3	1997	Feeding a high fat-high cholesterol diet raised HDL-C minimally in apoA-I knockout compared to the large increase seen in control mice, suggesting an interaction between diet and apoA-I genotype.	Cholesterol	24-35	apolipoprotein A-I	Mus musculus	179-185
9186920-5	1997	Compared to control mice there was more triglyceride and free cholesterol and less cholesteryl ester (CE), suggesting that apoA-I-deficient HDL is a poor substrate for hepatic lipase and lecithin:cholesterol acyltransferase (LCAT).	Triglycerides	40-52	apolipoprotein A-I	Mus musculus	123-129
9186920-5	1997	Compared to control mice there was more triglyceride and free cholesterol and less cholesteryl ester (CE), suggesting that apoA-I-deficient HDL is a poor substrate for hepatic lipase and lecithin:cholesterol acyltransferase (LCAT).	Cholesterol	62-73	apolipoprotein A-I	Mus musculus	123-129
9186920-9	1997	The low HDL-C state in the apoA-I-deficient mouse was associated with an absolute decrease in unidirectional transport of cholesterol from peripheral tissues to the liver but this did not lead to cholesterol accumulation in the periphery or a cholesterol deficit in the liver; nor was there altered peripheral tissue HMG-CoA reductase activity.	Cholesterol	122-133	apolipoprotein A-I	Mus musculus	27-33
9186920-11	1997	In the apoA-I knockout mouse model it appears that low HDL levels create a new steady state in which decreased cholesterol is delivered to both peripheral tissues and the liver.	Cholesterol	111-122	apolipoprotein A-I	Mus musculus	7-13
9046367-0	1997	Alcohol feeding impedes early atherosclerosis in low-density lipoprotein receptor knockout mice: factors in addition to high-density lipoprotein-apolipoprotein A1 are involved.	Alcohols	0-7	apolipoprotein A-I	Mus musculus	133-162
9046367-5	1997	By contrast, the lesion size of group B was not significantly different from that of group C. Serum high-density lipoprotein-apolipoprotein A1 (apo A1) A1 in LDLR-/- mice was suppressed by feeding the atherogenic diet, but the decrease was negated by alcohol (both groups A and B).	Alcohols	251-258	apolipoprotein A-I	Mus musculus	113-142
9046367-5	1997	By contrast, the lesion size of group B was not significantly different from that of group C. Serum high-density lipoprotein-apolipoprotein A1 (apo A1) A1 in LDLR-/- mice was suppressed by feeding the atherogenic diet, but the decrease was negated by alcohol (both groups A and B).	Alcohols	251-258	apolipoprotein A-I	Mus musculus	144-150
9046367-6	1997	The effectiveness of 5% alcohol to protect against atherosclerosis waned with time, but was still noticeable at 12 weeks, even though serum apo A1 remained high.	Alcohols	24-31	apolipoprotein A-I	Mus musculus	140-146
9046367-8	1997	Our data, therefore, show that: (1) alcohol-feeding impedes early atherosclerosis in LDLR-/- mice (this effect of alcohol is dose-dependent); (2) the protective effect of alcohol is not entirely attributable to an elevated serum high-density lipoprotein-apo A1; and (3) severe impairment of lipoprotein metabolism due to a lack of low-density lipoprotein receptors can eventually overwhelm the protective effect of alcohol against atherosclerosis.	Alcohols	36-43	apolipoprotein A-I	Mus musculus	254-260
8798380-3	1996	Apolipoprotein A-I knock-out (apoA-I0) mice have decreased HDL cholesterol, depleted adrenal cholesterol stores and impaired corticosteroid synthesis (Plump, A.S., Erickson, S.K., Weng, W., J. Clin.	Cholesterol	63-74	apolipoprotein A-I	Mus musculus	0-18
8798380-3	1996	Apolipoprotein A-I knock-out (apoA-I0) mice have decreased HDL cholesterol, depleted adrenal cholesterol stores and impaired corticosteroid synthesis (Plump, A.S., Erickson, S.K., Weng, W., J. Clin.	Cholesterol	93-104	apolipoprotein A-I	Mus musculus	0-18
8663356-5	1996	Cholesterol efflux from mouse macrophages loaded with 7kAcLDL, using apoA-I as a sterol acceptor, was impaired in cells containing >50 nmol of 7KC/mg of cell protein compared with cells loaded with oxysterol-free acetylated LDL.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	69-75
8663356-5	1996	Cholesterol efflux from mouse macrophages loaded with 7kAcLDL, using apoA-I as a sterol acceptor, was impaired in cells containing >50 nmol of 7KC/mg of cell protein compared with cells loaded with oxysterol-free acetylated LDL.	Sterols	5-11	apolipoprotein A-I	Mus musculus	69-75
8647932-4	1996	In contrast, plasma mouse apo A-I concentration was decreased after fenofibrate in nontransgenic mice.	Fenofibrate	68-79	apolipoprotein A-I	Mus musculus	26-33
8647932-5	1996	The increase in plasma human apo A-I levels after fenofibrate treatment was associated with a 97% increase in hepatic human apo A-I mRNA, whereas mouse apo A-I mRNA levels decreased to 51%.	Fenofibrate	50-61	apolipoprotein A-I	Mus musculus	124-131
8647932-7	1996	Nuclear run-on experiments demonstrated that the increase in human apo A-I and the decrease in mouse apo A-I gene expression after fenofibrate occurred at the transcriptional level.	Fenofibrate	131-142	apolipoprotein A-I	Mus musculus	101-108
8636092-13	1996	Feeding the transgenic mice a high fat, high cholesterol diet maintained the mouse apoA-I concentration at a normal level (69 +/- 14 mg/dl in line 11.1 compared with 71 +/- 6 mg/dl in nontransgenic controls) and prevented the appearance of HDL deficiency.	Cholesterol	45-56	apolipoprotein A-I	Mus musculus	83-89
8808496-2	1996	Analyses of re-isolated ox-LDL showed that apo A-I was transferred from DMPC/apo A-I to ox-LDL, which accounted for 10% of the total protein of ox-LDL.	Dimyristoylphosphatidylcholine	72-76	apolipoprotein A-I	Mus musculus	43-50
8808496-2	1996	Analyses of re-isolated ox-LDL showed that apo A-I was transferred from DMPC/apo A-I to ox-LDL, which accounted for 10% of the total protein of ox-LDL.	Dimyristoylphosphatidylcholine	72-76	apolipoprotein A-I	Mus musculus	77-84
8808496-8	1996	Thus, it is likely that the reduction in the ligand activity of ox-LDL by DMPC/apo A-I is explained by the change in the lipid moiety (mainly phospholipid) of ox-LDL.	Phospholipids	142-154	apolipoprotein A-I	Mus musculus	79-86
8555242-3	1996	All particles containing monomeric apoA-II, i.e., native HDL3 or reconstituted HDL with or without apoA-I, showed a higher ability to promote cholesterol efflux originating from plasma membrane and intracellular stores, compared to particles containing dimeric apoA-II.	Cholesterol	142-153	apolipoprotein A-I	Mus musculus	35-41
8919697-2	1996	More recent research with transgenic mice demonstrated that a high-fat, high-cholesterol diet raised plasma HDL-C and the production rate of apo A-I by a mechanism involving the regulation of translation of the apo A-I mRNA.	Cholesterol	77-88	apolipoprotein A-I	Mus musculus	141-148
8919697-2	1996	More recent research with transgenic mice demonstrated that a high-fat, high-cholesterol diet raised plasma HDL-C and the production rate of apo A-I by a mechanism involving the regulation of translation of the apo A-I mRNA.	Cholesterol	77-88	apolipoprotein A-I	Mus musculus	211-218
7794908-4	1995	This enhancement in cholesterol efflux to lipid-free apo AI from macrophages enriched with cholesterol was found to be controlled by the level of free cholesterol in the cells.	Cholesterol	20-31	apolipoprotein A-I	Mus musculus	53-59
7794908-4	1995	This enhancement in cholesterol efflux to lipid-free apo AI from macrophages enriched with cholesterol was found to be controlled by the level of free cholesterol in the cells.	Cholesterol	91-102	apolipoprotein A-I	Mus musculus	53-59
7794908-4	1995	This enhancement in cholesterol efflux to lipid-free apo AI from macrophages enriched with cholesterol was found to be controlled by the level of free cholesterol in the cells.	Cholesterol	91-102	apolipoprotein A-I	Mus musculus	53-59
7794908-5	1995	When cholesterol-enriched mouse macrophages were exposed to lipid-free apo AI at 20 micrograms/mL (706 nM), there was significant efflux of [14C]cholesterol and [3H]phospholipid (20% +/- 0.5%/24 h and 6% +/- 0.3%/24 h, respectively).	Cholesterol	5-16	apolipoprotein A-I	Mus musculus	71-77
7794908-5	1995	When cholesterol-enriched mouse macrophages were exposed to lipid-free apo AI at 20 micrograms/mL (706 nM), there was significant efflux of [14C]cholesterol and [3H]phospholipid (20% +/- 0.5%/24 h and 6% +/- 0.3%/24 h, respectively).	Carbon-14	141-144	apolipoprotein A-I	Mus musculus	71-77
7794908-5	1995	When cholesterol-enriched mouse macrophages were exposed to lipid-free apo AI at 20 micrograms/mL (706 nM), there was significant efflux of [14C]cholesterol and [3H]phospholipid (20% +/- 0.5%/24 h and 6% +/- 0.3%/24 h, respectively).	Cholesterol	145-156	apolipoprotein A-I	Mus musculus	71-77
7794908-5	1995	When cholesterol-enriched mouse macrophages were exposed to lipid-free apo AI at 20 micrograms/mL (706 nM), there was significant efflux of [14C]cholesterol and [3H]phospholipid (20% +/- 0.5%/24 h and 6% +/- 0.3%/24 h, respectively).	Tritium	162-164	apolipoprotein A-I	Mus musculus	71-77
7794908-5	1995	When cholesterol-enriched mouse macrophages were exposed to lipid-free apo AI at 20 micrograms/mL (706 nM), there was significant efflux of [14C]cholesterol and [3H]phospholipid (20% +/- 0.5%/24 h and 6% +/- 0.3%/24 h, respectively).	Phospholipids	165-177	apolipoprotein A-I	Mus musculus	71-77
7794908-8	1995	Peptides containing only one (18A) or two (37pA) amphipathic helical segments stimulated as much cholesterol efflux from both mouse macrophages and L-cells as apo AI.	Peptides	0-8	apolipoprotein A-I	Mus musculus	159-165
7794908-14	1995	These results suggest that the apo AI or peptides first interacted with the cell to form protein/phospholipid complexes, that could then accept cholesterol.	Phospholipids	97-109	apolipoprotein A-I	Mus musculus	31-37
7794908-14	1995	These results suggest that the apo AI or peptides first interacted with the cell to form protein/phospholipid complexes, that could then accept cholesterol.	Cholesterol	144-155	apolipoprotein A-I	Mus musculus	31-37
7749836-0	1995	Apolipoprotein A-I-mediated efflux of sterols from oxidized LDL-loaded macrophages.	Sterols	38-45	apolipoprotein A-I	Mus musculus	0-18
7989603-2	1994	Subsequent lipolysis of the triglyceride-enriched HDL by hepatic lipase leads to reductions of HDL size and apoA-I content.	Triglycerides	28-40	apolipoprotein A-I	Mus musculus	108-114
7989603-10	1994	However, coexpression of apoA-II with CETP results in HDL particles that are more triglyceride enriched and resistant to reductions in size and apoA-I content, reflecting inhibition of hepatic lipase by apoA-II.	Triglycerides	82-94	apolipoprotein A-I	Mus musculus	25-31
7857382-0	1994	Apolipoprotein A-I-containing particles and reverse cholesterol transport: evidence for connection between cholesterol efflux and atherosclerosis risk.	Cholesterol	107-118	apolipoprotein A-I	Mus musculus	0-18
7857382-8	1994	The results in mice transgenic for apo A-I indicate that overexpression of apo A-I induces more cholesterol efflux and protects C57BL/6 mice from atherosclerosis.	Cholesterol	96-107	apolipoprotein A-I	Mus musculus	35-42
7857382-8	1994	The results in mice transgenic for apo A-I indicate that overexpression of apo A-I induces more cholesterol efflux and protects C57BL/6 mice from atherosclerosis.	Cholesterol	96-107	apolipoprotein A-I	Mus musculus	75-82
7858910-4	1994	Unique new functions of apolipoprotein A-I-containing particles in modulating cytokines and lipid hydroperoxide transport, together with their role in antiatherogenesis, are also discussed.	Lipid Peroxides	92-111	apolipoprotein A-I	Mus musculus	24-42
8087941-4	1994	A 35% increase in HDL cholesterol and a 47% increase in total cholesterol were observed in mice infected with AdCMV apo A-I compared with control viruses.	Cholesterol	22-33	apolipoprotein A-I	Mus musculus	116-123
8087941-4	1994	A 35% increase in HDL cholesterol and a 47% increase in total cholesterol were observed in mice infected with AdCMV apo A-I compared with control viruses.	Cholesterol	62-73	apolipoprotein A-I	Mus musculus	116-123
7515279-3	1994	We have recently compared six different genetic variants of apo A-I and found that the apo A-I (Pro 165-->Arg) mutant is defective in promoting cellular cholesterol efflux from murine adipocytes and peritoneal macrophages and we have proposed that this region of apo A-I may be involved in their interaction with cells.	Arginine	109-112	apolipoprotein A-I	Mus musculus	60-67
7515279-3	1994	We have recently compared six different genetic variants of apo A-I and found that the apo A-I (Pro 165-->Arg) mutant is defective in promoting cellular cholesterol efflux from murine adipocytes and peritoneal macrophages and we have proposed that this region of apo A-I may be involved in their interaction with cells.	Arginine	109-112	apolipoprotein A-I	Mus musculus	87-94
7515279-3	1994	We have recently compared six different genetic variants of apo A-I and found that the apo A-I (Pro 165-->Arg) mutant is defective in promoting cellular cholesterol efflux from murine adipocytes and peritoneal macrophages and we have proposed that this region of apo A-I may be involved in their interaction with cells.	Arginine	109-112	apolipoprotein A-I	Mus musculus	87-94
7515279-3	1994	We have recently compared six different genetic variants of apo A-I and found that the apo A-I (Pro 165-->Arg) mutant is defective in promoting cellular cholesterol efflux from murine adipocytes and peritoneal macrophages and we have proposed that this region of apo A-I may be involved in their interaction with cells.	Cholesterol	156-167	apolipoprotein A-I	Mus musculus	87-94
7515279-3	1994	We have recently compared six different genetic variants of apo A-I and found that the apo A-I (Pro 165-->Arg) mutant is defective in promoting cellular cholesterol efflux from murine adipocytes and peritoneal macrophages and we have proposed that this region of apo A-I may be involved in their interaction with cells.	Cholesterol	156-167	apolipoprotein A-I	Mus musculus	87-94
8132527-0	1994	Apolipoprotein A-I metabolism in cholesteryl ester transfer protein transgenic mice.	Cholesterol Esters	33-50	apolipoprotein A-I	Mus musculus	0-18
8132527-10	1994	It was concluded that CETP expression enriched the core of the HDL with triglyceride, which rendered it vulnerable to lipolysis, causing apoA-I to be shed from the particle.	Triglycerides	72-84	apolipoprotein A-I	Mus musculus	137-143
8127890-7	1994	Plasma from normal and apoA-I-deficient mice, but not from apoE-deficient mice, released [3H]cholesterol from fibroblasts into a gamma-migrating lipoprotein.	Tritium	90-92	apolipoprotein A-I	Mus musculus	23-29
8127890-7	1994	Plasma from normal and apoA-I-deficient mice, but not from apoE-deficient mice, released [3H]cholesterol from fibroblasts into a gamma-migrating lipoprotein.	Cholesterol	93-104	apolipoprotein A-I	Mus musculus	23-29
8241102-2	1993	Inbred strain 129 mice homozygous for the inactive Apoa1 gene and maintained on regular mouse chow had markedly reduced total cholesterol (26% normal) and high-density lipoprotein (HDL) cholesterol (25% normal) levels in their plasma.	Cholesterol	126-137	apolipoprotein A-I	Mus musculus	51-56
8241102-2	1993	Inbred strain 129 mice homozygous for the inactive Apoa1 gene and maintained on regular mouse chow had markedly reduced total cholesterol (26% normal) and high-density lipoprotein (HDL) cholesterol (25% normal) levels in their plasma.	Cholesterol	186-197	apolipoprotein A-I	Mus musculus	51-56
8428938-1	1993	Evidence for reduced cholesterol efflux promotion by apoA-I(Pro165-->Arg).	Cholesterol	21-32	apolipoprotein A-I	Mus musculus	53-59
8428938-1	1993	Evidence for reduced cholesterol efflux promotion by apoA-I(Pro165-->Arg).	Arginine	72-75	apolipoprotein A-I	Mus musculus	53-59
8428938-2	1993	Interaction of cells with both native and reconstituted high density lipoproteins (rHDL) containing apolipoprotein (apo) A-I mediates efflux of cellular cholesterol.	Cholesterol	153-164	apolipoprotein A-I	Mus musculus	100-124
8428938-6	1993	265, 8610-8617) and demonstrated that all apoA-I variants except apoA-I(Lys107-->0) form discoidal HDL particles with phosphatidylcholine analogues indistinguishable from normal apoA-I (Jonas, A., von Eckardstein, A., Kezdy, K. E., Steinmetz, A., and Assmann, G. (1991) J.	Phosphatidylcholines	121-140	apolipoprotein A-I	Mus musculus	42-48
8428938-9	1993	In the present study, all apoA-I.DMPC complexes except those containing apoA-I(Pro165-->Arg) promoted cholesterol efflux as effectively as those containing normal apoA-I.	Dimyristoylphosphatidylcholine	33-37	apolipoprotein A-I	Mus musculus	26-32
8428938-9	1993	In the present study, all apoA-I.DMPC complexes except those containing apoA-I(Pro165-->Arg) promoted cholesterol efflux as effectively as those containing normal apoA-I.	Arginine	91-94	apolipoprotein A-I	Mus musculus	72-78
8428938-9	1993	In the present study, all apoA-I.DMPC complexes except those containing apoA-I(Pro165-->Arg) promoted cholesterol efflux as effectively as those containing normal apoA-I.	Arginine	91-94	apolipoprotein A-I	Mus musculus	72-78
8428938-9	1993	In the present study, all apoA-I.DMPC complexes except those containing apoA-I(Pro165-->Arg) promoted cholesterol efflux as effectively as those containing normal apoA-I.	Cholesterol	105-116	apolipoprotein A-I	Mus musculus	26-32
8428938-9	1993	In the present study, all apoA-I.DMPC complexes except those containing apoA-I(Pro165-->Arg) promoted cholesterol efflux as effectively as those containing normal apoA-I.	Cholesterol	105-116	apolipoprotein A-I	Mus musculus	72-78
8428938-9	1993	In the present study, all apoA-I.DMPC complexes except those containing apoA-I(Pro165-->Arg) promoted cholesterol efflux as effectively as those containing normal apoA-I.	Cholesterol	105-116	apolipoprotein A-I	Mus musculus	72-78
8428938-10	1993	Cholesterol efflux from adipocytes obtained after 180 min of incubation with apoA-I(Pro165-->Arg).DMPC complexes was decreased by 30% although this variant was bound to adipocytes with normal affinity.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	77-83
8428938-10	1993	Cholesterol efflux from adipocytes obtained after 180 min of incubation with apoA-I(Pro165-->Arg).DMPC complexes was decreased by 30% although this variant was bound to adipocytes with normal affinity.	Arginine	96-99	apolipoprotein A-I	Mus musculus	77-83
8428938-10	1993	Cholesterol efflux from adipocytes obtained after 180 min of incubation with apoA-I(Pro165-->Arg).DMPC complexes was decreased by 30% although this variant was bound to adipocytes with normal affinity.	Dimyristoylphosphatidylcholine	101-105	apolipoprotein A-I	Mus musculus	77-83
8428938-11	1993	By contrast, apoA-I(Lys107-->Met).DMPC complexes were decreased in their binding affinity compared to normal apoA-I.DMPC complexes but normally promoted cholesterol efflux.	Dimyristoylphosphatidylcholine	37-41	apolipoprotein A-I	Mus musculus	13-19
8428938-11	1993	By contrast, apoA-I(Lys107-->Met).DMPC complexes were decreased in their binding affinity compared to normal apoA-I.DMPC complexes but normally promoted cholesterol efflux.	Dimyristoylphosphatidylcholine	37-41	apolipoprotein A-I	Mus musculus	112-118
8428938-11	1993	By contrast, apoA-I(Lys107-->Met).DMPC complexes were decreased in their binding affinity compared to normal apoA-I.DMPC complexes but normally promoted cholesterol efflux.	Dimyristoylphosphatidylcholine	119-123	apolipoprotein A-I	Mus musculus	13-19
8428938-11	1993	By contrast, apoA-I(Lys107-->Met).DMPC complexes were decreased in their binding affinity compared to normal apoA-I.DMPC complexes but normally promoted cholesterol efflux.	Cholesterol	156-167	apolipoprotein A-I	Mus musculus	13-19
8428938-12	1993	Incubation of mouse peritoneal macrophages with apoA-I(Pro165-->Arg).DMPC complexes did also result in a 30% decreased efflux of radiolabeled cholesterol if compared to rHDL with the normal allele product from the same donor.	Arginine	67-70	apolipoprotein A-I	Mus musculus	48-54
8428938-12	1993	Incubation of mouse peritoneal macrophages with apoA-I(Pro165-->Arg).DMPC complexes did also result in a 30% decreased efflux of radiolabeled cholesterol if compared to rHDL with the normal allele product from the same donor.	Dimyristoylphosphatidylcholine	72-76	apolipoprotein A-I	Mus musculus	48-54
8428938-12	1993	Incubation of mouse peritoneal macrophages with apoA-I(Pro165-->Arg).DMPC complexes did also result in a 30% decreased efflux of radiolabeled cholesterol if compared to rHDL with the normal allele product from the same donor.	Cholesterol	145-156	apolipoprotein A-I	Mus musculus	48-54
8428938-13	1993	Together the observations suggest that the substitution of proline at residue 165 interferes with the formation of a structural domain in apoA-I that is crucial for cellular cholesterol efflux stimulation.	Proline	59-66	apolipoprotein A-I	Mus musculus	138-144
8428938-13	1993	Together the observations suggest that the substitution of proline at residue 165 interferes with the formation of a structural domain in apoA-I that is crucial for cellular cholesterol efflux stimulation.	Cholesterol	174-185	apolipoprotein A-I	Mus musculus	138-144
1596514-0	1992	Dietary fatty acids and dietary cholesterol differ in their effect on the in vivo regulation of apolipoprotein A-I and A-II gene expression in inbred strains of mice.	Fatty Acids	8-19	apolipoprotein A-I	Mus musculus	96-114
1596514-0	1992	Dietary fatty acids and dietary cholesterol differ in their effect on the in vivo regulation of apolipoprotein A-I and A-II gene expression in inbred strains of mice.	Cholesterol	32-43	apolipoprotein A-I	Mus musculus	96-114
1596360-2	1992	Apolipoprotein AI, the dominant protein component of serum high density lipoprotein, is intimately involved in cholesterol homeostasis.	Cholesterol	111-122	apolipoprotein A-I	Mus musculus	0-17
1596360-3	1992	Apo AI activates the lecithin-cholesterol acyltransferase within the HDL particle and functions as ligand for a putative HDL receptor--two properties, which render this apolipoprotein a key mediator in reversed cholesterol transport.	Cholesterol	30-41	apolipoprotein A-I	Mus musculus	0-6
1536847-3	1992	The cholesterol removal by the microemulsion was enhanced by some 30% only when apoA-I, -A-II, and -E were present in excess to provide their free forms in the medium, but apoC-III did not show such an effect even by its excess amount.	Cholesterol	4-15	apolipoprotein A-I	Mus musculus	80-101
1536847-9	1992	Thus, the data were consistent with a model that the free form of certain apolipoproteins, such as apoA-I, -A-II, and -E but not apoC-III, generates pre beta-HDL-like particles with cellular lipids in situ and these particles act as mediators for cholesterol transfer from the cells to other lipoproteins.	Cholesterol	247-258	apolipoprotein A-I	Mus musculus	99-120
1764091-0	1991	In vivo regulation of apolipoprotein A-I gene expression by estradiol and testosterone occurs at the translational level in inbred strains of mice.	Estradiol	60-69	apolipoprotein A-I	Mus musculus	22-40
1764091-0	1991	In vivo regulation of apolipoprotein A-I gene expression by estradiol and testosterone occurs at the translational level in inbred strains of mice.	Testosterone	74-86	apolipoprotein A-I	Mus musculus	22-40
1764091-1	1991	Testosterone and estrogen alter the hepatic synthesis of apoA-I in castrated inbred strains of mice, but apoA-I mRNA levels remain unaltered, suggesting post-transcriptional regulation of apoA-I production in liver.	Testosterone	0-12	apolipoprotein A-I	Mus musculus	57-63
1932099-0	1991	Cholesterol efflux from macrophages mediated by high-density lipoprotein subfractions, which differ principally in apolipoprotein A-I and apolipoprotein A-II ratios.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	115-133
1797939-1	1991	We tested the hypothesis that testosterone and estrogen modulate apoA-I gene expression and metabolism by different mechanisms that may be influenced by genetic factors.	Testosterone	30-42	apolipoprotein A-I	Mus musculus	65-71
1797939-13	1991	Testosterone increased and E2H decreased hepatic apoA-I synthesis.	e2h	27-30	apolipoprotein A-I	Mus musculus	49-55
2117920-3	1990	Chromatography of the soluble extract on DEAE-Trisacryl was followed by immunoaffinity chromatography of the complex apolipoprotein AI-binding proteins on anti-(apolipoprotein AI) coupled to Sepharose 4B and then by h.p.l.c.	Sepharose	191-200	apolipoprotein A-I	Mus musculus	117-134
2117920-3	1990	Chromatography of the soluble extract on DEAE-Trisacryl was followed by immunoaffinity chromatography of the complex apolipoprotein AI-binding proteins on anti-(apolipoprotein AI) coupled to Sepharose 4B and then by h.p.l.c.	Sepharose	191-200	apolipoprotein A-I	Mus musculus	161-178
2148897-1	1990	The treatment of HDL3 with malondialdehyde (MDA) results in an increase of the electrophoretic mobility of the particle and in aggregation of the apolipoprotein AI.	Malondialdehyde	27-42	apolipoprotein A-I	Mus musculus	146-163
2148897-1	1990	The treatment of HDL3 with malondialdehyde (MDA) results in an increase of the electrophoretic mobility of the particle and in aggregation of the apolipoprotein AI.	Malondialdehyde	44-47	apolipoprotein A-I	Mus musculus	146-163
19996385-4	2010	The present study showed that treatment with the LXR agonist T0901317 increased lipogenesis and apoA1-dependent cholesterol efflux in LXRalpha KO and WT myotubes but not in LXRbeta KO cells.	Cholesterol	112-123	apolipoprotein A-I	Mus musculus	96-101
34942193-3	2022	ApoA-I, the key apolipoprotein of HDL, was genetically deleted from BCO2 knockout (Bco2-/-) mouse, a macular pigment mouse model capable of accumulating carotenoids in the retina.	Carotenoids	153-164	apolipoprotein A-I	Mus musculus	0-6
34942193-5	2022	HPLC data demonstrated that the total carotenoids were increased in the livers but decreased in the serum, retinal pigment epithelium (RPE)/choroids, and retinas of ApoA-I-/-/Bco2-/- mice compared to Bco2-/- mice.	Carotenoids	38-49	apolipoprotein A-I	Mus musculus	165-171
34942193-7	2022	Furthermore, surface plasmon resonance spectroscopy (SPR) data showed that the binding affinity between ApoA-I and beta-carotene >> zeaxanthin > lutein.	beta Carotene	115-128	apolipoprotein A-I	Mus musculus	104-110
34942193-7	2022	Furthermore, surface plasmon resonance spectroscopy (SPR) data showed that the binding affinity between ApoA-I and beta-carotene >> zeaxanthin > lutein.	Zeaxanthins	132-142	apolipoprotein A-I	Mus musculus	104-110
34942193-7	2022	Furthermore, surface plasmon resonance spectroscopy (SPR) data showed that the binding affinity between ApoA-I and beta-carotene >> zeaxanthin > lutein.	Lutein	145-151	apolipoprotein A-I	Mus musculus	104-110
34942193-8	2022	Our results show that carotenoids are transported from the liver to the eye mainly by HDL, and ApoA-I may be involved in the selective delivery of macular carotenoids to the RPE.	Carotenoids	22-33	apolipoprotein A-I	Mus musculus	95-101
34942193-8	2022	Our results show that carotenoids are transported from the liver to the eye mainly by HDL, and ApoA-I may be involved in the selective delivery of macular carotenoids to the RPE.	Carotenoids	155-166	apolipoprotein A-I	Mus musculus	95-101
34737305-4	2021	ApoA-I increases the antibacterial activity of lysocin E when added in vitro, and the antibiotic displays reduced activity in ApoA-I gene knockout mice.	lysocin E	47-56	apolipoprotein A-I	Mus musculus	0-6
34737305-5	2021	Binding of ApoA-I to lysocin E is enhanced by lipid II, a cell-wall synthesis precursor found in the bacterial membrane.	lysocin E	21-30	apolipoprotein A-I	Mus musculus	11-17
34737305-5	2021	Binding of ApoA-I to lysocin E is enhanced by lipid II, a cell-wall synthesis precursor found in the bacterial membrane.	muramyl-NAc-(pentapeptide)pyrophosphoryl-undecaprenol	46-54	apolipoprotein A-I	Mus musculus	11-17
34716267-6	2021	While the adsorbed Apo A-I ameliorated the cytotoxic and proinflammatory effects of SiNPs, the protein was eliminated from the blood upon clearance of the NPs.	sinps	84-89	apolipoprotein A-I	Mus musculus	19-26
34716267-7	2021	However, supplementation of Apo A-I mimic peptide mitigated the atherosclerotic lesion induced by SiNPs.	sinps	98-103	apolipoprotein A-I	Mus musculus	28-35
34416563-8	2021	The cholesterol metabolism pathway was significantly enriched in the KEGG pathway analysis, and there was lower expression of three apolipoprotein genes (Apoa1, Apoa2, and Apoc3) at CT2 in the testes of Bmal1-/- mice than in those of WT mice.	Cholesterol	4-15	apolipoprotein A-I	Mus musculus	154-159
34416563-13	2021	Considering the vital role of Apo genes in high-density lipoprotein formation and cholesterol transport, the present data suggest that the circadian clock system regulates testosterone production by orchestrating the rhythmic expression of Apo genes.	Cholesterol	82-93	apolipoprotein A-I	Mus musculus	30-33
34416563-13	2021	Considering the vital role of Apo genes in high-density lipoprotein formation and cholesterol transport, the present data suggest that the circadian clock system regulates testosterone production by orchestrating the rhythmic expression of Apo genes.	Cholesterol	82-93	apolipoprotein A-I	Mus musculus	240-243
34416563-13	2021	Considering the vital role of Apo genes in high-density lipoprotein formation and cholesterol transport, the present data suggest that the circadian clock system regulates testosterone production by orchestrating the rhythmic expression of Apo genes.	Testosterone	172-184	apolipoprotein A-I	Mus musculus	30-33
34416563-13	2021	Considering the vital role of Apo genes in high-density lipoprotein formation and cholesterol transport, the present data suggest that the circadian clock system regulates testosterone production by orchestrating the rhythmic expression of Apo genes.	Testosterone	172-184	apolipoprotein A-I	Mus musculus	240-243
34364980-8	2021	Proteomics demonstrated the presence of MDA adducts on Lysine residues of HDL proteins, mainly ApoA-I.	Lysine	55-61	apolipoprotein A-I	Mus musculus	95-101
34660746-11	2021	SBC-115076 used to inhibit PCSK9 largely alleviated lipid accumulation and reversed the cholesterol efflux to apolipoprotein-I(apoA-I) and high-density lipoprotein (HDL) mediated by ABCA1 and ABCG1.	Cholesterol	88-99	apolipoprotein A-I	Mus musculus	127-133
34926792-7	2021	Further, the ApoA1-LXR PA nanofibers targeted plaque within an atherosclerotic mouse model in vivo and activated ATP-binding cassette A1 (ABCA1) expression as well as LXR alone with reduced liver toxicity.	Protactinium	23-25	apolipoprotein A-I	Mus musculus	13-18
34733976-2	2021	Apolipoprotein A-1 (ApoA-1) has been reported to ameliorate the bleomycin (BLM)-induced IPF model.	Bleomycin	64-73	apolipoprotein A-I	Mus musculus	0-18
34733976-2	2021	Apolipoprotein A-1 (ApoA-1) has been reported to ameliorate the bleomycin (BLM)-induced IPF model.	Bleomycin	64-73	apolipoprotein A-I	Mus musculus	20-26
34733976-2	2021	Apolipoprotein A-1 (ApoA-1) has been reported to ameliorate the bleomycin (BLM)-induced IPF model.	Bleomycin	75-78	apolipoprotein A-I	Mus musculus	0-18
34733976-2	2021	Apolipoprotein A-1 (ApoA-1) has been reported to ameliorate the bleomycin (BLM)-induced IPF model.	Bleomycin	75-78	apolipoprotein A-I	Mus musculus	20-26
34422975-11	2021	High-level PON1 increased the antioxidative and anti-inflammatory properties, promoted HDL maturation and macrophage cholesterol efflux through increasing HDL functional proteins components apolipoprotein A1 (APOA1), apolipoprotein E (APOE), and lecithin-cholesterol acyltransferase (LCAT), while decreased inflammatory protein markers, such as serum amyloid A (SAA), apolipoprotein A4 (APOA4) and alpha 1 antitrypsin (A1AT).	Cholesterol	117-128	apolipoprotein A-I	Mus musculus	190-207
34095317-1	2021	Background and Aims: Apolipoprotein A-I (ApoA-I), the main component of high-density lipoprotein (HDL), not only promotes reverse cholesterol transport (RCT) in atherosclerosis but also increases insulin secretion in pancreatic beta-cells, suggesting that interventions which raise HDL levels may be beneficial in diabetes-associated cardiovascular disease (CVD).	Cholesterol	130-141	apolipoprotein A-I	Mus musculus	21-39
34095317-1	2021	Background and Aims: Apolipoprotein A-I (ApoA-I), the main component of high-density lipoprotein (HDL), not only promotes reverse cholesterol transport (RCT) in atherosclerosis but also increases insulin secretion in pancreatic beta-cells, suggesting that interventions which raise HDL levels may be beneficial in diabetes-associated cardiovascular disease (CVD).	Cholesterol	130-141	apolipoprotein A-I	Mus musculus	41-47
35611698-5	2022	METHODS AND RESULTS: Loss of miR-223 in macrophages decreases Abca1 gene and protein expression as well as cholesterol efflux to apoA1 (Apolipoprotein A1) and enhances proinflammatory gene expression.	Cholesterol	107-118	apolipoprotein A-I	Mus musculus	129-134
35611698-5	2022	METHODS AND RESULTS: Loss of miR-223 in macrophages decreases Abca1 gene and protein expression as well as cholesterol efflux to apoA1 (Apolipoprotein A1) and enhances proinflammatory gene expression.	Cholesterol	107-118	apolipoprotein A-I	Mus musculus	136-153
35587694-1	2022	BACKGROUND: HDL (High-density lipoprotein) and its major protein component, apoA-I (apolipoprotein A-I), play a unique role in cholesterol homeostasis and immunity.	Cholesterol	127-138	apolipoprotein A-I	Mus musculus	76-82
35587694-1	2022	BACKGROUND: HDL (High-density lipoprotein) and its major protein component, apoA-I (apolipoprotein A-I), play a unique role in cholesterol homeostasis and immunity.	Cholesterol	127-138	apolipoprotein A-I	Mus musculus	84-102
35563223-2	2022	APOA1 is a central regulator of high-density lipoprotein cholesterol (HDL-C) metabolism, and thus HDL; our recent work showed that deficiency of APOA1 increases bone marrow adiposity in mice.	Cholesterol	57-68	apolipoprotein A-I	Mus musculus	0-5
35563223-2	2022	APOA1 is a central regulator of high-density lipoprotein cholesterol (HDL-C) metabolism, and thus HDL; our recent work showed that deficiency of APOA1 increases bone marrow adiposity in mice.	Cholesterol	57-68	apolipoprotein A-I	Mus musculus	145-150
35453650-4	2022	The results showed that apolipoprotein A1 (ApoA1)-modified liposomes (BAA1) significantly enhanced BA"s cellular uptake and specific distribution in the liver.	baicalin	99-101	apolipoprotein A-I	Mus musculus	24-41
35453650-4	2022	The results showed that apolipoprotein A1 (ApoA1)-modified liposomes (BAA1) significantly enhanced BA"s cellular uptake and specific distribution in the liver.	baicalin	99-101	apolipoprotein A-I	Mus musculus	43-48
35453650-7	2022	Based on the findings, we propose that the ApoA1-modified liposomes aid BA in inhibiting HBV transcription and replication by augmenting its bioavailability and the HNFs-ERs axis.	baicalin	72-74	apolipoprotein A-I	Mus musculus	43-48
35078048-3	2022	In vitro and in vivo assays revealed that the lead compound (E)-4-styrylphenoxy-propanamide (5b) removed 14C-cholesterol from the foam cells through apolipoprotein A-I and High-Density Lipoprotein-2.	(e)-4-styrylphenoxy-propanamide	60-91	apolipoprotein A-I	Mus musculus	149-167
35078048-3	2022	In vitro and in vivo assays revealed that the lead compound (E)-4-styrylphenoxy-propanamide (5b) removed 14C-cholesterol from the foam cells through apolipoprotein A-I and High-Density Lipoprotein-2.	14c-cholesterol	105-120	apolipoprotein A-I	Mus musculus	149-167
35120132-5	2022	In males and females, lesion progression was studied over time, and both apoA1 and 4WF transgenic mice vs. LDLr KO mice had significant and similar delayed lesion progression and reduced non-HDL cholesterol.	Cholesterol	195-206	apolipoprotein A-I	Mus musculus	73-78
35237969-7	2022	While lipid-free ApoA-1 mediates ChE via only ATP-binding cassette (ABC)A1 transporter, the remaining acceptors mediate ChE via ABCA1 , ABCG1 and scavenger receptor class B type 1 (SRB1) transporters.	che	33-36	apolipoprotein A-I	Mus musculus	17-23
3129297-3	1988	Transfection of mouse C127 cells with a recombinant vector containing the Tangier apoA-I gene (pSV2-gpt apoA-I) allowed selection of stable clones resistant to aminopterin and mycophenolic acid.	Aminopterin	160-171	apolipoprotein A-I	Mus musculus	82-88
3129297-3	1988	Transfection of mouse C127 cells with a recombinant vector containing the Tangier apoA-I gene (pSV2-gpt apoA-I) allowed selection of stable clones resistant to aminopterin and mycophenolic acid.	Aminopterin	160-171	apolipoprotein A-I	Mus musculus	104-110
3129297-3	1988	Transfection of mouse C127 cells with a recombinant vector containing the Tangier apoA-I gene (pSV2-gpt apoA-I) allowed selection of stable clones resistant to aminopterin and mycophenolic acid.	Mycophenolic Acid	176-193	apolipoprotein A-I	Mus musculus	82-88
3129297-3	1988	Transfection of mouse C127 cells with a recombinant vector containing the Tangier apoA-I gene (pSV2-gpt apoA-I) allowed selection of stable clones resistant to aminopterin and mycophenolic acid.	Mycophenolic Acid	176-193	apolipoprotein A-I	Mus musculus	104-110
2829803-4	1988	We demonstrated that apolipoprotein A-I containing high density lipoproteins (HDL) bind to specific receptor sites on macrophages, are internalized, take up cholesterol, and are then released from the cells as native lipoproteins.	Cholesterol	157-168	apolipoprotein A-I	Mus musculus	21-39
3017445-6	1986	The binding of 125I-labeled apolipoprotein AI- and 125I-labeled apolipoprotein AII-containing liposomes was competitively inhibited by HDL3, apolipoprotein AI- and apolipoprotein AII-containing liposomes.	Iodine-125	15-19	apolipoprotein A-I	Mus musculus	28-45
6572912-6	1983	Finally, we show that there is a differential effect of a diet high in saturated fat and cholesterol on apo A-1 mRNA levels in liver and small intestine.	saturated fat	71-84	apolipoprotein A-I	Mus musculus	104-111
6572912-6	1983	Finally, we show that there is a differential effect of a diet high in saturated fat and cholesterol on apo A-1 mRNA levels in liver and small intestine.	Cholesterol	89-100	apolipoprotein A-I	Mus musculus	104-111
33441025-5	2021	It promotes cholesterol efflux to apo AI in macrophage cells, and this effect depends on ABCA1.	Cholesterol	12-23	apolipoprotein A-I	Mus musculus	34-40
33983968-15	2021	Atorvastatin combined with GRT significantly downregulated mRNA expression of Apoa1 (p = 0.03), whilst upregulating the expression of Ppargamma (p = 0.03), Pparalpha (p = 0.002), Srebp1 (p = 0.002), and Fasn (p = 0.04).	Atorvastatin	0-12	apolipoprotein A-I	Mus musculus	78-83
33983968-16	2021	The GRT-pioglitazone-atorvastatin combination therapy downregulated Apoa1 (p = 0.006), whilst upregulating Fasn (p = 0.005), Pparalpha (p = 0.041), and Srebp1 (p = 0.03).	Pioglitazone	8-20	apolipoprotein A-I	Mus musculus	68-73
33983968-16	2021	The GRT-pioglitazone-atorvastatin combination therapy downregulated Apoa1 (p = 0.006), whilst upregulating Fasn (p = 0.005), Pparalpha (p = 0.041), and Srebp1 (p = 0.03).	Atorvastatin	21-33	apolipoprotein A-I	Mus musculus	68-73
33861588-8	2021	Our observations suggest that oxidative damage of apoA-I and HDL involves MPO-dependent site-specific tyrosine chlorination, raising the feasibility of producing MPO-resistant forms of apoA-I that have stronger antiatherosclerotic activity in vivo.	Tyrosine	102-110	apolipoprotein A-I	Mus musculus	50-56
33861588-8	2021	Our observations suggest that oxidative damage of apoA-I and HDL involves MPO-dependent site-specific tyrosine chlorination, raising the feasibility of producing MPO-resistant forms of apoA-I that have stronger antiatherosclerotic activity in vivo.	Tyrosine	102-110	apolipoprotein A-I	Mus musculus	185-191
33924461-5	2021	In the fed state, niacin increased expression of apolipoprotein-A1 mRNA and decreased sterol regulatory element-binding protein 1 mRNA independent of genotype, suggesting a possible GPR109a independent mechanism by which niacin increases high-density lipoprotein (HDL) production and limits transcriptional upregulation of lipogenic genes.	Niacin	18-24	apolipoprotein A-I	Mus musculus	49-66
33650825-2	2021	Here, we have investigated whether cyclodextrin (CD) and apolipoprotein A-I (apoA-I) induce the same signal to inhibit cell cholesterol accumulation by focusing on the main proteins involved in cholesterol homeostasis in response to CD and apoA-I treatment.	Cyclodextrins	35-47	apolipoprotein A-I	Mus musculus	240-246
33650825-2	2021	Here, we have investigated whether cyclodextrin (CD) and apolipoprotein A-I (apoA-I) induce the same signal to inhibit cell cholesterol accumulation by focusing on the main proteins involved in cholesterol homeostasis in response to CD and apoA-I treatment.	Cholesterol	124-135	apolipoprotein A-I	Mus musculus	77-83
33650825-2	2021	Here, we have investigated whether cyclodextrin (CD) and apolipoprotein A-I (apoA-I) induce the same signal to inhibit cell cholesterol accumulation by focusing on the main proteins involved in cholesterol homeostasis in response to CD and apoA-I treatment.	Cholesterol	194-205	apolipoprotein A-I	Mus musculus	77-83
33650825-2	2021	Here, we have investigated whether cyclodextrin (CD) and apolipoprotein A-I (apoA-I) induce the same signal to inhibit cell cholesterol accumulation by focusing on the main proteins involved in cholesterol homeostasis in response to CD and apoA-I treatment.	Cyclodextrins	233-235	apolipoprotein A-I	Mus musculus	77-83
33650825-7	2021	Both apoA-I and CD increased cholesterol release in the medium.	Cholesterol	29-40	apolipoprotein A-I	Mus musculus	5-11
33650825-9	2021	Conclusion: CD, like apoA-I, depletes cellular cholesterol.	Cyclodextrins	12-14	apolipoprotein A-I	Mus musculus	21-27
33650825-9	2021	Conclusion: CD, like apoA-I, depletes cellular cholesterol.	Cholesterol	47-58	apolipoprotein A-I	Mus musculus	21-27
33650825-10	2021	This depletion occurs in a different way from apoA-I that is through cholesterol efflux.	Cholesterol	69-80	apolipoprotein A-I	Mus musculus	46-52
33050984-6	2021	The co-administration of RAPA and ATV improved the serum lipid profile and raised the expression levels of proteins involved in reverse cholesterol transport (LXRalpha, CYP7A1, ABCG1, PPARgamma, ApoA1) in the liver.	Sirolimus	25-29	apolipoprotein A-I	Mus musculus	195-200
33050984-6	2021	The co-administration of RAPA and ATV improved the serum lipid profile and raised the expression levels of proteins involved in reverse cholesterol transport (LXRalpha, CYP7A1, ABCG1, PPARgamma, ApoA1) in the liver.	Atorvastatin	34-37	apolipoprotein A-I	Mus musculus	195-200
33050984-6	2021	The co-administration of RAPA and ATV improved the serum lipid profile and raised the expression levels of proteins involved in reverse cholesterol transport (LXRalpha, CYP7A1, ABCG1, PPARgamma, ApoA1) in the liver.	Cholesterol	136-147	apolipoprotein A-I	Mus musculus	195-200
33327742-8	2021	The reduced atherosclerotic burden in the aorta of EKO mice expressing high levels of apoA-I was accompanied by a reduced activation of immune system markers, as well as reduced perturbation of lysosomal activity and a better regulation of the sphingolipid synthesis pathway.	Sphingolipids	244-256	apolipoprotein A-I	Mus musculus	86-92
33483533-6	2021	We found that cholesterol depletion was accompanied by a substantial decrease in HDL cholesterol mediated by lowered ApoA-I and ApoA-II protein levels and not by inhibited lecithin-cholesterol transferase activity.	Cholesterol	14-25	apolipoprotein A-I	Mus musculus	117-123
33483533-6	2021	We found that cholesterol depletion was accompanied by a substantial decrease in HDL cholesterol mediated by lowered ApoA-I and ApoA-II protein levels and not by inhibited lecithin-cholesterol transferase activity.	Cholesterol	85-96	apolipoprotein A-I	Mus musculus	117-123
33483533-6	2021	We found that cholesterol depletion was accompanied by a substantial decrease in HDL cholesterol mediated by lowered ApoA-I and ApoA-II protein levels and not by inhibited lecithin-cholesterol transferase activity.	Cholesterol	85-96	apolipoprotein A-I	Mus musculus	117-123
33086869-7	2020	Treatment of pancreatic alphaTC1 clone 6 cells with HDL or ApoA-1 for 24 hours resulted in a significant reduction of glucagon expression (P<0.04) and secretion (P<0.01) after an hypoglycemic stimulus and increased Akt (RAC-alpha serine/threonine-protein kinase) and FoxO1 (forkhead/winged helix box gene, group O-1) phosphorylation.	Serine	230-236	apolipoprotein A-I	Mus musculus	59-65
32810603-8	2020	CONCLUSION: Studies of DMPC microsolubilization show that proline residues are essential to the optimal interaction of APOA1 with membranes, the initial step in cholesterol efflux and HDL production.	Dimyristoylphosphatidylcholine	23-27	apolipoprotein A-I	Mus musculus	119-124
32810603-8	2020	CONCLUSION: Studies of DMPC microsolubilization show that proline residues are essential to the optimal interaction of APOA1 with membranes, the initial step in cholesterol efflux and HDL production.	Proline	58-65	apolipoprotein A-I	Mus musculus	119-124
32810603-8	2020	CONCLUSION: Studies of DMPC microsolubilization show that proline residues are essential to the optimal interaction of APOA1 with membranes, the initial step in cholesterol efflux and HDL production.	Cholesterol	161-172	apolipoprotein A-I	Mus musculus	119-124
32810603-9	2020	In contrast, P A substitutions modestly reduce the cholesterol efflux capacity of APOA1, have no effect on LCAT activation, but according to the profound reduction in the size of HDL formed in vivo, P A substitutions alter HDL biogenesis, thereby implicating other cellular and in vivo processes as determinants of HDL metabolism and function.	Cholesterol	51-62	apolipoprotein A-I	Mus musculus	82-87
32241173-3	2020	The objective of the study was to develop a novel stabilized d-rHDL by replacing cholesterol and apoA-I with mono-cholesterol glutarate (MCG) modified apoA-I (termed as mA) and to evaluate its allosteric behavior and glioma targeting.	mono-cholesterol glutarate	109-135	apolipoprotein A-I	Mus musculus	151-157
33093642-0	2020	A short peptide of the C-terminal class Y helices of apolipoprotein A-I has preserved functions in cholesterol efflux and in vivo metabolic control.	Cholesterol	99-110	apolipoprotein A-I	Mus musculus	53-71
33093642-1	2020	Apolipoprotein A-I (ApoA-I) of high-density lipoprotein (HDL) induces glucose uptake by muscle tissues and stimulates pancreatic insulin secretion, and also facilitates cholesterol transport in circulation, and is explored for anti-diabetic and anti-atherosclerotic treatments.	Glucose	70-77	apolipoprotein A-I	Mus musculus	0-18
33093642-1	2020	Apolipoprotein A-I (ApoA-I) of high-density lipoprotein (HDL) induces glucose uptake by muscle tissues and stimulates pancreatic insulin secretion, and also facilitates cholesterol transport in circulation, and is explored for anti-diabetic and anti-atherosclerotic treatments.	Glucose	70-77	apolipoprotein A-I	Mus musculus	20-26
33093642-1	2020	Apolipoprotein A-I (ApoA-I) of high-density lipoprotein (HDL) induces glucose uptake by muscle tissues and stimulates pancreatic insulin secretion, and also facilitates cholesterol transport in circulation, and is explored for anti-diabetic and anti-atherosclerotic treatments.	Cholesterol	169-180	apolipoprotein A-I	Mus musculus	0-18
33093642-1	2020	Apolipoprotein A-I (ApoA-I) of high-density lipoprotein (HDL) induces glucose uptake by muscle tissues and stimulates pancreatic insulin secretion, and also facilitates cholesterol transport in circulation, and is explored for anti-diabetic and anti-atherosclerotic treatments.	Cholesterol	169-180	apolipoprotein A-I	Mus musculus	20-26
33093642-4	2020	We here investigate a short peptide (33mer, RG33) that corresponds to the two last helical segments (aa 209-241) of the ApoA-I structure (so-called class Y-helices which forms amphipathic helices) for stability and solubility in serum, for in vitro cholesterol efflux capability, and for providing in vivo glucose control in an insulin resistant mouse model.	rg33	44-48	apolipoprotein A-I	Mus musculus	120-126
33093642-4	2020	We here investigate a short peptide (33mer, RG33) that corresponds to the two last helical segments (aa 209-241) of the ApoA-I structure (so-called class Y-helices which forms amphipathic helices) for stability and solubility in serum, for in vitro cholesterol efflux capability, and for providing in vivo glucose control in an insulin resistant mouse model.	Cholesterol	249-260	apolipoprotein A-I	Mus musculus	120-126
33093642-4	2020	We here investigate a short peptide (33mer, RG33) that corresponds to the two last helical segments (aa 209-241) of the ApoA-I structure (so-called class Y-helices which forms amphipathic helices) for stability and solubility in serum, for in vitro cholesterol efflux capability, and for providing in vivo glucose control in an insulin resistant mouse model.	Glucose	306-313	apolipoprotein A-I	Mus musculus	120-126
32726461-1	2020	BACKGROUND AND PURPOSE: Apolipoprotein A-I (apoA-I) mimetic peptides (AMPs) are short peptides that can mimic the physiological effects of apoA-I, including the suppression of atherosclerosis by reversely transporting peripheral cholesterol to the liver.	Cholesterol	229-240	apolipoprotein A-I	Mus musculus	24-42
32726461-1	2020	BACKGROUND AND PURPOSE: Apolipoprotein A-I (apoA-I) mimetic peptides (AMPs) are short peptides that can mimic the physiological effects of apoA-I, including the suppression of atherosclerosis by reversely transporting peripheral cholesterol to the liver.	Cholesterol	229-240	apolipoprotein A-I	Mus musculus	44-50
32726461-1	2020	BACKGROUND AND PURPOSE: Apolipoprotein A-I (apoA-I) mimetic peptides (AMPs) are short peptides that can mimic the physiological effects of apoA-I, including the suppression of atherosclerosis by reversely transporting peripheral cholesterol to the liver.	Cholesterol	229-240	apolipoprotein A-I	Mus musculus	139-145
32726461-2	2020	As the hydrophobicity of apoA-I is considered important for its lipid transport, novel AMPs were designed and synthesized in this study by gradually increasing the hydrophobicity of the parent peptide and their anti-atherosclerotic effects were tested.	adenosine 5'-phosphorothioate	87-91	apolipoprotein A-I	Mus musculus	25-31
32726461-3	2020	EXPERIMENTAL APPROACH: Seventeen new AMPs (P1-P17) with incrementally increased hydrophobicity were designed and synthesized by replacing the amino acids 221-240 of apoA-I (VLESFKVSFLSALEEYTKKL).	adenosine 5'-phosphorothioate	37-41	apolipoprotein A-I	Mus musculus	165-171
32681583-8	2020	Furthermore, we unveil ApoA1"s beneficial impact on cell viability and calcium homeostasis of cultured enteric neurons of 5xFAD animals.	Calcium	71-78	apolipoprotein A-I	Mus musculus	23-28
32713273-9	2020	Administration of an apoA-I (apolipoprotein A-I) mimetic peptide, Tg6F (transgenic 6F), which is known to prevent accumulation of circulating oxidized lipids, not only inhibited pulmonary arterial endothelial cell apoptosis but also prevented and rescued 15-HETE-induced pulmonary hypertension in mice.	15-Hete	255-262	apolipoprotein A-I	Mus musculus	21-27
32713273-9	2020	Administration of an apoA-I (apolipoprotein A-I) mimetic peptide, Tg6F (transgenic 6F), which is known to prevent accumulation of circulating oxidized lipids, not only inhibited pulmonary arterial endothelial cell apoptosis but also prevented and rescued 15-HETE-induced pulmonary hypertension in mice.	15-Hete	255-262	apolipoprotein A-I	Mus musculus	29-47
32678293-3	2020	We explore the unique property of the apolipoprotein A-I (apoA-I) binding protein (AIBP) that enhances cholesterol efflux from endothelial cells and macrophages to thereby limit angiogenesis and inflammation to tackle anti-VEGF resistance in CNV.	Cholesterol	103-114	apolipoprotein A-I	Mus musculus	38-56
32685494-11	2020	Further, we found that HT might regulate cholesterol metabolism via decreasing phosphorylation of p38, followed by activation of AMPK and inactivation of NF-kappaB, which in turn triggered the blockade of SREBP2/PCSK9 and upregulation of LDLR, apoAI, and ABCA1, finally leading to a reduction of LDL-C and increase of HDL-C in the circulation.	Cholesterol	41-52	apolipoprotein A-I	Mus musculus	244-249
32092318-5	2020	Endogenous ApoA-I in macrophages has anti-inflammatory and cholesterol efflux effects.	Cholesterol	59-70	apolipoprotein A-I	Mus musculus	11-17
32244181-0	2020	ApoA-1 improves glucose tolerance by increasing glucose uptake into heart and skeletal muscle independently of AMPKalpha2.	Glucose	16-23	apolipoprotein A-I	Mus musculus	0-6
32244181-0	2020	ApoA-1 improves glucose tolerance by increasing glucose uptake into heart and skeletal muscle independently of AMPKalpha2.	Glucose	48-55	apolipoprotein A-I	Mus musculus	0-6
32244181-1	2020	OBJECTIVE: Acute administration of the main protein component of high-density lipoprotein, apolipoprotein A-I (ApoA-1), improves glucose uptake in skeletal muscle.	Glucose	129-136	apolipoprotein A-I	Mus musculus	91-109
32244181-1	2020	OBJECTIVE: Acute administration of the main protein component of high-density lipoprotein, apolipoprotein A-I (ApoA-1), improves glucose uptake in skeletal muscle.	Glucose	129-136	apolipoprotein A-I	Mus musculus	111-117
32244181-3	2020	We therefore investigated whether AMPK is necessary for ApoA-1-stimulated glucose uptake in intact heart and skeletal muscle in vivo.	Glucose	74-81	apolipoprotein A-I	Mus musculus	56-62
32244181-12	2020	CONCLUSIONS: In conclusion, ApoA-1 stimulates in vivo glucose disposal into skeletal and heart muscle independently of AMPKalpha2.	Glucose	54-61	apolipoprotein A-I	Mus musculus	28-34
32084429-1	2020	BACKGROUND: Apolipoprotein A-I (ApoA-I) is involved in reverse cholesterol transport as a major component of HDL, but also conveys anti-thrombotic, anti-oxidative, anti-inflammatory and immune-regulatory properties that are pertinent to its protective roles in cardiovascular, inflammatory and malignant pathologies.	Cholesterol	63-74	apolipoprotein A-I	Mus musculus	12-30
32084429-1	2020	BACKGROUND: Apolipoprotein A-I (ApoA-I) is involved in reverse cholesterol transport as a major component of HDL, but also conveys anti-thrombotic, anti-oxidative, anti-inflammatory and immune-regulatory properties that are pertinent to its protective roles in cardiovascular, inflammatory and malignant pathologies.	Cholesterol	63-74	apolipoprotein A-I	Mus musculus	32-38
32084429-10	2020	Given the established role of ApoA-I in HDL-mediated reverse cholesterol transport, this mode of ApoA-I regulation may reflect a hepatocellular response to the organismal requirement for maintenance of cholesterol and lipid reserves under conditions of nutrient scarcity.	Cholesterol	61-72	apolipoprotein A-I	Mus musculus	30-36
32084429-10	2020	Given the established role of ApoA-I in HDL-mediated reverse cholesterol transport, this mode of ApoA-I regulation may reflect a hepatocellular response to the organismal requirement for maintenance of cholesterol and lipid reserves under conditions of nutrient scarcity.	Cholesterol	61-72	apolipoprotein A-I	Mus musculus	97-103
32084429-10	2020	Given the established role of ApoA-I in HDL-mediated reverse cholesterol transport, this mode of ApoA-I regulation may reflect a hepatocellular response to the organismal requirement for maintenance of cholesterol and lipid reserves under conditions of nutrient scarcity.	Cholesterol	202-213	apolipoprotein A-I	Mus musculus	97-103
33479646-1	2020	ATP binding cassette transporter A1 (ABCA1) is a critical transporter that mediates cellular cholesterol efflux from macrophages to apolipoprotein A-I (ApoA-I).	Cholesterol	93-104	apolipoprotein A-I	Mus musculus	132-150
33479646-1	2020	ATP binding cassette transporter A1 (ABCA1) is a critical transporter that mediates cellular cholesterol efflux from macrophages to apolipoprotein A-I (ApoA-I).	Cholesterol	93-104	apolipoprotein A-I	Mus musculus	152-158
31765698-6	2020	In high glucose environment, pre-incubation of beta cells and isolated murine islets with ApoA-I augmented insulin secretion.	Glucose	8-15	apolipoprotein A-I	Mus musculus	90-96
31907281-10	2020	We further detected oxPL cross-link adducts of HDL apoproteins in plasma and aorta of hyperlipidemic LDLR-/- mice, including cross-link adducts of apoA-I His-165-apoA-I Lys-93, apoA-I His-154-apoA-I Lys-105, apoA-I His-154-apoA-IV Lys-149, and apoA-II Lys-30-apoE His-227.	His-His-His-His-His-His	154-157	apolipoprotein A-I	Mus musculus	147-153
31907281-10	2020	We further detected oxPL cross-link adducts of HDL apoproteins in plasma and aorta of hyperlipidemic LDLR-/- mice, including cross-link adducts of apoA-I His-165-apoA-I Lys-93, apoA-I His-154-apoA-I Lys-105, apoA-I His-154-apoA-IV Lys-149, and apoA-II Lys-30-apoE His-227.	pentalysine	169-172	apolipoprotein A-I	Mus musculus	147-153
31907281-10	2020	We further detected oxPL cross-link adducts of HDL apoproteins in plasma and aorta of hyperlipidemic LDLR-/- mice, including cross-link adducts of apoA-I His-165-apoA-I Lys-93, apoA-I His-154-apoA-I Lys-105, apoA-I His-154-apoA-IV Lys-149, and apoA-II Lys-30-apoE His-227.	His-His-His-His-His-His	184-187	apolipoprotein A-I	Mus musculus	147-153
31907281-10	2020	We further detected oxPL cross-link adducts of HDL apoproteins in plasma and aorta of hyperlipidemic LDLR-/- mice, including cross-link adducts of apoA-I His-165-apoA-I Lys-93, apoA-I His-154-apoA-I Lys-105, apoA-I His-154-apoA-IV Lys-149, and apoA-II Lys-30-apoE His-227.	pentalysine	199-202	apolipoprotein A-I	Mus musculus	147-153
31907281-10	2020	We further detected oxPL cross-link adducts of HDL apoproteins in plasma and aorta of hyperlipidemic LDLR-/- mice, including cross-link adducts of apoA-I His-165-apoA-I Lys-93, apoA-I His-154-apoA-I Lys-105, apoA-I His-154-apoA-IV Lys-149, and apoA-II Lys-30-apoE His-227.	His-His-His-His-His-His	184-187	apolipoprotein A-I	Mus musculus	147-153
31907281-10	2020	We further detected oxPL cross-link adducts of HDL apoproteins in plasma and aorta of hyperlipidemic LDLR-/- mice, including cross-link adducts of apoA-I His-165-apoA-I Lys-93, apoA-I His-154-apoA-I Lys-105, apoA-I His-154-apoA-IV Lys-149, and apoA-II Lys-30-apoE His-227.	pentalysine	199-202	apolipoprotein A-I	Mus musculus	147-153
31907281-10	2020	We further detected oxPL cross-link adducts of HDL apoproteins in plasma and aorta of hyperlipidemic LDLR-/- mice, including cross-link adducts of apoA-I His-165-apoA-I Lys-93, apoA-I His-154-apoA-I Lys-105, apoA-I His-154-apoA-IV Lys-149, and apoA-II Lys-30-apoE His-227.	pentalysine	199-202	apolipoprotein A-I	Mus musculus	147-153
31907281-10	2020	We further detected oxPL cross-link adducts of HDL apoproteins in plasma and aorta of hyperlipidemic LDLR-/- mice, including cross-link adducts of apoA-I His-165-apoA-I Lys-93, apoA-I His-154-apoA-I Lys-105, apoA-I His-154-apoA-IV Lys-149, and apoA-II Lys-30-apoE His-227.	His-His-His-His-His-His	184-187	apolipoprotein A-I	Mus musculus	147-153
31914125-8	2020	RESULTS: Treatment with apo-AI mimetic peptides D-4F and L-5F showed: (i) improved blood glucose clearance (D-4F 1.40-fold AUC decrease compared to HFD, P<0.05; L-4F 1.17-fold AUC decrease compared to HFD, ns) in the glucose tolerance test; (ii) improved insulin tolerance (D-4F 1.63-fold AUC decrease compared to HFD, P<0.05; L-5F 1.39-fold AUC compared to HFD, P<0.05) in the insulin tolerance test.	Glucose	89-96	apolipoprotein A-I	Mus musculus	24-30
31914125-8	2020	RESULTS: Treatment with apo-AI mimetic peptides D-4F and L-5F showed: (i) improved blood glucose clearance (D-4F 1.40-fold AUC decrease compared to HFD, P<0.05; L-4F 1.17-fold AUC decrease compared to HFD, ns) in the glucose tolerance test; (ii) improved insulin tolerance (D-4F 1.63-fold AUC decrease compared to HFD, P<0.05; L-5F 1.39-fold AUC compared to HFD, P<0.05) in the insulin tolerance test.	Glucose	217-224	apolipoprotein A-I	Mus musculus	24-30
31914125-10	2020	CONCLUSION: Apo-AI mimetic peptides treatment led to improved glucose homeostasis.	Peptides	27-35	apolipoprotein A-I	Mus musculus	12-18
31660677-7	2020	Tryptophan-fluorescence-quenching assay showed that lyso-DGTS interacts spontaneously with the entire HDL lipoprotein and with apolipoprotein A1 (ApoA1), the major structural and functional HDL protein, with high affinity (Ka = 2.17 x 104  M-1 at 37 C).	Tryptophan	0-10	apolipoprotein A-I	Mus musculus	127-144
31660677-7	2020	Tryptophan-fluorescence-quenching assay showed that lyso-DGTS interacts spontaneously with the entire HDL lipoprotein and with apolipoprotein A1 (ApoA1), the major structural and functional HDL protein, with high affinity (Ka = 2.17 x 104  M-1 at 37 C).	Tryptophan	0-10	apolipoprotein A-I	Mus musculus	146-151
31660677-7	2020	Tryptophan-fluorescence-quenching assay showed that lyso-DGTS interacts spontaneously with the entire HDL lipoprotein and with apolipoprotein A1 (ApoA1), the major structural and functional HDL protein, with high affinity (Ka = 2.17 x 104  M-1 at 37 C).	1(3),2-diacylglyceryl-3(1)-O-4'-(N,N,N-trimethyl)homoserine	52-61	apolipoprotein A-I	Mus musculus	127-144
31660677-7	2020	Tryptophan-fluorescence-quenching assay showed that lyso-DGTS interacts spontaneously with the entire HDL lipoprotein and with apolipoprotein A1 (ApoA1), the major structural and functional HDL protein, with high affinity (Ka = 2.17 x 104  M-1 at 37 C).	1(3),2-diacylglyceryl-3(1)-O-4'-(N,N,N-trimethyl)homoserine	52-61	apolipoprotein A-I	Mus musculus	146-151
31660677-8	2020	Lyso-DGTS added to HDL and to ApoA1 increased cholesterol efflux from macrophage cells, the main antiatherogenic function of HDL, dose-dependently, and significantly increased HDL"s ability to induce nitric oxide production from endothelial cells.	Cholesterol	46-57	apolipoprotein A-I	Mus musculus	30-35
31660677-8	2020	Lyso-DGTS added to HDL and to ApoA1 increased cholesterol efflux from macrophage cells, the main antiatherogenic function of HDL, dose-dependently, and significantly increased HDL"s ability to induce nitric oxide production from endothelial cells.	Nitric Oxide	200-212	apolipoprotein A-I	Mus musculus	30-35
31666337-5	2019	ONE crosslinked apolipoprotein A-I (apoA-I) on HDL at a concentration of > 3 mol ONE per 10 mol apoA-I (0.3 eq), which was 100-fold lower than HNE, but comparable to the potent protein crosslinker isolevuglandin.	isolevuglandin	197-211	apolipoprotein A-I	Mus musculus	36-42
31666337-9	2019	LC-MS/MS analysis revealed that Lys-12, Lys-23, Lys-96, and Lys-226 in apoA-I are modified by ONE ketoamide adducts.	Lysine	32-35	apolipoprotein A-I	Mus musculus	71-77
31666337-9	2019	LC-MS/MS analysis revealed that Lys-12, Lys-23, Lys-96, and Lys-226 in apoA-I are modified by ONE ketoamide adducts.	Lysine	40-43	apolipoprotein A-I	Mus musculus	71-77
31666337-9	2019	LC-MS/MS analysis revealed that Lys-12, Lys-23, Lys-96, and Lys-226 in apoA-I are modified by ONE ketoamide adducts.	Lysine	40-43	apolipoprotein A-I	Mus musculus	71-77
31666337-9	2019	LC-MS/MS analysis revealed that Lys-12, Lys-23, Lys-96, and Lys-226 in apoA-I are modified by ONE ketoamide adducts.	Lysine	40-43	apolipoprotein A-I	Mus musculus	71-77
31666337-9	2019	LC-MS/MS analysis revealed that Lys-12, Lys-23, Lys-96, and Lys-226 in apoA-I are modified by ONE ketoamide adducts.	oxoazanide	98-107	apolipoprotein A-I	Mus musculus	71-77
31842455-0	2019	The Mechanism of Bisphenol A Atherogenicity Involves Apolipoprotein A-I Downregulation through NF-kappaB Activation.	bisphenol A	17-28	apolipoprotein A-I	Mus musculus	53-71
31842455-6	2019	Real-Time PCR data showed that BPA treatment decreased hepatic apoA-I expression.	bisphenol A	31-34	apolipoprotein A-I	Mus musculus	63-69
31842455-7	2019	BPA downregulated the activity of the apoA-I promoter in a dose-dependent manner.	bisphenol A	0-3	apolipoprotein A-I	Mus musculus	38-44
31842455-9	2019	Transfection experiments using apoA-I promoter deletion mutants, chromatin immunoprecipitation, and protein-DNA interaction assays demonstrated that treatment of hepatocytes with BPA induced NF-kappaB signaling and thus the recruitment of p65/50 proteins to the multiple NF-kappaB binding sites located in the apoA-I promoter.	bisphenol A	179-182	apolipoprotein A-I	Mus musculus	31-37
31842455-9	2019	Transfection experiments using apoA-I promoter deletion mutants, chromatin immunoprecipitation, and protein-DNA interaction assays demonstrated that treatment of hepatocytes with BPA induced NF-kappaB signaling and thus the recruitment of p65/50 proteins to the multiple NF-kappaB binding sites located in the apoA-I promoter.	bisphenol A	179-182	apolipoprotein A-I	Mus musculus	310-316
31842455-10	2019	In conclusion, BPA exerts pro-atherogenic effects downregulating apoA-I by MEKK1 signaling and NF-kappaB activation in hepatocytes.	bisphenol A	15-18	apolipoprotein A-I	Mus musculus	65-71
31290708-0	2019	Development of synthetic high-density lipoprotein-based ApoA-I mimetic peptide-loaded docetaxel as a drug delivery nanocarrier for breast cancer chemotherapy.	Docetaxel	86-95	apolipoprotein A-I	Mus musculus	56-62
31662443-4	2019	In vitro, our data showed that CXCL12 reduced ABCA1 expression and it-mediated cholesterol efflux from THP-1-derived macrophages to apoA-I.	Cholesterol	79-90	apolipoprotein A-I	Mus musculus	132-138
31520916-12	2019	Apoa-1 and Apoc-1 were closely related to cholesterol transport, lipid metabolism balance, and airway epithelial integrity; Cfd participated in immune response, affecting the occurrence and development of inflammation; EGFR and Lrg1 were involved in epithelial cell proliferation, influencing the process of airway remodeling.	Cholesterol	42-53	apolipoprotein A-I	Mus musculus	0-6
31708728-2	2019	We investigate whether L-4F, an economical ApoA-I mimetic peptide, reduces neurovascular and white-matter damage in db/db type-2 diabetic (T2DM) stroke mice.	L-4F peptide	23-27	apolipoprotein A-I	Mus musculus	43-49
31176760-5	2019	Results showed that naringenin increased cholesterol efflux to both apoA-I and HDL and gene expressions in ABCA1, ABCG1 and LXRalpha in RAW264.7 macrophages.	naringenin	20-30	apolipoprotein A-I	Mus musculus	68-74
31176760-5	2019	Results showed that naringenin increased cholesterol efflux to both apoA-I and HDL and gene expressions in ABCA1, ABCG1 and LXRalpha in RAW264.7 macrophages.	Cholesterol	41-52	apolipoprotein A-I	Mus musculus	68-74
31567014-15	2019	CONCLUSIONS: Raising apolipoprotein AI and functional levels of HDL promotes multiple favorable changes in the production of monocytes and neutrophils and in the inflammatory environment of atherosclerotic plaques of diabetic mice after cholesterol lowering and may represent a novel approach to reduce cardiovascular disease risk in people with diabetes mellitus.	Cholesterol	237-248	apolipoprotein A-I	Mus musculus	21-38
31085374-7	2019	Furthermore, polydatin may facilitate RCT by stimulating cholesterol efflux through ATP-binding cassette transporters (ABC) A1, ABCG1 and scavenger receptor class B type I (SR-BI) in macrophages, increasing serum levels of high density lipoprotein and apolipoprotein A-I, promoting of SR-BI-mediated cholesterol uptake of liver, increasing secretion of cholesterol into bile by ABCG5/ABCG8 and improving cholesterol metabolism by CYP7A1 pathway.	polydatin	13-22	apolipoprotein A-I	Mus musculus	252-270
31129217-1	2019	In this study, the purified water-soluble polysaccharide (ALP-1) from Arctium lappa was used to intervene lipopolysaccharide-induced RAW264.7 macrophage and systemic inflammatory mice.	Water	28-33	apolipoprotein A-I	Mus musculus	58-63
31129217-1	2019	In this study, the purified water-soluble polysaccharide (ALP-1) from Arctium lappa was used to intervene lipopolysaccharide-induced RAW264.7 macrophage and systemic inflammatory mice.	Polysaccharides	42-56	apolipoprotein A-I	Mus musculus	58-63
31129217-6	2019	Besides, ALP-1 could significantly enhance the production of short chain fatty acids (SCFAs) in gut.	Fatty Acids, Volatile	61-84	apolipoprotein A-I	Mus musculus	9-14
31129217-6	2019	Besides, ALP-1 could significantly enhance the production of short chain fatty acids (SCFAs) in gut.	Fatty Acids, Volatile	86-91	apolipoprotein A-I	Mus musculus	9-14
30821416-0	2019	Pharmacological inhibition of the F1 -ATPase/P2Y1 pathway suppresses the effect of apolipoprotein A1 on endothelial nitric oxide synthesis and vasorelaxation.	Nitric Oxide	116-128	apolipoprotein A-I	Mus musculus	83-100
31069401-0	2019	ApoAI-derived peptide increases glucose tolerance and prevents formation of atherosclerosis in mice.	Glucose	32-39	apolipoprotein A-I	Mus musculus	0-5
30970222-2	2019	ApoA-I also accepts cholesterol that effluxes from cells expressing ATP-binding cassette transporter A1 (ABCA1) and ATP-binding cassette transporter G1 (ABCG1).	Cholesterol	20-31	apolipoprotein A-I	Mus musculus	0-6
31184596-5	2019	The apolipoprotein A-I (APOA1) mimetic 4F mitigated disease in both the Cox2 MKO/CCHF and piroxicam-accelerated Il10-/- models of inflammatory bowel disease (IBD) and reduced elevated levels of pro-inflammatory mediators in tissue and plasma.	mko	77-80	apolipoprotein A-I	Mus musculus	4-22
31184596-5	2019	The apolipoprotein A-I (APOA1) mimetic 4F mitigated disease in both the Cox2 MKO/CCHF and piroxicam-accelerated Il10-/- models of inflammatory bowel disease (IBD) and reduced elevated levels of pro-inflammatory mediators in tissue and plasma.	mko	77-80	apolipoprotein A-I	Mus musculus	24-29
31184596-5	2019	The apolipoprotein A-I (APOA1) mimetic 4F mitigated disease in both the Cox2 MKO/CCHF and piroxicam-accelerated Il10-/- models of inflammatory bowel disease (IBD) and reduced elevated levels of pro-inflammatory mediators in tissue and plasma.	Piroxicam	90-99	apolipoprotein A-I	Mus musculus	4-22
31184596-5	2019	The apolipoprotein A-I (APOA1) mimetic 4F mitigated disease in both the Cox2 MKO/CCHF and piroxicam-accelerated Il10-/- models of inflammatory bowel disease (IBD) and reduced elevated levels of pro-inflammatory mediators in tissue and plasma.	Piroxicam	90-99	apolipoprotein A-I	Mus musculus	24-29
31184596-6	2019	APOA1 mimetic Tg6F therapy was also effective in reducing intestinal inflammation in the Cox2 MKO/CCHF model.	tg6f	14-18	apolipoprotein A-I	Mus musculus	0-5
31184596-6	2019	APOA1 mimetic Tg6F therapy was also effective in reducing intestinal inflammation in the Cox2 MKO/CCHF model.	mko	94-97	apolipoprotein A-I	Mus musculus	0-5
31002281-0	2019	Treatment with apolipoprotein A1 protects mice against doxorubicin-induced cardiotoxicity in a scavenger receptor class B, type I-dependent manner.	Doxorubicin	55-66	apolipoprotein A-I	Mus musculus	15-32
31002281-9	2019	Pharmacological administration of purified apolipoprotein A1 dramatically protected wild-type mice from doxorubicin-induced cardiotoxicity and left ventricular dysfunction, whereas this protection was lost in scavenger receptor class B, type I-deficient mice.	Doxorubicin	104-115	apolipoprotein A-I	Mus musculus	43-60
31002281-12	2019	We also demonstrate that pharmacological treatment with apolipoprotein A1, the major HDL structural protein, protects mice against doxorubicin-induced cardiomyocyte apoptosis and left ventricular dysfunction in an SR-B1-dependent manner.	Doxorubicin	131-142	apolipoprotein A-I	Mus musculus	56-73
30879693-1	2019	In this study, water-soluble polysaccharide from Arctium lappa was extracted, isolated and purified to be a fraction (ALP-1).	Water	15-20	apolipoprotein A-I	Mus musculus	118-123
30879693-1	2019	In this study, water-soluble polysaccharide from Arctium lappa was extracted, isolated and purified to be a fraction (ALP-1).	Polysaccharides	29-43	apolipoprotein A-I	Mus musculus	118-123
30879693-3	2019	ALP-1 was composed of (2  1)-beta-d-fructofuranose backbone linked to a terminal of (2   1)-alpha-d-glucopyranose at the non-reducing end and a (2   6)-beta-d-fructofuranose branching.	(2  1)-beta-d-fructofuranose	22-50	apolipoprotein A-I	Mus musculus	0-5
30879693-3	2019	ALP-1 was composed of (2  1)-beta-d-fructofuranose backbone linked to a terminal of (2   1)-alpha-d-glucopyranose at the non-reducing end and a (2   6)-beta-d-fructofuranose branching.	(2   1)-alpha-d-glucopyranose	84-113	apolipoprotein A-I	Mus musculus	0-5
30879693-3	2019	ALP-1 was composed of (2  1)-beta-d-fructofuranose backbone linked to a terminal of (2   1)-alpha-d-glucopyranose at the non-reducing end and a (2   6)-beta-d-fructofuranose branching.	(2   6)-beta-d-fructofuranose	144-173	apolipoprotein A-I	Mus musculus	0-5
31101050-0	2019	AIBP and APOA-I synergistically inhibit intestinal tumor growth and metastasis by promoting cholesterol efflux.	Cholesterol	92-103	apolipoprotein A-I	Mus musculus	9-15
31101050-3	2019	APOA-I binding protein (AIBP) promotes the reverse cholesterol transport pathway (RCT) in cooperation with Apolipoprotein A-I (APOA-I) or high-density lipoprotein cholesterol.	Cholesterol	51-62	apolipoprotein A-I	Mus musculus	107-125
31101050-3	2019	APOA-I binding protein (AIBP) promotes the reverse cholesterol transport pathway (RCT) in cooperation with Apolipoprotein A-I (APOA-I) or high-density lipoprotein cholesterol.	Cholesterol	51-62	apolipoprotein A-I	Mus musculus	0-6
31101050-3	2019	APOA-I binding protein (AIBP) promotes the reverse cholesterol transport pathway (RCT) in cooperation with Apolipoprotein A-I (APOA-I) or high-density lipoprotein cholesterol.	Cholesterol	163-174	apolipoprotein A-I	Mus musculus	0-6
31101050-12	2019	Moreover, cyclosporine A, a cholesterol efflux inhibitor, rescued the inhibitory effect induced by the combination of AIBP and APOA-I.	Cyclosporine	10-24	apolipoprotein A-I	Mus musculus	127-133
31101050-12	2019	Moreover, cyclosporine A, a cholesterol efflux inhibitor, rescued the inhibitory effect induced by the combination of AIBP and APOA-I.	Cholesterol	28-39	apolipoprotein A-I	Mus musculus	127-133
31101050-13	2019	CONCLUSIONS: These results indicate that the combination of APOA-I and AIBP has an obvious anticancer effect on colorectal cancer by promoting cholesterol efflux.	Cholesterol	143-154	apolipoprotein A-I	Mus musculus	60-66
30783475-10	2019	ApoA1, ApoA5, Cyp2c37, Cyp2J5, Cyp2b9 and Cyp2b10 were differently expressed after rosiglitazone treatment, which may be accountable for affecting cardiovascular outcomes and glycemic control in T2DM.	Rosiglitazone	83-96	apolipoprotein A-I	Mus musculus	0-5
30717414-0	2019	Human ApoA-I Overexpression Enhances Macrophage-Specific Reverse Cholesterol Transport but Fails to Prevent Inherited Diabesity in Mice.	Cholesterol	65-76	apolipoprotein A-I	Mus musculus	6-12
30543107-5	2019	Pathway analysis demonstrated that several metabolic pathways such as aminoacyl-tRNA biosynthesis, arginine and proline metabolism, and phenylalanine, tyrosine, and tryptophan biosynthesis were dysregulated in apoA-I knockout mice.	Arginine	99-107	apolipoprotein A-I	Mus musculus	210-216
30543107-5	2019	Pathway analysis demonstrated that several metabolic pathways such as aminoacyl-tRNA biosynthesis, arginine and proline metabolism, and phenylalanine, tyrosine, and tryptophan biosynthesis were dysregulated in apoA-I knockout mice.	Proline	112-119	apolipoprotein A-I	Mus musculus	210-216
30543107-5	2019	Pathway analysis demonstrated that several metabolic pathways such as aminoacyl-tRNA biosynthesis, arginine and proline metabolism, and phenylalanine, tyrosine, and tryptophan biosynthesis were dysregulated in apoA-I knockout mice.	Phenylalanine	136-149	apolipoprotein A-I	Mus musculus	210-216
30543107-5	2019	Pathway analysis demonstrated that several metabolic pathways such as aminoacyl-tRNA biosynthesis, arginine and proline metabolism, and phenylalanine, tyrosine, and tryptophan biosynthesis were dysregulated in apoA-I knockout mice.	Tyrosine	151-159	apolipoprotein A-I	Mus musculus	210-216
30543107-5	2019	Pathway analysis demonstrated that several metabolic pathways such as aminoacyl-tRNA biosynthesis, arginine and proline metabolism, and phenylalanine, tyrosine, and tryptophan biosynthesis were dysregulated in apoA-I knockout mice.	Tryptophan	165-175	apolipoprotein A-I	Mus musculus	210-216
30473024-6	2018	In functional study, the expression of ApoA-1 was decreased in hepatocytes with steatosis and was inversely associated with the concentration of oleic acid.	Oleic Acid	145-155	apolipoprotein A-I	Mus musculus	39-45
30333155-7	2018	The data obtained indicate that when APOE is absent, particles containing APOA1, APOA4, and APOJ still transport cholesterol in the intraretinal space, but these particles are not taken up by retinal cells.	Cholesterol	113-124	apolipoprotein A-I	Mus musculus	74-79
30419936-10	2018	Compared to HDL obtained by ultracentrifugation, HDL isolated by PEG precipitation show a lower ApoE/ApoA-I proportion and reduced cholesterol content.	Polyethylene Glycols	65-68	apolipoprotein A-I	Mus musculus	101-107
30354238-4	2018	Approach and Results- We found that V-ATPase inhibitors dose-dependently decreased ABCA1-mediated cholesterol efflux to apoA1 in baby hamster kidney cells and RAW264.7 cells; and similarly, siRNA knockdown of ATP6V0C inhibited ABCA1-mediated cholesterol efflux to apoA1 in RAW264.7 cells.	Cholesterol	98-109	apolipoprotein A-I	Mus musculus	120-125
30354238-4	2018	Approach and Results- We found that V-ATPase inhibitors dose-dependently decreased ABCA1-mediated cholesterol efflux to apoA1 in baby hamster kidney cells and RAW264.7 cells; and similarly, siRNA knockdown of ATP6V0C inhibited ABCA1-mediated cholesterol efflux to apoA1 in RAW264.7 cells.	Cholesterol	98-109	apolipoprotein A-I	Mus musculus	264-269
30354238-6	2018	We generated a fluorescein isothiocyanate/Alexa647 double-labeled fluorescent ratiometric apoA1 pH indicator whose fluorescein isothiocyanate/Alexa647 emission ratio decreased as the pH drops.	Fluorescein-5-isothiocyanate	15-41	apolipoprotein A-I	Mus musculus	90-95
30354238-6	2018	We generated a fluorescein isothiocyanate/Alexa647 double-labeled fluorescent ratiometric apoA1 pH indicator whose fluorescein isothiocyanate/Alexa647 emission ratio decreased as the pH drops.	Alexa Fluor 647	42-50	apolipoprotein A-I	Mus musculus	90-95
30354238-6	2018	We generated a fluorescein isothiocyanate/Alexa647 double-labeled fluorescent ratiometric apoA1 pH indicator whose fluorescein isothiocyanate/Alexa647 emission ratio decreased as the pH drops.	Fluorescein-5-isothiocyanate	115-141	apolipoprotein A-I	Mus musculus	90-95
30354238-6	2018	We generated a fluorescein isothiocyanate/Alexa647 double-labeled fluorescent ratiometric apoA1 pH indicator whose fluorescein isothiocyanate/Alexa647 emission ratio decreased as the pH drops.	Alexa Fluor 647	142-150	apolipoprotein A-I	Mus musculus	90-95
30354238-10	2018	We showed that acidic pH facilitated apoA1 unfolding, apoA1 solubilization of phosphatidycholine:phosphatidyserine liposomes, and increased lipid fluidity of these liposomes.	phosphatidycholine	78-96	apolipoprotein A-I	Mus musculus	54-59
30354238-10	2018	We showed that acidic pH facilitated apoA1 unfolding, apoA1 solubilization of phosphatidycholine:phosphatidyserine liposomes, and increased lipid fluidity of these liposomes.	phosphatidyserine	97-114	apolipoprotein A-I	Mus musculus	54-59
30425683-0	2018	Possible Insulinotropic Action of Apolipoprotein A-I Through the ABCA1/Cdc42/cAMP/PKA Pathway in MIN6 Cells.	Cyclic AMP	77-81	apolipoprotein A-I	Mus musculus	34-52
30425683-5	2018	Results: Addition of ApoA-I produced cAMP and increased insulin secretion, dose-dependently in high glucose concentration (25 mmmol/l).	Cyclic AMP	37-41	apolipoprotein A-I	Mus musculus	21-27
30425683-5	2018	Results: Addition of ApoA-I produced cAMP and increased insulin secretion, dose-dependently in high glucose concentration (25 mmmol/l).	Glucose	100-107	apolipoprotein A-I	Mus musculus	21-27
30425683-9	2018	Both cAMP inhibiror (SQ22536) and protein kinases inhibitor (Rp-cAMPS) strongly inhibited the effects of ApoA-I on insulin secretion.	Cyclic AMP	5-9	apolipoprotein A-I	Mus musculus	105-111
30425683-9	2018	Both cAMP inhibiror (SQ22536) and protein kinases inhibitor (Rp-cAMPS) strongly inhibited the effects of ApoA-I on insulin secretion.	9-(tetrahydro-2-furyl)-adenine	21-28	apolipoprotein A-I	Mus musculus	105-111
30425683-10	2018	Conclusions: We demonstrated that ApoA-I enhances glucose-stimulated insulin release in high glucose at least partially through the ABCA1/Cdc42/cAMP/ Protein kinase A (PKA) pathway.	Glucose	50-57	apolipoprotein A-I	Mus musculus	34-40
30425683-10	2018	Conclusions: We demonstrated that ApoA-I enhances glucose-stimulated insulin release in high glucose at least partially through the ABCA1/Cdc42/cAMP/ Protein kinase A (PKA) pathway.	Glucose	93-100	apolipoprotein A-I	Mus musculus	34-40
30216355-8	2018	Furthermore, ex vivo cholesterol efflux was reduced in ob/ob liver and adipose tissue towards apoA-I and HDL.	Cholesterol	21-32	apolipoprotein A-I	Mus musculus	94-100
29991652-6	2018	apoA-I-/- mice exhibited key components of metabolic disease, like increased fat mass, fasting glucose levels, hepatic triglyceride content, and hepatic glucose output compared with apoA-I+/+ controls.	Glucose	95-102	apolipoprotein A-I	Mus musculus	0-6
29991652-6	2018	apoA-I-/- mice exhibited key components of metabolic disease, like increased fat mass, fasting glucose levels, hepatic triglyceride content, and hepatic glucose output compared with apoA-I+/+ controls.	Triglycerides	119-131	apolipoprotein A-I	Mus musculus	0-6
30233285-5	2018	In vitro studies of the effects of PPAR-gamma on lipid homeostasis in macrophage cells suggested a role for PPAR-gamma in the regulation of ABCA1-dependent cholesterol efflux to apoA-I pathway.	Cholesterol	156-167	apolipoprotein A-I	Mus musculus	178-184
30132720-0	2018	Development and Characterization of Monoclonal Antibodies Against Nitro-166Tyrosine of High-Density Lipoprotein: Apolipoprotein A1.	nitro-166tyrosine	66-83	apolipoprotein A-I	Mus musculus	113-130
30132720-4	2018	It has been reported that the oxidation of the amino acids such as methionine, tyrosine, and tryptophan residues at specific sites of ApoA1 renders it not only dysfunctional but also proinflammatory and proatherogenic.	Methionine	67-77	apolipoprotein A-I	Mus musculus	134-139
30132720-4	2018	It has been reported that the oxidation of the amino acids such as methionine, tyrosine, and tryptophan residues at specific sites of ApoA1 renders it not only dysfunctional but also proinflammatory and proatherogenic.	Tyrosine	79-87	apolipoprotein A-I	Mus musculus	134-139
30132720-4	2018	It has been reported that the oxidation of the amino acids such as methionine, tyrosine, and tryptophan residues at specific sites of ApoA1 renders it not only dysfunctional but also proinflammatory and proatherogenic.	Tryptophan	93-103	apolipoprotein A-I	Mus musculus	134-139
30132720-6	2018	In this study, we developed monoclonal antibodies (mAbs) specific to modified ApoA1 with its tyrosine residue at the 166th position nitrated to 3-nitrotyrosine.	Tyrosine	93-101	apolipoprotein A-I	Mus musculus	78-83
30132720-6	2018	In this study, we developed monoclonal antibodies (mAbs) specific to modified ApoA1 with its tyrosine residue at the 166th position nitrated to 3-nitrotyrosine.	3-nitrotyrosine	144-159	apolipoprotein A-I	Mus musculus	78-83
30100992-2	2018	Previously, we reported that doxorubicin (Dox), a prototypical reactive oxygen species (ROS)-producing anti-cancer drug, results in oxidation of plasma proteins, including apolipoprotein A-I (ApoA-I) leading to tumor necrosis factor-alpha (TNF-alpha)-mediated oxidative stress in plasma and brain.	Doxorubicin	29-40	apolipoprotein A-I	Mus musculus	172-190
30100992-2	2018	Previously, we reported that doxorubicin (Dox), a prototypical reactive oxygen species (ROS)-producing anti-cancer drug, results in oxidation of plasma proteins, including apolipoprotein A-I (ApoA-I) leading to tumor necrosis factor-alpha (TNF-alpha)-mediated oxidative stress in plasma and brain.	Doxorubicin	29-40	apolipoprotein A-I	Mus musculus	192-198
30100992-2	2018	Previously, we reported that doxorubicin (Dox), a prototypical reactive oxygen species (ROS)-producing anti-cancer drug, results in oxidation of plasma proteins, including apolipoprotein A-I (ApoA-I) leading to tumor necrosis factor-alpha (TNF-alpha)-mediated oxidative stress in plasma and brain.	Doxorubicin	42-45	apolipoprotein A-I	Mus musculus	172-190
30100992-2	2018	Previously, we reported that doxorubicin (Dox), a prototypical reactive oxygen species (ROS)-producing anti-cancer drug, results in oxidation of plasma proteins, including apolipoprotein A-I (ApoA-I) leading to tumor necrosis factor-alpha (TNF-alpha)-mediated oxidative stress in plasma and brain.	Doxorubicin	42-45	apolipoprotein A-I	Mus musculus	192-198
30100992-2	2018	Previously, we reported that doxorubicin (Dox), a prototypical reactive oxygen species (ROS)-producing anti-cancer drug, results in oxidation of plasma proteins, including apolipoprotein A-I (ApoA-I) leading to tumor necrosis factor-alpha (TNF-alpha)-mediated oxidative stress in plasma and brain.	Reactive Oxygen Species	63-86	apolipoprotein A-I	Mus musculus	192-198
30100992-2	2018	Previously, we reported that doxorubicin (Dox), a prototypical reactive oxygen species (ROS)-producing anti-cancer drug, results in oxidation of plasma proteins, including apolipoprotein A-I (ApoA-I) leading to tumor necrosis factor-alpha (TNF-alpha)-mediated oxidative stress in plasma and brain.	Reactive Oxygen Species	88-91	apolipoprotein A-I	Mus musculus	172-190
29899427-0	2018	Treating the Intestine with Oral ApoA-I Mimetic Tg6F Reduces Tumor Burden in Mouse Models of Metastatic Lung Cancer.	tg6f	48-52	apolipoprotein A-I	Mus musculus	33-39
29555084-1	2018	BACKGROUND AND AIMS: ApoA-1 binding protein (AIBP) is a secreted protein that interacts with apoA-I and accelerates cholesterol efflux from cells.	Cholesterol	116-127	apolipoprotein A-I	Mus musculus	21-27
29555084-1	2018	BACKGROUND AND AIMS: ApoA-1 binding protein (AIBP) is a secreted protein that interacts with apoA-I and accelerates cholesterol efflux from cells.	Cholesterol	116-127	apolipoprotein A-I	Mus musculus	93-99
29453462-11	2018	Furthermore, GQ-11 reduced triglycerides and VLDL cholesterol and increased HDL-cholesterol by upregulation of Apoa1 and Abca1 gene expression in the liver.	gq-11	13-18	apolipoprotein A-I	Mus musculus	111-116
29564886-7	2018	On the basis of molecular recognition between phospholipids on EV lipid bilayer membranes and ApoA-I mimetic peptides, we have developed methotrexate (MTX)-loaded EVs functionalized with therapeutic [Lys-Leu-Ala (KLA)] and targeted [low-density lipoprotein (LDL)] peptides.	Methotrexate	137-149	apolipoprotein A-I	Mus musculus	94-100
29564886-7	2018	On the basis of molecular recognition between phospholipids on EV lipid bilayer membranes and ApoA-I mimetic peptides, we have developed methotrexate (MTX)-loaded EVs functionalized with therapeutic [Lys-Leu-Ala (KLA)] and targeted [low-density lipoprotein (LDL)] peptides.	Methotrexate	151-154	apolipoprotein A-I	Mus musculus	94-100
29578333-4	2018	Cross-linking and size-exclusion chromatography showed that the mutations resulted in reduced self-association, generating a predominantly monomeric apoA-I when five or six lysine residues were substituted.	Lysine	173-179	apolipoprotein A-I	Mus musculus	149-155
29578333-5	2018	The rate of phosphatidylcholine vesicle solubilization was enhanced for all variants, with approximately a threefold rate enhancement for apoA-I lacking Lys 206, 208, 238, and 239, or Glu 234 and 235.	Phosphatidylcholines	12-31	apolipoprotein A-I	Mus musculus	138-144
29578333-5	2018	The rate of phosphatidylcholine vesicle solubilization was enhanced for all variants, with approximately a threefold rate enhancement for apoA-I lacking Lys 206, 208, 238, and 239, or Glu 234 and 235.	Lysine	153-156	apolipoprotein A-I	Mus musculus	138-144
29578333-7	2018	ApoA-I mediated cellular lipid efflux from wild-type mice macrophage foam cells was decreased for the variant with five lysine mutations.	Lysine	120-126	apolipoprotein A-I	Mus musculus	0-6
29578333-10	2018	Taken together, this study indicates that ionic interactions in the C-terminal domain of apoA-I favor self-association and that monomeric apoA-I is more active in solubilizing phospholipid bilayers.	Phospholipids	176-188	apolipoprotein A-I	Mus musculus	138-144
29505790-2	2018	The ATP-binding cassette transporter A1 (ABCA1) protein mediates the transport of cholesterol and phospholipids from cells to apolipoprotein A-I (apoA-I) to generate nascent HDL particles.	Cholesterol	82-93	apolipoprotein A-I	Mus musculus	126-144
29505790-2	2018	The ATP-binding cassette transporter A1 (ABCA1) protein mediates the transport of cholesterol and phospholipids from cells to apolipoprotein A-I (apoA-I) to generate nascent HDL particles.	Cholesterol	82-93	apolipoprotein A-I	Mus musculus	146-152
29505790-2	2018	The ATP-binding cassette transporter A1 (ABCA1) protein mediates the transport of cholesterol and phospholipids from cells to apolipoprotein A-I (apoA-I) to generate nascent HDL particles.	Phospholipids	98-111	apolipoprotein A-I	Mus musculus	126-144
29505790-2	2018	The ATP-binding cassette transporter A1 (ABCA1) protein mediates the transport of cholesterol and phospholipids from cells to apolipoprotein A-I (apoA-I) to generate nascent HDL particles.	Phospholipids	98-111	apolipoprotein A-I	Mus musculus	146-152
29545616-6	2018	Furthermore, injection of lipid-free Apolipoprotein AI (ApoAI) into ApoE-/- mice reduces intracellular cholesterol levels in Treg cells and prevents their conversion into Tfh cells.	Cholesterol	103-114	apolipoprotein A-I	Mus musculus	37-54
29545616-6	2018	Furthermore, injection of lipid-free Apolipoprotein AI (ApoAI) into ApoE-/- mice reduces intracellular cholesterol levels in Treg cells and prevents their conversion into Tfh cells.	Cholesterol	103-114	apolipoprotein A-I	Mus musculus	56-61
29385802-6	2018	A synthetic S-nitrosylated (SNO) phospholipid (1,2-dipalmitoyl-sn-glycero-3-phosphonitrosothioethanol) was synthesized and assembled with S-containing phospholipids and the principal protein of HDL, apolipoprotein A-I, to construct NO-delivering HDL-like particles (SNO HDL NPs).	sno	28-31	apolipoprotein A-I	Mus musculus	199-217
29385802-6	2018	A synthetic S-nitrosylated (SNO) phospholipid (1,2-dipalmitoyl-sn-glycero-3-phosphonitrosothioethanol) was synthesized and assembled with S-containing phospholipids and the principal protein of HDL, apolipoprotein A-I, to construct NO-delivering HDL-like particles (SNO HDL NPs).	Phospholipids	33-45	apolipoprotein A-I	Mus musculus	199-217
29385802-6	2018	A synthetic S-nitrosylated (SNO) phospholipid (1,2-dipalmitoyl-sn-glycero-3-phosphonitrosothioethanol) was synthesized and assembled with S-containing phospholipids and the principal protein of HDL, apolipoprotein A-I, to construct NO-delivering HDL-like particles (SNO HDL NPs).	1,2-dipalmitoyl-sn-glycero-3-phosphonitrosothioethanol	47-101	apolipoprotein A-I	Mus musculus	199-217
29174964-8	2018	Macrophage cholesterol efflux to apolipoprotein A-I was significantly reduced by miR-212, which was accompanied by reduced ABCA1 expression.	Cholesterol	11-22	apolipoprotein A-I	Mus musculus	33-51
29361501-3	2018	Here we describe an enlightened strategy using phospholipid reconstituted apoA-I peptide (22A)-derived synthetic HDL (sHDL) to deliver LXR agonists to the atheroma and examine their effect on atherosclerosis regression in vivo.	Phospholipids	47-59	apolipoprotein A-I	Mus musculus	74-80
28982731-2	2018	Similarly, previous studies in our laboratory have shown that chow-fed mice lacking apolipoprotein (apo) A-I, the major protein in HDL, have low HDL-cholesterol (HDL-C) concentrations and smaller fetuses in midgestation.	Cholesterol	149-160	apolipoprotein A-I	Mus musculus	84-108
28982731-4	2018	As expected, we found the differences in apoA-I expression led to changes in HDL particle size and protein cargo as well as plasma cholesterol concentrations.	Cholesterol	131-142	apolipoprotein A-I	Mus musculus	41-47
28982731-7	2018	Glucose tolerance tests were improved in the mice with the highest level of apoA-I, suggesting increased insulin-induced uptake of glucose by tissues of apoA-I transgenic mice.	Glucose	131-138	apolipoprotein A-I	Mus musculus	76-82
28982731-7	2018	Glucose tolerance tests were improved in the mice with the highest level of apoA-I, suggesting increased insulin-induced uptake of glucose by tissues of apoA-I transgenic mice.	Glucose	131-138	apolipoprotein A-I	Mus musculus	153-159
29350757-5	2018	It was found that the treatment of sophoricoside decreased the hepatic cholesterol and triglyceride levels, and serum low-density lipoprotein-cholesterol and apolipoprotein-B levels, and elevated the serum high-density lipoprotein-cholesterol and apolipoprotein-A1 levels.	sophoricoside	35-48	apolipoprotein A-I	Mus musculus	247-264
28986362-6	2018	After treatment, apoA1+/+ mice displayed cardiac dysfunction, as evidenced by reduced left ventricular end-systolic pressure and +dP/d t, and histological analysis revealed cardiomyocyte atrophy and increased cardiomyocyte apoptosis after doxorubicin treatment.	Doxorubicin	239-250	apolipoprotein A-I	Mus musculus	17-22
28986362-10	2018	Our findings provide proof of concept that raising apoA1 to supraphysiological levels can dramatically protect against doxorubicin-induced cardiotoxicity via a pathway that is mediated by SR-B1 and involves Akt1/2 activation in cardiomyocytes.	Doxorubicin	119-130	apolipoprotein A-I	Mus musculus	51-56
30010117-6	2018	In vitro, these decreases reduce cholesterol exchange across the BBB, particularly for high-density lipoproteins and ApoA-I particles.	Cholesterol	33-44	apolipoprotein A-I	Mus musculus	117-123
29074589-1	2017	OBJECTIVE: Reverse cholesterol transport comprises cholesterol efflux from ABCA1-expressing macrophages to apolipoprotein (apo) AI, giving nascent high-density lipoprotein (nHDL), esterification of nHDL-free cholesterol (FC), selective hepatic extraction of HDL lipids, and hepatic conversion of HDL cholesterol to bile salts, which are excreted.	Cholesterol	19-30	apolipoprotein A-I	Mus musculus	107-130
29074589-1	2017	OBJECTIVE: Reverse cholesterol transport comprises cholesterol efflux from ABCA1-expressing macrophages to apolipoprotein (apo) AI, giving nascent high-density lipoprotein (nHDL), esterification of nHDL-free cholesterol (FC), selective hepatic extraction of HDL lipids, and hepatic conversion of HDL cholesterol to bile salts, which are excreted.	Cholesterol	51-62	apolipoprotein A-I	Mus musculus	107-130
29074589-1	2017	OBJECTIVE: Reverse cholesterol transport comprises cholesterol efflux from ABCA1-expressing macrophages to apolipoprotein (apo) AI, giving nascent high-density lipoprotein (nHDL), esterification of nHDL-free cholesterol (FC), selective hepatic extraction of HDL lipids, and hepatic conversion of HDL cholesterol to bile salts, which are excreted.	Cholesterol	51-62	apolipoprotein A-I	Mus musculus	107-130
29074589-1	2017	OBJECTIVE: Reverse cholesterol transport comprises cholesterol efflux from ABCA1-expressing macrophages to apolipoprotein (apo) AI, giving nascent high-density lipoprotein (nHDL), esterification of nHDL-free cholesterol (FC), selective hepatic extraction of HDL lipids, and hepatic conversion of HDL cholesterol to bile salts, which are excreted.	Cholesterol	51-62	apolipoprotein A-I	Mus musculus	107-130
29074589-1	2017	OBJECTIVE: Reverse cholesterol transport comprises cholesterol efflux from ABCA1-expressing macrophages to apolipoprotein (apo) AI, giving nascent high-density lipoprotein (nHDL), esterification of nHDL-free cholesterol (FC), selective hepatic extraction of HDL lipids, and hepatic conversion of HDL cholesterol to bile salts, which are excreted.	Bile Acids and Salts	315-325	apolipoprotein A-I	Mus musculus	107-130
29074589-3	2017	APPROACH AND RESULTS: During in vitro incubation of human serum, nHDL-[3H]FC and [14C]PL rapidly transfer to HDL and low-density lipoproteins (t1/2=2-7 minutes), whereas nHDL-[125I]apo AI transfers solely to HDL (t1/2&lt;10 minutes) and to the lipid-free form (t1/2&gt;480 minutes).	Tritium	71-73	apolipoprotein A-I	Mus musculus	181-187
29285103-10	2017	These results indicated that sphingomyelin and cholesterol content may increase in the liver dysfunction of sepsis by increasing the expression of SMS2, HMGCR, SR-B1 and ABCA1, and downregulating Apo A1.	Sphingomyelins	29-42	apolipoprotein A-I	Mus musculus	196-202
29285103-10	2017	These results indicated that sphingomyelin and cholesterol content may increase in the liver dysfunction of sepsis by increasing the expression of SMS2, HMGCR, SR-B1 and ABCA1, and downregulating Apo A1.	Cholesterol	47-58	apolipoprotein A-I	Mus musculus	196-202
28941727-1	2017	Beyond the crucial role of apolipoprotein A-I (ApoA-I) on peripheral cholesterol metabolism, this apolipoprotein has also been implicated in beta amyloid (Abeta)-related neuropathologies.	Cholesterol	69-80	apolipoprotein A-I	Mus musculus	27-45
28941727-1	2017	Beyond the crucial role of apolipoprotein A-I (ApoA-I) on peripheral cholesterol metabolism, this apolipoprotein has also been implicated in beta amyloid (Abeta)-related neuropathologies.	Cholesterol	69-80	apolipoprotein A-I	Mus musculus	47-53
28882873-8	2017	Overexpression of wild-type but not mutant ABCA8 resulted in a significant increase (1.8-fold; P=0.01) of cholesterol efflux to apolipoprotein AI in vitro.	Cholesterol	106-117	apolipoprotein A-I	Mus musculus	128-145
28720595-7	2017	Sterol metabolism genes were those promoting cholesterol supply (Scarb1, Sqle, Apoa1) and disposal (Cyp27a1, Cyp7b1).	Sterols	0-6	apolipoprotein A-I	Mus musculus	79-84
28720595-7	2017	Sterol metabolism genes were those promoting cholesterol supply (Scarb1, Sqle, Apoa1) and disposal (Cyp27a1, Cyp7b1).	Cholesterol	45-56	apolipoprotein A-I	Mus musculus	79-84
28648864-3	2017	Here, we study the effects of four major plasma proteins - serum albumin (SA), transferrin (Tf), apolipoprotein A1 (ApoA1) and fibrinogen (Fib) - on the temperature-dependent release of fluorescein di-beta-D-galactopyranoside (FDG) from TSLs.	fluorescein-digalactoside	186-225	apolipoprotein A-I	Mus musculus	97-114
28648864-3	2017	Here, we study the effects of four major plasma proteins - serum albumin (SA), transferrin (Tf), apolipoprotein A1 (ApoA1) and fibrinogen (Fib) - on the temperature-dependent release of fluorescein di-beta-D-galactopyranoside (FDG) from TSLs.	fluorescein-digalactoside	186-225	apolipoprotein A-I	Mus musculus	116-121
28668625-0	2017	Plasma activated coating immobilizes apolipoprotein A-I to stainless steel surfaces in its bioactive form and enhances biocompatibility.	Stainless Steel	59-74	apolipoprotein A-I	Mus musculus	37-55
28668625-1	2017	We utilized a plasma activated coating (PAC) to covalently bind the active component of high density lipoproteins (HDL), apolipoprotein (apo) A-I, to stainless steel (SS) surfaces.	Stainless Steel	150-165	apolipoprotein A-I	Mus musculus	121-145
28668625-3	2017	PAC-coated SS significantly increased the covalent attachment of apoA-I, compared to SS alone.	pac	0-3	apolipoprotein A-I	Mus musculus	65-71
28668625-3	2017	PAC-coated SS significantly increased the covalent attachment of apoA-I, compared to SS alone.	Stainless Steel	11-13	apolipoprotein A-I	Mus musculus	65-71
28668625-3	2017	PAC-coated SS significantly increased the covalent attachment of apoA-I, compared to SS alone.	Stainless Steel	85-87	apolipoprotein A-I	Mus musculus	65-71
29158815-0	2017	Tethering Interleukin-22 to Apolipoprotein A-I Ameliorates Mice from Acetaminophen-induced Liver Injury.	Acetaminophen	69-82	apolipoprotein A-I	Mus musculus	28-46
29158815-7	2017	These studies demonstrated that IL-22 tethered to apolipoprotein A-I could target and ameliorate acetaminophen-induced acute liver injury, which highlighted that a targeted strategy for IL-22 delivery might have broad utility for the protection of hepatocellular damage.	Acetaminophen	97-110	apolipoprotein A-I	Mus musculus	50-68
28939717-1	2017	BACKGROUND: Subcutaneously injected lipid-free apoA-I (apolipoprotein A-I) reduces accumulation of lipid and immune cells within the aortic root of hypercholesterolemic mice without increasing high-density lipoprotein-cholesterol concentrations.	Cholesterol	153-164	apolipoprotein A-I	Mus musculus	47-53
28939717-1	2017	BACKGROUND: Subcutaneously injected lipid-free apoA-I (apolipoprotein A-I) reduces accumulation of lipid and immune cells within the aortic root of hypercholesterolemic mice without increasing high-density lipoprotein-cholesterol concentrations.	Cholesterol	153-164	apolipoprotein A-I	Mus musculus	55-73
28487312-7	2017	Further studies with either genetic deletion or pharmacological inhibition of Cd39 in macrophages revealed increased cholesterol efflux mediated via ABCA1 to ApoA1.	Cholesterol	117-128	apolipoprotein A-I	Mus musculus	158-163
28438023-5	2017	We revealed Apoa1 to be a biomarker of DHA-PL effects on hyperlipidemic mice by DHA-PL diet.	dha-pl	39-45	apolipoprotein A-I	Mus musculus	12-17
28438023-5	2017	We revealed Apoa1 to be a biomarker of DHA-PL effects on hyperlipidemic mice by DHA-PL diet.	dha-pl	80-86	apolipoprotein A-I	Mus musculus	12-17
28242047-5	2017	METHODS: Hypocholesterolemic apolipoprotein A1 (apoA1) knockout mice were administered high dose simvastatin twice daily for 3 days.	Simvastatin	97-108	apolipoprotein A-I	Mus musculus	29-46
28242047-5	2017	METHODS: Hypocholesterolemic apolipoprotein A1 (apoA1) knockout mice were administered high dose simvastatin twice daily for 3 days.	Simvastatin	97-108	apolipoprotein A-I	Mus musculus	48-53
28242047-8	2017	Upon injection with adrenocorticotropic hormone, control-treated apoA1 knockout mice already showed only a mild increase in plasma corticosterone levels, indicative of relative glucocorticoid insufficiency.	Corticosterone	131-145	apolipoprotein A-I	Mus musculus	65-70
28325782-3	2017	We showed previously that AIBP (apolipoprotein A-I [apoA-I]-binding protein)-regulated cholesterol efflux in endothelial cells controls zebra fish embryonic angiogenesis.	Cholesterol	87-98	apolipoprotein A-I	Mus musculus	52-58
28579886-2	2017	D-4F is the apolipoprotein A-I mimetic peptide which has been revealed a critical role in regulation cholesterol.	Cholesterol	101-112	apolipoprotein A-I	Mus musculus	12-30
28167355-5	2017	METHODS: Fluorescence quenching was obtained by saturation of Cy5.5 fluorophore molecules on apoA-I protein.	cyanine dye 5	62-65	apolipoprotein A-I	Mus musculus	93-99
28167355-7	2017	In vitro proteolysis of the apoA-I probe by a variety of proteases including serine, cysteine, and metalloproteases resulted in an up to 11-fold increase in fluorescence (n = 5, p &lt;= 0.05).	Serine	77-83	apolipoprotein A-I	Mus musculus	28-34
28167355-7	2017	In vitro proteolysis of the apoA-I probe by a variety of proteases including serine, cysteine, and metalloproteases resulted in an up to 11-fold increase in fluorescence (n = 5, p &lt;= 0.05).	Cysteine	85-93	apolipoprotein A-I	Mus musculus	28-34
28126411-6	2017	Proteomic profile analysis indicated that many changed proteins after PFOA treatment, including intersectin 1 (ITSN1), serine protease inhibitor A3K (Serpina3k), and apolipoprotein a1 (APOA1), were involved in endocytosis and blood-testis barrier (BTB) processes.	perfluorooctanoic acid	70-74	apolipoprotein A-I	Mus musculus	166-183
28126411-6	2017	Proteomic profile analysis indicated that many changed proteins after PFOA treatment, including intersectin 1 (ITSN1), serine protease inhibitor A3K (Serpina3k), and apolipoprotein a1 (APOA1), were involved in endocytosis and blood-testis barrier (BTB) processes.	perfluorooctanoic acid	70-74	apolipoprotein A-I	Mus musculus	185-190
28093456-0	2017	Effect of lipid-bound apolipoprotein A-I cysteine mutant on ATF3 in RAW264.7 cells.	Cysteine	41-49	apolipoprotein A-I	Mus musculus	22-40
28093456-6	2017	In summary, the different anti-inflammatory mechanisms of the ApoA-I cysteine mutants might be associated with the regulation of ATF3 level.	Cysteine	69-77	apolipoprotein A-I	Mus musculus	62-68
27702801-8	2016	These effects were increased by the stimulation of cholesterol efflux through a lipid acceptor, the apolipoprotein A1.	Cholesterol	51-62	apolipoprotein A-I	Mus musculus	100-117
27898742-2	2016	In the circulation, it can be sequestered by a high-density lipoprotein, HDL, which carries cholesterol, triglycerides, phospholipids and apolipoproteins (Apo-AI).	Cholesterol	92-103	apolipoprotein A-I	Mus musculus	155-161
27898742-2	2016	In the circulation, it can be sequestered by a high-density lipoprotein, HDL, which carries cholesterol, triglycerides, phospholipids and apolipoproteins (Apo-AI).	Triglycerides	105-118	apolipoprotein A-I	Mus musculus	155-161
27824936-4	2016	While in the brain apoE is the main cholesterol transporter, in the periphery apoE and apoA-I both serve as the major cholesterol transporters.	Cholesterol	118-129	apolipoprotein A-I	Mus musculus	87-93
27824936-8	2016	Similarly, the levels of plasma apoA-I were lower in the apoE4 mice compared to apoE3 mice, and this effect was partially reversed by CS-6253.	CS-6253	134-141	apolipoprotein A-I	Mus musculus	32-38
27821400-0	2016	Lipid-Free Apolipoprotein A-I Reduces Progression of Atherosclerosis by Mobilizing Microdomain Cholesterol and Attenuating the Number of CD131 Expressing Cells: Monitoring Cholesterol Homeostasis Using the Cellular Ester to Total Cholesterol Ratio.	Cholesterol	95-106	apolipoprotein A-I	Mus musculus	11-29
27821400-0	2016	Lipid-Free Apolipoprotein A-I Reduces Progression of Atherosclerosis by Mobilizing Microdomain Cholesterol and Attenuating the Number of CD131 Expressing Cells: Monitoring Cholesterol Homeostasis Using the Cellular Ester to Total Cholesterol Ratio.	Cholesterol	172-183	apolipoprotein A-I	Mus musculus	11-29
27821400-0	2016	Lipid-Free Apolipoprotein A-I Reduces Progression of Atherosclerosis by Mobilizing Microdomain Cholesterol and Attenuating the Number of CD131 Expressing Cells: Monitoring Cholesterol Homeostasis Using the Cellular Ester to Total Cholesterol Ratio.	Esters	215-220	apolipoprotein A-I	Mus musculus	11-29
27821400-0	2016	Lipid-Free Apolipoprotein A-I Reduces Progression of Atherosclerosis by Mobilizing Microdomain Cholesterol and Attenuating the Number of CD131 Expressing Cells: Monitoring Cholesterol Homeostasis Using the Cellular Ester to Total Cholesterol Ratio.	Cholesterol	172-183	apolipoprotein A-I	Mus musculus	11-29
27821400-7	2016	Mice treated with lipid-free apoA-I showed a decrease in cholesterol deposition and immune cell retention in the aortic root compared with albumin-treated mice, regardless of genotype.	Cholesterol	57-68	apolipoprotein A-I	Mus musculus	29-35
27821400-9	2016	In addition, apoA-I treatment altered microdomain cholesterol composition that shifted CD131, the common beta subunit of the interleukin 3 receptor, from lipid raft to nonraft fractions of the plasma membrane.	Cholesterol	50-61	apolipoprotein A-I	Mus musculus	13-19
27821400-10	2016	CONCLUSIONS: ApoA-I treatment reduced lipid and immune cell accumulation within the aortic root by systemically reducing microdomain cholesterol content in immune cells.	Cholesterol	133-144	apolipoprotein A-I	Mus musculus	13-19
27821400-11	2016	These data suggest that lipid-free apoA-I mediates beneficial effects through attenuation of immune cell lipid raft cholesterol content, which affects numerous types of signal transduction pathways that rely on microdomain integrity for assembly and activation.	Cholesterol	116-127	apolipoprotein A-I	Mus musculus	35-41
27531623-6	2016	The prototype of the HDL-mimicking alpha-tocopherol-coated NPs contained phosphatidylserine (a negative charged phospholipid) and d-alpha-Tocopheryl polyethylene glycol succinate (a source of vitamin E) to enhance the entrapment efficiency of apolipoprotein A-I in the NPs.	alpha-Tocopherol	35-51	apolipoprotein A-I	Mus musculus	243-261
27567428-3	2016	It was found that the up-regulation of apoA1 and hnRNP-E1 were dependent on the presence and status of blastocysts, on endometrial decidualization and on the progesterone and 17beta-oestradiol status.	Estradiol	175-192	apolipoprotein A-I	Mus musculus	39-44
27579791-8	2016	The effects of SQ and DQ to increase ABCA1 and cell cholesterol release induced by apolipoprotein A-I were dependent on expression of caveolin-1.	Cholesterol	52-63	apolipoprotein A-I	Mus musculus	83-101
27514935-0	2016	PI(4,5)P2 Is Translocated by ABCA1 to the Cell Surface Where It Mediates Apolipoprotein A1 Binding and Nascent HDL Assembly.	(4,5)p2	2-9	apolipoprotein A-I	Mus musculus	73-90
27514935-3	2016	METHODS AND RESULTS: Using multiple biochemical and biophysical methods, we found that apoA1 binds specifically to phosphatidylinositol (4,5) bis-phosphate (PIP2).	Phosphatidylinositol 4,5-Diphosphate	115-155	apolipoprotein A-I	Mus musculus	87-92
27514935-3	2016	METHODS AND RESULTS: Using multiple biochemical and biophysical methods, we found that apoA1 binds specifically to phosphatidylinositol (4,5) bis-phosphate (PIP2).	Phosphatidylinositol 4,5-Diphosphate	157-161	apolipoprotein A-I	Mus musculus	87-92
27514935-5	2016	Enzymatic cleavage of cell surface PIP2 or decreased cellular PIP2 by knockdown of phosphatidylinositol-5-phosphate 4-kinase impaired apoA1 binding and cholesterol efflux to apoA1.	Phosphatidylinositol 4,5-Diphosphate	35-39	apolipoprotein A-I	Mus musculus	134-139
27514935-5	2016	Enzymatic cleavage of cell surface PIP2 or decreased cellular PIP2 by knockdown of phosphatidylinositol-5-phosphate 4-kinase impaired apoA1 binding and cholesterol efflux to apoA1.	Phosphatidylinositol 4,5-Diphosphate	35-39	apolipoprotein A-I	Mus musculus	174-179
27514935-5	2016	Enzymatic cleavage of cell surface PIP2 or decreased cellular PIP2 by knockdown of phosphatidylinositol-5-phosphate 4-kinase impaired apoA1 binding and cholesterol efflux to apoA1.	Phosphatidylinositol 4,5-Diphosphate	62-66	apolipoprotein A-I	Mus musculus	134-139
27514935-5	2016	Enzymatic cleavage of cell surface PIP2 or decreased cellular PIP2 by knockdown of phosphatidylinositol-5-phosphate 4-kinase impaired apoA1 binding and cholesterol efflux to apoA1.	Phosphatidylinositol 4,5-Diphosphate	62-66	apolipoprotein A-I	Mus musculus	174-179
27514935-5	2016	Enzymatic cleavage of cell surface PIP2 or decreased cellular PIP2 by knockdown of phosphatidylinositol-5-phosphate 4-kinase impaired apoA1 binding and cholesterol efflux to apoA1.	phosphatidylinositol 5-phosphate	83-115	apolipoprotein A-I	Mus musculus	134-139
27514935-5	2016	Enzymatic cleavage of cell surface PIP2 or decreased cellular PIP2 by knockdown of phosphatidylinositol-5-phosphate 4-kinase impaired apoA1 binding and cholesterol efflux to apoA1.	phosphatidylinositol 5-phosphate	83-115	apolipoprotein A-I	Mus musculus	174-179
27514935-5	2016	Enzymatic cleavage of cell surface PIP2 or decreased cellular PIP2 by knockdown of phosphatidylinositol-5-phosphate 4-kinase impaired apoA1 binding and cholesterol efflux to apoA1.	Cholesterol	152-163	apolipoprotein A-I	Mus musculus	174-179
27514935-6	2016	PIP2 also increased the spontaneous solubilization of phospholipid liposomes by apoA1.	Phosphatidylinositol 4,5-Diphosphate	0-4	apolipoprotein A-I	Mus musculus	80-85
27514935-6	2016	PIP2 also increased the spontaneous solubilization of phospholipid liposomes by apoA1.	Phospholipids	54-66	apolipoprotein A-I	Mus musculus	80-85
27514935-8	2016	Furthermore, we discovered that PIP2 is effluxed from cells to apoA1, where it is associated with HDL in plasma, and that PIP2 on HDL is taken up by target cells in a scavenger receptor-BI-dependent manner.	Phosphatidylinositol 4,5-Diphosphate	32-36	apolipoprotein A-I	Mus musculus	63-68
27514935-10	2016	CONCLUSIONS: ABCA1 has PIP2 floppase activity, which increases cell surface PIP2 levels that mediate apoA1 binding and lipid efflux during nascent HDL assembly.	Phosphatidylinositol 4,5-Diphosphate	23-27	apolipoprotein A-I	Mus musculus	101-106
27514935-11	2016	We found that PIP2 itself is effluxed to apoA1 and it circulates on plasma HDL, where it can be taken up via the HDL receptor scavenger receptor-BI.	Phosphatidylinositol 4,5-Diphosphate	14-18	apolipoprotein A-I	Mus musculus	41-46
27601313-4	2016	The SERMs impaired cholesterol efflux to apolipoprotein A-I and HDL, and lowered ABCA1 and ABCG1 expression.	Cholesterol	19-30	apolipoprotein A-I	Mus musculus	41-59
27425846-8	2016	Increased susceptibility to DSS-induced inflammation was noted in apoA-I(-/-) mice.	dss	28-31	apolipoprotein A-I	Mus musculus	66-72
27193916-0	2016	In vivo PET imaging with [(18)F]FDG to explain improved glucose uptake in an apolipoprotein A-I treated mouse model of diabetes.	Glucose	56-63	apolipoprotein A-I	Mus musculus	77-95
27193916-4	2016	METHODS: This study used kinetic modelling to investigate the impact of increasing plasma apoA-I levels on the metabolism of glucose in the db/db mouse model.	Glucose	125-132	apolipoprotein A-I	Mus musculus	90-96
27193916-5	2016	RESULTS: Treatment of db/db mice with apoA-I for 2 h significantly improved both glucose tolerance (AUC 2574 +- 70 mmol/l x min vs 2927 +- 137 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.05) and insulin sensitivity (AUC 388.8 +- 23.8 mmol/l x min vs 194.1 +- 19.6 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.001).	Glucose	81-88	apolipoprotein A-I	Mus musculus	38-44
27193916-5	2016	RESULTS: Treatment of db/db mice with apoA-I for 2 h significantly improved both glucose tolerance (AUC 2574 +- 70 mmol/l x min vs 2927 +- 137 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.05) and insulin sensitivity (AUC 388.8 +- 23.8 mmol/l x min vs 194.1 +- 19.6 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.001).	Lead	172-175	apolipoprotein A-I	Mus musculus	38-44
27193916-5	2016	RESULTS: Treatment of db/db mice with apoA-I for 2 h significantly improved both glucose tolerance (AUC 2574 +- 70 mmol/l x min vs 2927 +- 137 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.05) and insulin sensitivity (AUC 388.8 +- 23.8 mmol/l x min vs 194.1 +- 19.6 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.001).	Lead	172-175	apolipoprotein A-I	Mus musculus	161-167
27193916-5	2016	RESULTS: Treatment of db/db mice with apoA-I for 2 h significantly improved both glucose tolerance (AUC 2574 +- 70 mmol/l x min vs 2927 +- 137 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.05) and insulin sensitivity (AUC 388.8 +- 23.8 mmol/l x min vs 194.1 +- 19.6 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.001).	Lead	172-175	apolipoprotein A-I	Mus musculus	161-167
27193916-5	2016	RESULTS: Treatment of db/db mice with apoA-I for 2 h significantly improved both glucose tolerance (AUC 2574 +- 70 mmol/l x min vs 2927 +- 137 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.05) and insulin sensitivity (AUC 388.8 +- 23.8 mmol/l x min vs 194.1 +- 19.6 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.001).	Lead	306-309	apolipoprotein A-I	Mus musculus	38-44
27193916-5	2016	RESULTS: Treatment of db/db mice with apoA-I for 2 h significantly improved both glucose tolerance (AUC 2574 +- 70 mmol/l x min vs 2927 +- 137 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.05) and insulin sensitivity (AUC 388.8 +- 23.8 mmol/l x min vs 194.1 +- 19.6 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.001).	Lead	306-309	apolipoprotein A-I	Mus musculus	161-167
27193916-5	2016	RESULTS: Treatment of db/db mice with apoA-I for 2 h significantly improved both glucose tolerance (AUC 2574 +- 70 mmol/l x min vs 2927 +- 137 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.05) and insulin sensitivity (AUC 388.8 +- 23.8 mmol/l x min vs 194.1 +- 19.6 mmol/l x min, for apoA-I and PBS, respectively; p &lt; 0.001).	Lead	306-309	apolipoprotein A-I	Mus musculus	161-167
27193916-6	2016	ApoA-I treatment also increased glucose uptake by skeletal muscle in both an insulin-dependent and insulin-independent manner as evidenced by increased uptake of fludeoxyglucose ([(18)F]FDG) from plasma into gastrocnemius muscle in apoA-I treated mice, both in the absence and presence of insulin.	Glucose	32-39	apolipoprotein A-I	Mus musculus	0-6
27193916-6	2016	ApoA-I treatment also increased glucose uptake by skeletal muscle in both an insulin-dependent and insulin-independent manner as evidenced by increased uptake of fludeoxyglucose ([(18)F]FDG) from plasma into gastrocnemius muscle in apoA-I treated mice, both in the absence and presence of insulin.	Fluorodeoxyglucose F18	162-177	apolipoprotein A-I	Mus musculus	0-6
27193916-6	2016	ApoA-I treatment also increased glucose uptake by skeletal muscle in both an insulin-dependent and insulin-independent manner as evidenced by increased uptake of fludeoxyglucose ([(18)F]FDG) from plasma into gastrocnemius muscle in apoA-I treated mice, both in the absence and presence of insulin.	Fluorodeoxyglucose F18	162-177	apolipoprotein A-I	Mus musculus	232-238
27193916-8	2016	Treatment of L6 rat skeletal muscle cells with apoA-I for 2 h indicated that increased hexokinase activity mediated the increased rate of glucose phosphorylation.	Glucose	138-145	apolipoprotein A-I	Mus musculus	47-53
27193916-9	2016	CONCLUSIONS/INTERPRETATION: These findings indicate that apoA-I improves glucose disposal in db/db mice by improving insulin sensitivity and enhancing glucose phosphorylation.	Glucose	73-80	apolipoprotein A-I	Mus musculus	57-63
27193916-9	2016	CONCLUSIONS/INTERPRETATION: These findings indicate that apoA-I improves glucose disposal in db/db mice by improving insulin sensitivity and enhancing glucose phosphorylation.	Glucose	151-158	apolipoprotein A-I	Mus musculus	57-63
27236528-5	2016	For radiolabeling with zirconium-89 ((89)Zr), the chelator deferoxamine B was introduced by conjugation to apo A-I or as a phospholipid-chelator (1,2-distearoyl-sn-glycero-3-phosphoethanolamine-deferoxamine B).	Deferoxamine	59-73	apolipoprotein A-I	Mus musculus	107-114
27447612-6	2016	Reduction of the cholesterol level in the lipid rafts by infusion of reconstituted high-density lipoprotein (HDL) or its major apolipoprotein, apoA-I, reverses hypercholesterolemia-induced HSPC expansion.	Cholesterol	17-28	apolipoprotein A-I	Mus musculus	143-149
27150392-12	2016	CONCLUSIONS: Reductions in Dio1 expression reduce the expression of ApoA-I in a 3,5,3"-triiodothyronine-/thyroid hormone response element-independent manner.	3,5,3"-triiodothyronine	80-103	apolipoprotein A-I	Mus musculus	68-74
27207515-0	2016	Dual Actions of Apolipoprotein A-I on Glucose-Stimulated Insulin Secretion and Insulin-Independent Peripheral Tissue Glucose Uptake Lead to Increased Heart and Skeletal Muscle Glucose Disposal.	Glucose	38-45	apolipoprotein A-I	Mus musculus	16-34
27207515-1	2016	Apolipoprotein A-I (apoA-I) of HDL is central to the transport of cholesterol in circulation.	Cholesterol	66-77	apolipoprotein A-I	Mus musculus	0-18
27207515-1	2016	Apolipoprotein A-I (apoA-I) of HDL is central to the transport of cholesterol in circulation.	Cholesterol	66-77	apolipoprotein A-I	Mus musculus	20-26
27207515-2	2016	ApoA-I also provides glucose control with described in vitro effects of apoA-I on beta-cell insulin secretion and muscle glucose uptake.	Glucose	21-28	apolipoprotein A-I	Mus musculus	0-6
27207515-2	2016	ApoA-I also provides glucose control with described in vitro effects of apoA-I on beta-cell insulin secretion and muscle glucose uptake.	Glucose	121-128	apolipoprotein A-I	Mus musculus	0-6
27207515-3	2016	In addition, apoA-I injections in insulin-resistant diet-induced obese (DIO) mice lead to increased glucose-stimulated insulin secretion (GSIS) and peripheral tissue glucose uptake.	Glucose	100-107	apolipoprotein A-I	Mus musculus	13-19
27207515-3	2016	In addition, apoA-I injections in insulin-resistant diet-induced obese (DIO) mice lead to increased glucose-stimulated insulin secretion (GSIS) and peripheral tissue glucose uptake.	Glucose	166-173	apolipoprotein A-I	Mus musculus	13-19
27207515-6	2016	Data demonstrate that apoA-I to an equal extent enhances GSIS and acts as peripheral tissue activator of insulin-independent glucose uptake and verify skeletal muscle as an apoA-I target tissue.	Glucose	125-132	apolipoprotein A-I	Mus musculus	22-28
27207515-7	2016	Intriguingly, our analyses also identify the heart as an important target tissue for the apoA-I-stimulated glucose uptake, with potential implications in diabetic cardiomyopathy.	Glucose	107-114	apolipoprotein A-I	Mus musculus	89-95
27433174-8	2016	The silica-induced lung fibrosis model was established using ApoA1 overexpressing transgenic mice.	Silicon Dioxide	4-10	apolipoprotein A-I	Mus musculus	61-66
27433174-13	2016	In a mouse model of silica-induced lung fibrosis, ApoA1 overexpression reduced the silica-mediated effects, which were increased N-cadherin and decreased E-cadherin expression in the alveolar epithelium.	Silicon Dioxide	20-26	apolipoprotein A-I	Mus musculus	50-55
27433174-13	2016	In a mouse model of silica-induced lung fibrosis, ApoA1 overexpression reduced the silica-mediated effects, which were increased N-cadherin and decreased E-cadherin expression in the alveolar epithelium.	Silicon Dioxide	83-89	apolipoprotein A-I	Mus musculus	50-55
27320924-4	2016	These changes displaced ABCA1 from the cell surface but created new binding sites for apolipoprotein A-I, resulting in enhanced cholesterol efflux.	Cholesterol	128-139	apolipoprotein A-I	Mus musculus	86-104
27108950-7	2016	Pemafibrate treatment of hapoA-I tg mice increases plasma HDL cholesterol, apoA-I and stimulates RCT to feces.	Cholesterol	62-73	apolipoprotein A-I	Mus musculus	26-32
26759003-3	2016	We used the mouse osteocyte cell line (MLO-Y4) to investigate the effects of TNF alpha on the expression of cholesterol acceptor proteins such as apolipoprotein A-I (apo A-I) and apolipoprotein E (apo E), as well as on the cholesterol transporters ATP-binding cassette-1 (ABCA1), scavenger receptor class B type 1 (SRB1), and cluster of differentiation 36 (CD36).	Cholesterol	108-119	apolipoprotein A-I	Mus musculus	146-164
26759003-5	2016	Treatment of MLO-Y4 cells with TNF alpha had no effect on SRB1, CD36, and osteocalcin levels; however, TNF alpha reduced ABCA1 protein levels in a dose-dependent manner and cholesterol efflux to apo A-I.	Cholesterol	173-184	apolipoprotein A-I	Mus musculus	195-202
26965683-3	2016	Apolipoprotein A-I (apoA-I) exerts anti-inflammatory effects on adipocytes by effluxing cholesterol from the cells via the ATP binding cassette transporter A1 (ABCA1).	Cholesterol	88-99	apolipoprotein A-I	Mus musculus	0-18
26965683-3	2016	Apolipoprotein A-I (apoA-I) exerts anti-inflammatory effects on adipocytes by effluxing cholesterol from the cells via the ATP binding cassette transporter A1 (ABCA1).	Cholesterol	88-99	apolipoprotein A-I	Mus musculus	20-26
27017606-9	2016	COT administration reduced lipid accumulation in the liver, ameliorated the pathological changes, and lessened liver injury, the levels of TG, TC, and non-HDL-C in plasma were decreased significantly, and COT led to a significant increase in plasma HDL-C and apolipoprotein A (apoA1).	Carbon	0-1	apolipoprotein A-I	Mus musculus	277-282
27105909-0	2016	Heparin interactions with apoA1 and SAA in inflammation-associated HDL.	Heparin	0-7	apolipoprotein A-I	Mus musculus	26-31
27105909-1	2016	Apolipoprotein A1 (apoA1) is the main protein component responsible for transportation of cholesterol on high-density lipoprotein (HDL).	Cholesterol	90-101	apolipoprotein A-I	Mus musculus	0-17
27105909-1	2016	Apolipoprotein A1 (apoA1) is the main protein component responsible for transportation of cholesterol on high-density lipoprotein (HDL).	Cholesterol	90-101	apolipoprotein A-I	Mus musculus	19-24
27105909-4	2016	We report herein that the polysaccharide heparin interacts with both apoA1 and SAA in HDL isolated from plasma of inflamed mice.	Polysaccharides	26-40	apolipoprotein A-I	Mus musculus	69-74
27105909-4	2016	We report herein that the polysaccharide heparin interacts with both apoA1 and SAA in HDL isolated from plasma of inflamed mice.	Heparin	41-48	apolipoprotein A-I	Mus musculus	69-74
26279300-5	2016	We show that ApoA-I is expressed at higher levels in the proximal compared with the distal part of the colon and its ablation in mice results in exaggerated DSS-induced colitis and disruption of epithelial architecture in larger areas of the large intestine.	dss	157-160	apolipoprotein A-I	Mus musculus	13-19
26279300-7	2016	Genetic interference with ApoA-I levels in vivo impacted on the number, size and distribution of AOM/DSS-induced colon tumors.	dss	101-104	apolipoprotein A-I	Mus musculus	26-32
26454209-2	2016	HDL/apoA-I particles are produced by the liver and intestine and, in addition to removing excess cholesterol from the body, are increasingly recognized to have vasoprotective functions.	Cholesterol	97-108	apolipoprotein A-I	Mus musculus	4-10
26828321-0	2016	Apolipoprotein A-I Mimetic Peptide D-4F Reduces Cardiac Hypertrophy and Improves Apolipoprotein A-I-Mediated Reverse Cholesterol Transport From Cardiac Tissue in LDL Receptor-null Mice Fed a Western Diet.	Cholesterol	117-128	apolipoprotein A-I	Mus musculus	0-18
26828321-0	2016	Apolipoprotein A-I Mimetic Peptide D-4F Reduces Cardiac Hypertrophy and Improves Apolipoprotein A-I-Mediated Reverse Cholesterol Transport From Cardiac Tissue in LDL Receptor-null Mice Fed a Western Diet.	Cholesterol	117-128	apolipoprotein A-I	Mus musculus	81-99
26828321-2	2016	Because high-density lipoprotein and its major protein apolipoprotein A-I (apoA-I) mediate reverse cholesterol transport (RCT) and have cardiac protective effects, we hypothesized that the apoA-I mimetic peptide D-4F could promote RCT in cardiac tissue and decrease cardiac hypertrophy induced by hypercholesterolemia.	Cholesterol	99-110	apolipoprotein A-I	Mus musculus	55-73
26828321-2	2016	Because high-density lipoprotein and its major protein apolipoprotein A-I (apoA-I) mediate reverse cholesterol transport (RCT) and have cardiac protective effects, we hypothesized that the apoA-I mimetic peptide D-4F could promote RCT in cardiac tissue and decrease cardiac hypertrophy induced by hypercholesterolemia.	Cholesterol	99-110	apolipoprotein A-I	Mus musculus	75-81
26828321-2	2016	Because high-density lipoprotein and its major protein apolipoprotein A-I (apoA-I) mediate reverse cholesterol transport (RCT) and have cardiac protective effects, we hypothesized that the apoA-I mimetic peptide D-4F could promote RCT in cardiac tissue and decrease cardiac hypertrophy induced by hypercholesterolemia.	Cholesterol	99-110	apolipoprotein A-I	Mus musculus	189-195
26848156-3	2016	APPROACH AND RESULTS: Spiroquinone and diphenoquinone increased ATP-binding cassette transporter A1 protein (2.8- and 2.6-fold, respectively, P&lt;0.01) and apolipoprotein A-I-mediated cholesterol release (1.4- and 1.4-fold, P&lt;0.01 and P&lt;0.05, respectively) in RAW264.7 cells.	spiroquinone	22-34	apolipoprotein A-I	Mus musculus	157-175
26848156-3	2016	APPROACH AND RESULTS: Spiroquinone and diphenoquinone increased ATP-binding cassette transporter A1 protein (2.8- and 2.6-fold, respectively, P&lt;0.01) and apolipoprotein A-I-mediated cholesterol release (1.4- and 1.4-fold, P&lt;0.01 and P&lt;0.05, respectively) in RAW264.7 cells.	diphenoquinone	39-53	apolipoprotein A-I	Mus musculus	157-175
26891738-4	2016	Genetic deletion of APOA1 in LDL receptor (LDLR) knockout mice was associated with HDL deficiency and a parallel increase in the level of cholesterol associated with nonHDL fractions.	Cholesterol	138-149	apolipoprotein A-I	Mus musculus	20-25
26814636-0	2016	The ApoA-I mimetic peptide FAMP promotes recovery from hindlimb ischemia through a nitric oxide (NO)-related pathway.	fludarabine phosphate	27-31	apolipoprotein A-I	Mus musculus	4-10
26814636-0	2016	The ApoA-I mimetic peptide FAMP promotes recovery from hindlimb ischemia through a nitric oxide (NO)-related pathway.	Nitric Oxide	83-95	apolipoprotein A-I	Mus musculus	4-10
26749169-5	2016	SUMMARY:  BACKGROUND: The ATP-binding cassette transporter ABCA1 is required for the conversion of apolipoprotein A-1 to high-density lipoprotein (HDL), and its defect causes Tangier disease, a rare disorder characterized by an absence of HDL and accumulation of cholesterol in peripheral tissues.	Cholesterol	263-274	apolipoprotein A-I	Mus musculus	99-117
26487692-2	2016	The process involves cholesterol efflux from foam cells to extracellular acceptors such as apolipoprotein A-I (apoA-I) and high-density lipoprotein (HDL) that mediate transport to the liver.	Cholesterol	21-32	apolipoprotein A-I	Mus musculus	91-109
26487692-2	2016	The process involves cholesterol efflux from foam cells to extracellular acceptors such as apolipoprotein A-I (apoA-I) and high-density lipoprotein (HDL) that mediate transport to the liver.	Cholesterol	21-32	apolipoprotein A-I	Mus musculus	111-117
26487692-9	2016	PLIN2 deficiency and apoA-I cumulatively reduced LDs and cholesterol ester content in cultured macrophages.	Cholesterol Esters	57-74	apolipoprotein A-I	Mus musculus	21-27
26673204-6	2016	In contrast, ABCA1-specific cholesterol efflux correlated strongly with HDL"s content of APOA1, APOC3, and APOD, but not RBP4 and PLTP.	Cholesterol	28-39	apolipoprotein A-I	Mus musculus	89-94
26086425-3	2016	Although apolipoprotein A-1 (ApoA1) has antiinflammatory and antioxidant properties as well as cholesterol efflux potential, its role in cigarette smoke (CS)-induced emphysema has not been determined.	Cesium	154-156	apolipoprotein A-I	Mus musculus	29-34
26086425-7	2016	Compared with the control TG mice, ApoA1 overexpression attenuated lung inflammation, oxidative stress, metalloprotease activation, and apoptosis in CS-exposed mouse lungs.	Cesium	149-151	apolipoprotein A-I	Mus musculus	35-40
26086425-8	2016	To explore a plausible mechanism of antiapoptotic activity of ApoA1, alveolar epithelial cells (A549) were treated with CS extract (CSE).	Cesium	120-122	apolipoprotein A-I	Mus musculus	62-67
26086425-9	2016	ApoA1 prevented CSE-induced translocation of Fas and downstream death-inducing signaling complex into lipid rafts, thereby inhibiting Fas-mediated apoptosis.	ammonium ferrous sulfate	45-48	apolipoprotein A-I	Mus musculus	0-5
26086425-10	2016	Taken together, the data showed that ApoA1 overexpression attenuated CS-induced lung inflammation and emphysema in mice.	Cesium	69-71	apolipoprotein A-I	Mus musculus	37-42
26427927-8	2016	The IFNbeta-induced increase in lipid content was also associated with decreased ApoA1-mediated cholesterol efflux, in response to decreased ABCA1 protein and gene expression.	Cholesterol	96-107	apolipoprotein A-I	Mus musculus	81-86
27192798-3	2016	Reverse cholesterol transport (RCT) is believed to be a primary atheroprotective property of HDL and its major protein, apolipoprotein A-I(apoA-I).	Cholesterol	8-19	apolipoprotein A-I	Mus musculus	120-138
27192798-3	2016	Reverse cholesterol transport (RCT) is believed to be a primary atheroprotective property of HDL and its major protein, apolipoprotein A-I(apoA-I).	Cholesterol	8-19	apolipoprotein A-I	Mus musculus	139-145
27192798-4	2016	HDL and apoA-I have been shown to promote the efflux of excess cholesterol from macrophage-derived foam cells via the cholesterol transporters, ATP-binding cassette transporter A1 (ABCA1), ABCG1, and scavenger receptor class B, type I (SR-BI), and then transport it back to the liver for excretion into bile and eventually into the feces.	Cholesterol	63-74	apolipoprotein A-I	Mus musculus	8-14
26510953-1	2015	UNLABELLED: ATP binding cassette transporter A1 (encoded by ABCA1) regulates cholesterol efflux from cells to apolipoproteins A-I and E (ApoA-I and APOE; encoded by APOA1 and APOE, respectively) and the generation of high density lipoproteins.	Cholesterol	77-88	apolipoprotein A-I	Mus musculus	110-135
26510953-1	2015	UNLABELLED: ATP binding cassette transporter A1 (encoded by ABCA1) regulates cholesterol efflux from cells to apolipoproteins A-I and E (ApoA-I and APOE; encoded by APOA1 and APOE, respectively) and the generation of high density lipoproteins.	Cholesterol	77-88	apolipoprotein A-I	Mus musculus	137-143
26510953-1	2015	UNLABELLED: ATP binding cassette transporter A1 (encoded by ABCA1) regulates cholesterol efflux from cells to apolipoproteins A-I and E (ApoA-I and APOE; encoded by APOA1 and APOE, respectively) and the generation of high density lipoproteins.	Cholesterol	77-88	apolipoprotein A-I	Mus musculus	165-170
26429563-8	2015	LDLr(-/-) and ApoA1(-/-) myocytes contained more cholesterol than WT (34.4+-2.8 and 36.5+-2.4 versus 25.5+-0.4 mumol/g protein).	Cholesterol	49-60	apolipoprotein A-I	Mus musculus	14-19
26429563-10	2015	The L-type calcium current (I(Ca)), however, was larger in LDLr(-/-) and ApoA1(-/-) than in WT (12.1+-0.7 and 12.8+-0.8 versus 9.4+-1.1 pA/pF).	Calcium	11-18	apolipoprotein A-I	Mus musculus	73-78
26429563-11	2015	Calcium transient amplitude and fractional sarcoplasmic reticulum calcium release were larger and action potential and QTc duration longer in LDLr(-/-) and ApoA1(-/-) than in WT mice (action potential duration at 90% of repolarization: 102+-4 and 106+-3 versus 84+-3.1 ms; QTc: 50.9+-1.3 and 52.8+-0.8 versus 43.5+-1.2 ms).	Calcium	0-7	apolipoprotein A-I	Mus musculus	156-161
26253613-4	2015	Macrophage cholesterol efflux to apolipoprotein A1 and HDL and reverse cholesterol transport to plasma, liver, and feces were reduced in diabetic macrophages through RAGE.	Cholesterol	11-22	apolipoprotein A-I	Mus musculus	33-50
26466956-0	2015	Cholesterol-Independent Suppression of Lymphocyte Activation, Autoimmunity, and Glomerulonephritis by Apolipoprotein A-I in Normocholesterolemic Lupus-Prone Mice.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	102-120
26466956-1	2015	Apolipoprotein (Apo)A-I, the major lipid-binding protein of high-density lipoprotein, can prevent autoimmunity and suppress inflammation in hypercholesterolemic mice by attenuating lymphocyte cholesterol accumulation and removing tissue-oxidized lipids.	Cholesterol	145-156	apolipoprotein A-I	Mus musculus	16-23
26466956-4	2015	Increased ApoA-I in ApoA-I(tg) mice suppressed CD4(+) T and B cell activation without changing lymphocyte cholesterol levels or reducing major ApoA-I-binding oxidized fatty acids.	Fatty Acids	167-178	apolipoprotein A-I	Mus musculus	10-16
26466956-5	2015	Unexpectedly, oxidized fatty acid peroxisome proliferator-activated receptor gamma ligands 13- and 9-hydroxyoctadecadienoic acid were increased in lymphocytes of autoimmune ApoA-I(tg) mice.	Fatty Acids	23-33	apolipoprotein A-I	Mus musculus	173-183
26466956-5	2015	Unexpectedly, oxidized fatty acid peroxisome proliferator-activated receptor gamma ligands 13- and 9-hydroxyoctadecadienoic acid were increased in lymphocytes of autoimmune ApoA-I(tg) mice.	13- and 9-hydroxyoctadecadienoic acid	91-128	apolipoprotein A-I	Mus musculus	173-183
26420354-0	2015	Deficiency in apolipoprotein A-I ablates the pharmacological effects of metformin on plasma glucose homeostasis and hepatic lipid deposition.	Metformin	72-81	apolipoprotein A-I	Mus musculus	14-32
26420354-0	2015	Deficiency in apolipoprotein A-I ablates the pharmacological effects of metformin on plasma glucose homeostasis and hepatic lipid deposition.	Glucose	92-99	apolipoprotein A-I	Mus musculus	14-32
26420354-2	2015	Here we investigated the potential involvement of ApoA-I in the pharmacological effects of metformin on glucose intolerance and NAFLD development.	Metformin	91-100	apolipoprotein A-I	Mus musculus	50-56
26420354-5	2015	Metformin treatment led to a comparable reduction in plasma insulin levels in both C57BL/6 and apoa1(-/-) mice following intraperitoneal glucose tolerance test.	Metformin	0-9	apolipoprotein A-I	Mus musculus	95-100
26420354-7	2015	Similarly, deficiency in ApoA-I ablated the effect of metformin on hepatic lipid deposition and NAFLD development.	Metformin	54-63	apolipoprotein A-I	Mus musculus	25-31
26420354-8	2015	Gene expression analysis indicated that the effects of ApoA-I on metformin treatment may be independent of adenosine monophosphate-activated protein kinase (AMPK) activation and de novo lipogenesis.	Metformin	65-74	apolipoprotein A-I	Mus musculus	55-61
26420354-9	2015	Interestingly, metformin treatment reduced mitochondrial oxidative phosphorylation function only in apoa1(-/-) mice.	Metformin	15-24	apolipoprotein A-I	Mus musculus	100-105
26420354-10	2015	Our data show that the role of ApoA-I in diabetes extends to the modulation of the pharmacological actions of metformin, a common drug for the treatment of type 2 diabetes.	Metformin	110-119	apolipoprotein A-I	Mus musculus	31-37
26363436-5	2015	RESULTS: The expression of either apoA-I mutant was associated with markedly reduced serum apoA-I (&lt;10% of WT apoA-I), total and HDL-cholesterol levels (~20% and ~7% of WT apoA-I, respectively) and the formation of few small size HDL particles with prebeta2 and alpha3, alpha4 electrophoretic mobility.	Cholesterol	136-147	apolipoprotein A-I	Mus musculus	34-40
26363436-7	2015	However, the apoA-I(L141R)Pisa or apoA-I(L159R)FIN-containing HDL particles demonstrated increased capacity to promote ATP-Binding Cassette Transporter A1-mediated cholesterol efflux from macrophages.	Cholesterol	164-175	apolipoprotein A-I	Mus musculus	13-19
26363436-7	2015	However, the apoA-I(L141R)Pisa or apoA-I(L159R)FIN-containing HDL particles demonstrated increased capacity to promote ATP-Binding Cassette Transporter A1-mediated cholesterol efflux from macrophages.	Cholesterol	164-175	apolipoprotein A-I	Mus musculus	34-40
26368306-0	2015	Perhexiline activates KLF14 and reduces atherosclerosis by modulating ApoA-I production.	Perhexiline	0-11	apolipoprotein A-I	Mus musculus	70-76
26368306-7	2015	Indeed, in WT mice, treatment with perhexiline increased HDL-C levels and cholesterol efflux capacity via KLF14-mediated upregulation of ApoA-I expression.	Perhexiline	35-46	apolipoprotein A-I	Mus musculus	137-143
26255968-4	2015	Administration of high-density lipoprotein (HDL) or apolipoprotein AI (apoAI) to the apical compartment enhanced transendothelial cholesterol transport in a concentration-dependent manner.	Cholesterol	130-141	apolipoprotein A-I	Mus musculus	52-69
26377330-9	2015	(14)C-cholesterol efflux mediated by apo A-I and HDL2 and the uptake of (3)H-cholesteryl oleoyl ether ((3)H-COE)-acetylated-LDL were determined in macrophages isolated from sedentary and trained animals 48 h after the last exercise session.	Cholesterol	6-17	apolipoprotein A-I	Mus musculus	37-44
26119689-3	2015	In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1).	Retinoids	58-67	apolipoprotein A-I	Mus musculus	174-191
26119689-3	2015	In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1).	Retinoids	58-67	apolipoprotein A-I	Mus musculus	193-199
26119689-3	2015	In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1).	all-trans	82-91	apolipoprotein A-I	Mus musculus	174-191
26119689-3	2015	In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1).	all-trans	82-91	apolipoprotein A-I	Mus musculus	193-199
26119689-3	2015	In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1).	Tretinoin	92-105	apolipoprotein A-I	Mus musculus	174-191
26119689-3	2015	In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1).	Tretinoin	92-105	apolipoprotein A-I	Mus musculus	193-199
26119689-3	2015	In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1).	Tretinoin	107-111	apolipoprotein A-I	Mus musculus	174-191
26119689-3	2015	In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1).	Tretinoin	107-111	apolipoprotein A-I	Mus musculus	193-199
26119689-3	2015	In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1).	Cholesterol	152-163	apolipoprotein A-I	Mus musculus	174-191
26119689-3	2015	In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1).	Cholesterol	152-163	apolipoprotein A-I	Mus musculus	193-199
26119689-6	2015	RAs elevated StAR promoter activity in macrophages, and an increase in StAR levels augmented cholesterol efflux to Apo-A1, suggesting retinoid-mediated efflux of cholesterol involves enhanced oxysterol production.	Cholesterol	93-104	apolipoprotein A-I	Mus musculus	115-121
26119689-6	2015	RAs elevated StAR promoter activity in macrophages, and an increase in StAR levels augmented cholesterol efflux to Apo-A1, suggesting retinoid-mediated efflux of cholesterol involves enhanced oxysterol production.	Retinoids	134-142	apolipoprotein A-I	Mus musculus	115-121
26119689-6	2015	RAs elevated StAR promoter activity in macrophages, and an increase in StAR levels augmented cholesterol efflux to Apo-A1, suggesting retinoid-mediated efflux of cholesterol involves enhanced oxysterol production.	Cholesterol	162-173	apolipoprotein A-I	Mus musculus	115-121
26005953-0	2015	Newly developed apolipoprotein A-I mimetic peptide promotes macrophage reverse cholesterol transport in vivo.	Cholesterol	79-90	apolipoprotein A-I	Mus musculus	16-34
26005953-1	2015	BACKGROUND: We elucidated the effect of newly developed Fukuoka Apolipoprotein A-I Mimetic Peptide (FAMP) on in vivo macrophage reverse cholesterol transport (RCT) and the underlying mechanisms.	Cholesterol	136-147	apolipoprotein A-I	Mus musculus	64-82
26112022-6	2015	(89)Zr was complexed with deferoxamine (also known as desferrioxamine B, desferoxamine B), conjugated either to a phospholipid or to apoA-I to generate (89)Zr-PL-HDL and (89)Zr-AI-HDL, respectively.	Deferoxamine	26-38	apolipoprotein A-I	Mus musculus	133-139
26112022-6	2015	(89)Zr was complexed with deferoxamine (also known as desferrioxamine B, desferoxamine B), conjugated either to a phospholipid or to apoA-I to generate (89)Zr-PL-HDL and (89)Zr-AI-HDL, respectively.	Deferoxamine	54-71	apolipoprotein A-I	Mus musculus	133-139
26112022-6	2015	(89)Zr was complexed with deferoxamine (also known as desferrioxamine B, desferoxamine B), conjugated either to a phospholipid or to apoA-I to generate (89)Zr-PL-HDL and (89)Zr-AI-HDL, respectively.	Deferoxamine	73-88	apolipoprotein A-I	Mus musculus	133-139
25838426-1	2015	OBJECTIVE: By excreting cellular cholesterol to apolipoprotein A-I, ATP-binding cassette transporter A1 (ABCA1) mediates the biogenesis of high-density lipoprotein in hepatocytes and prevents foam cell formation from macrophages.	Cholesterol	33-44	apolipoprotein A-I	Mus musculus	48-66
25572138-6	2015	This coincided with a 30% decrease in the capacity of macrophages to efflux cholesterol to apolipoprotein A1.	Cholesterol	76-87	apolipoprotein A-I	Mus musculus	91-108
25761370-1	2015	ABCA1 plays a key role in the initial lipidation of apoA-I, which generates circulating HDL cholesterol.	Cholesterol	92-103	apolipoprotein A-I	Mus musculus	52-58
25790332-1	2015	The reaction of Streptococcal serum opacity factor (SOF) against plasma high-density lipoproteins (HDL) produces a large cholesteryl ester-rich microemulsion (CERM), a smaller neo HDL that is apolipoprotein (apo) AI-poor, and lipid-free apo AI.	Cholesterol Esters	121-138	apolipoprotein A-I	Mus musculus	237-243
25790332-8	2015	Chaotropic perturbation studies using guanidine hydrochloride showed that apo AI-null HDL was more stable than WT HDL.	Guanidine	38-61	apolipoprotein A-I	Mus musculus	74-80
25790332-10	2015	Both SOF and guanidine hydrochloride displaced apo AI from the reconstituted HDL.	Guanidine	13-36	apolipoprotein A-I	Mus musculus	47-53
25550459-6	2015	Treatment of apoA-I and HDL with MMP-8 resulted in significant reduction (up to 84%, P &lt; 0.001) in their ability to facilitate cholesterol efflux from cholesterol-loaded THP-1 macrophages.	Cholesterol	130-141	apolipoprotein A-I	Mus musculus	13-19
25550459-6	2015	Treatment of apoA-I and HDL with MMP-8 resulted in significant reduction (up to 84%, P &lt; 0.001) in their ability to facilitate cholesterol efflux from cholesterol-loaded THP-1 macrophages.	Cholesterol	154-165	apolipoprotein A-I	Mus musculus	13-19
25550459-7	2015	The cleavage of apoA-I by MMP-8 and the reduction in its cholesterol efflux capacity was inhibited by doxycycline.	Cholesterol	57-68	apolipoprotein A-I	Mus musculus	16-22
25550459-7	2015	The cleavage of apoA-I by MMP-8 and the reduction in its cholesterol efflux capacity was inhibited by doxycycline.	Doxycycline	102-113	apolipoprotein A-I	Mus musculus	16-22
25550459-10	2015	Proteolytic modification of apoA-I by MMP-8 may impair the first steps of reverse cholesterol transport, leading to increased accumulation of cholesterol in the vessel walls.	Cholesterol	82-93	apolipoprotein A-I	Mus musculus	28-34
25550459-10	2015	Proteolytic modification of apoA-I by MMP-8 may impair the first steps of reverse cholesterol transport, leading to increased accumulation of cholesterol in the vessel walls.	Cholesterol	142-153	apolipoprotein A-I	Mus musculus	28-34
25477345-8	2015	To further investigate the mechanisms behind the reduction in plasma apolipoprotein A-I and high-density lipoprotein lipids, we measured apolipoprotein A-I-mediated cholesterol efflux in adipose tissue explants and found that endogenous and exogenous PLTP significantly increased cholesterol efflux from the explants.	Cholesterol	165-176	apolipoprotein A-I	Mus musculus	137-155
25524771-7	2015	In addition, transfection of murine macrophages with miR-302a attenuated cholesterol efflux to apolipoprotein A-1 (apoA-1) by 38%.	Cholesterol	73-84	apolipoprotein A-I	Mus musculus	95-113
25524771-7	2015	In addition, transfection of murine macrophages with miR-302a attenuated cholesterol efflux to apolipoprotein A-1 (apoA-1) by 38%.	Cholesterol	73-84	apolipoprotein A-I	Mus musculus	115-121
25395590-1	2015	Apolipoprotein A-I (apoA-I) mimetic peptides are currently being developed as possible new agents for the treatment of cardiovascular disease based on their ability to promote cholesterol efflux and their other beneficial antiatherogenic properties.	Cholesterol	176-187	apolipoprotein A-I	Mus musculus	0-18
25395590-1	2015	Apolipoprotein A-I (apoA-I) mimetic peptides are currently being developed as possible new agents for the treatment of cardiovascular disease based on their ability to promote cholesterol efflux and their other beneficial antiatherogenic properties.	Cholesterol	176-187	apolipoprotein A-I	Mus musculus	20-26
25332231-9	2015	Functionally, the absence of FHL2 resulted in attenuated cholesterol efflux to both ApoA-1 and high-density lipoprotein (HDL), in agreement with reduced LXR signaling.	Cholesterol	57-68	apolipoprotein A-I	Mus musculus	84-90
28247863-5	2015	Mucosal damage from colitis induced by dextran sodium sulphate (DSS) and 2,4,6-trinitrobenzenesulfonic acid (TNBS) was scored by colonoscopy and histology in apoA-I transgenic (Tg) and apoA-I knockout (KO) and wild-type (WT) mice.	dss	64-67	apolipoprotein A-I	Mus musculus	158-164
28247863-5	2015	Mucosal damage from colitis induced by dextran sodium sulphate (DSS) and 2,4,6-trinitrobenzenesulfonic acid (TNBS) was scored by colonoscopy and histology in apoA-I transgenic (Tg) and apoA-I knockout (KO) and wild-type (WT) mice.	Trinitrobenzenesulfonic Acid	109-113	apolipoprotein A-I	Mus musculus	158-164
28247863-9	2015	DSS/TNBS-treated apoA-I KO mice displayed increased mucosal damage upon both colonoscopy and histology, increased intestinal MPO activity and mRNA expression of TNF and ICAM as compared with WT and apoA-I Tg mice.	dss	0-3	apolipoprotein A-I	Mus musculus	17-23
28247863-9	2015	DSS/TNBS-treated apoA-I KO mice displayed increased mucosal damage upon both colonoscopy and histology, increased intestinal MPO activity and mRNA expression of TNF and ICAM as compared with WT and apoA-I Tg mice.	dss	0-3	apolipoprotein A-I	Mus musculus	198-204
28247863-9	2015	DSS/TNBS-treated apoA-I KO mice displayed increased mucosal damage upon both colonoscopy and histology, increased intestinal MPO activity and mRNA expression of TNF and ICAM as compared with WT and apoA-I Tg mice.	Trinitrobenzenesulfonic Acid	4-8	apolipoprotein A-I	Mus musculus	17-23
28247863-9	2015	DSS/TNBS-treated apoA-I KO mice displayed increased mucosal damage upon both colonoscopy and histology, increased intestinal MPO activity and mRNA expression of TNF and ICAM as compared with WT and apoA-I Tg mice.	Trinitrobenzenesulfonic Acid	4-8	apolipoprotein A-I	Mus musculus	198-204
28247863-10	2015	In contrast, apoA-I Tg mice showed less severe symptoms monitored by colonoscopy and MPO activity in both the DSS and TNBS colitis models.	dss	110-113	apolipoprotein A-I	Mus musculus	13-19
24844148-1	2014	ATP-binding cassette transporter A1 (ABCA1) mediates cholesterol efflux to lipid-free apolipoprotein A-I (apoA-I) and apolipoprotein E (apoE).	Cholesterol	53-64	apolipoprotein A-I	Mus musculus	86-104
24844148-1	2014	ATP-binding cassette transporter A1 (ABCA1) mediates cholesterol efflux to lipid-free apolipoprotein A-I (apoA-I) and apolipoprotein E (apoE).	Cholesterol	53-64	apolipoprotein A-I	Mus musculus	106-112
25451254-0	2014	Apolipoprotein A-I expression suppresses COX-2 expression by reducing reactive oxygen species in hepatocytes.	Reactive Oxygen Species	70-93	apolipoprotein A-I	Mus musculus	0-18
25451254-2	2014	Apolipoprotein A-I (apoA-I) accepts cellular cholesterol and phospholipids transported by ATP-binding cassette transporter A1 to generate nascent high density lipoprotein particles.	Cholesterol	45-56	apolipoprotein A-I	Mus musculus	0-18
25451254-2	2014	Apolipoprotein A-I (apoA-I) accepts cellular cholesterol and phospholipids transported by ATP-binding cassette transporter A1 to generate nascent high density lipoprotein particles.	Cholesterol	45-56	apolipoprotein A-I	Mus musculus	20-26
25451254-2	2014	Apolipoprotein A-I (apoA-I) accepts cellular cholesterol and phospholipids transported by ATP-binding cassette transporter A1 to generate nascent high density lipoprotein particles.	Phospholipids	61-74	apolipoprotein A-I	Mus musculus	0-18
25451254-2	2014	Apolipoprotein A-I (apoA-I) accepts cellular cholesterol and phospholipids transported by ATP-binding cassette transporter A1 to generate nascent high density lipoprotein particles.	Phospholipids	61-74	apolipoprotein A-I	Mus musculus	20-26
25451254-4	2014	Here, we examined the effect of apoA-I overexpression on ROS and genes involved in inflammation in both BEL-7402 hepatocytes and mice.	Reactive Oxygen Species	57-60	apolipoprotein A-I	Mus musculus	32-38
25451254-6	2014	The overexpression of apoA-I in both models resulted in decreased ROS and lipid peroxidation levels, as well as a reduced MAPK phosphorylation and decreased expression levels of c-Fos and COX-2.	Reactive Oxygen Species	66-69	apolipoprotein A-I	Mus musculus	22-28
25451254-7	2014	These results suggest that apoA-I overexpression can reduce steatosis by decreasing ROS levels and suppressing COX-2-induced inflammation in hepatocytes.	Reactive Oxygen Species	84-87	apolipoprotein A-I	Mus musculus	27-33
24813055-1	2014	Apolipoprotein A-I (apoA-I) is an important component of high-density lipoprotein particles that mediates reverse cholesterol transport out of cells by interacting with the ATP-binding cassette transporter 1 (ABCA1).	Cholesterol	114-125	apolipoprotein A-I	Mus musculus	0-18
24813055-1	2014	Apolipoprotein A-I (apoA-I) is an important component of high-density lipoprotein particles that mediates reverse cholesterol transport out of cells by interacting with the ATP-binding cassette transporter 1 (ABCA1).	Cholesterol	114-125	apolipoprotein A-I	Mus musculus	20-26
25014134-4	2014	In the present study, we have identified several critical genes in lipid homeostasis (Apoa1, Apoa2 and ApoF) that are repressed by RA-treatment in a SHP dependent manner, in vitro and also in vivo with the use of the SHP null mice.	Tretinoin	131-133	apolipoprotein A-I	Mus musculus	86-91
25347070-2	2014	ORP8 downregulates ABCA1 expression in macrophages and cellular cholesterol efflux to apolipoprotein A-I.	Cholesterol	64-75	apolipoprotein A-I	Mus musculus	86-104
25037389-1	2014	A new water-soluble polysaccharide (SEP-2), with a molecular weight of 6.78 x 10(5)Da, was isolated from Strongylocentrotus nudus eggs under the extraction conditions optimized by response surface methodology (RSM).	Water	6-11	apolipoprotein A-I	Mus musculus	36-41
25037389-1	2014	A new water-soluble polysaccharide (SEP-2), with a molecular weight of 6.78 x 10(5)Da, was isolated from Strongylocentrotus nudus eggs under the extraction conditions optimized by response surface methodology (RSM).	Polysaccharides	20-34	apolipoprotein A-I	Mus musculus	36-41
25037389-2	2014	Preliminary characterization of SEP-2 was performed by HPSEC and GC-MS, indicating that SEP-2 could be a D-glucan containing a (1   4)-linked D-Glcp backbone with (1   3)-linked D-Glcp side chains.	polyglucosan	105-113	apolipoprotein A-I	Mus musculus	32-37
25037389-2	2014	Preliminary characterization of SEP-2 was performed by HPSEC and GC-MS, indicating that SEP-2 could be a D-glucan containing a (1   4)-linked D-Glcp backbone with (1   3)-linked D-Glcp side chains.	polyglucosan	105-113	apolipoprotein A-I	Mus musculus	88-93
25037389-2	2014	Preliminary characterization of SEP-2 was performed by HPSEC and GC-MS, indicating that SEP-2 could be a D-glucan containing a (1   4)-linked D-Glcp backbone with (1   3)-linked D-Glcp side chains.	-glcp	143-148	apolipoprotein A-I	Mus musculus	32-37
25037389-2	2014	Preliminary characterization of SEP-2 was performed by HPSEC and GC-MS, indicating that SEP-2 could be a D-glucan containing a (1   4)-linked D-Glcp backbone with (1   3)-linked D-Glcp side chains.	-glcp	143-148	apolipoprotein A-I	Mus musculus	88-93
25037389-3	2014	In subsequent immunostimulatory studies, significantly enhanced ROS level, NO production and inflammatory cytokines secretion (IL-1beta, IL-6, and TNF-alpha) were observed in SEP-2 treated murine macrophage cell line RAW264.7.	ros	64-67	apolipoprotein A-I	Mus musculus	175-180
25249180-0	2014	The discovery of I-BET726 (GSK1324726A), a potent tetrahydroquinoline ApoA1 up-regulator and selective BET bromodomain inhibitor.	4-(1-acetyl-4-((4-chlorophenyl)amino)-2-methyl-1,2,3,4-tetrahydroquinolin-6-yl)benzoic acid	17-25	apolipoprotein A-I	Mus musculus	70-75
25249180-0	2014	The discovery of I-BET726 (GSK1324726A), a potent tetrahydroquinoline ApoA1 up-regulator and selective BET bromodomain inhibitor.	4-(1-acetyl-4-((4-chlorophenyl)amino)-2-methyl-1,2,3,4-tetrahydroquinolin-6-yl)benzoic acid	27-38	apolipoprotein A-I	Mus musculus	70-75
25249180-0	2014	The discovery of I-BET726 (GSK1324726A), a potent tetrahydroquinoline ApoA1 up-regulator and selective BET bromodomain inhibitor.	1,2,3,4-tetrahydroquinoline	50-69	apolipoprotein A-I	Mus musculus	70-75
25249180-4	2014	Here we describe the identification of a novel tetrahydroquinoline series through up-regulation of apolipoprotein A1 and the optimization into potent compounds active in murine models of septic shock and neuroblastoma.	1,2,3,4-tetrahydroquinoline	47-66	apolipoprotein A-I	Mus musculus	99-116
24868095-8	2014	Paraoxon inhibited cholesterol efflux to apoA-I or HDL, while 76-0079 did not.	Paraoxon	0-8	apolipoprotein A-I	Mus musculus	41-47
24868095-8	2014	Paraoxon inhibited cholesterol efflux to apoA-I or HDL, while 76-0079 did not.	Cholesterol	19-30	apolipoprotein A-I	Mus musculus	41-47
24969774-7	2014	ApoA-I infusion inhibited HSPC cell proliferation, Akt phosphorylation and reactive oxygen species production in HSPC and plaque progression in low-density lipoprotein receptor knockout (LDLr(-/-)) apoA-I(-/-) mice on HFD but had no effect on SR-BI(-/-) mice on HFD.	Reactive Oxygen Species	75-98	apolipoprotein A-I	Mus musculus	0-6
25060793-6	2014	Lipid-free apoA-I had a greater efflux capacity in the presence of PLTP than in the absence of PLTP, suggesting that PLTP may promote ATP-binding cassette transporter A1-mediated cholesterol and phospholipid efflux.	Cholesterol	179-190	apolipoprotein A-I	Mus musculus	11-17
25060793-6	2014	Lipid-free apoA-I had a greater efflux capacity in the presence of PLTP than in the absence of PLTP, suggesting that PLTP may promote ATP-binding cassette transporter A1-mediated cholesterol and phospholipid efflux.	Phospholipids	195-207	apolipoprotein A-I	Mus musculus	11-17
25084135-8	2014	Cholesterol transport assays revealed that miR-19b dramatically suppressed apolipoprotein AI-mediated ABCA1-dependent cholesterol efflux, resulting in the increased levels of total cholesterol (TC), free cholesterol (FC) and cholesterol ester (CE) as revealed by HPLC.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	75-92
25084135-8	2014	Cholesterol transport assays revealed that miR-19b dramatically suppressed apolipoprotein AI-mediated ABCA1-dependent cholesterol efflux, resulting in the increased levels of total cholesterol (TC), free cholesterol (FC) and cholesterol ester (CE) as revealed by HPLC.	Cholesterol	118-129	apolipoprotein A-I	Mus musculus	75-92
25084135-8	2014	Cholesterol transport assays revealed that miR-19b dramatically suppressed apolipoprotein AI-mediated ABCA1-dependent cholesterol efflux, resulting in the increased levels of total cholesterol (TC), free cholesterol (FC) and cholesterol ester (CE) as revealed by HPLC.	Cholesterol	181-192	apolipoprotein A-I	Mus musculus	75-92
25084135-8	2014	Cholesterol transport assays revealed that miR-19b dramatically suppressed apolipoprotein AI-mediated ABCA1-dependent cholesterol efflux, resulting in the increased levels of total cholesterol (TC), free cholesterol (FC) and cholesterol ester (CE) as revealed by HPLC.	Technetium	194-196	apolipoprotein A-I	Mus musculus	75-92
25084135-8	2014	Cholesterol transport assays revealed that miR-19b dramatically suppressed apolipoprotein AI-mediated ABCA1-dependent cholesterol efflux, resulting in the increased levels of total cholesterol (TC), free cholesterol (FC) and cholesterol ester (CE) as revealed by HPLC.	Cholesterol	181-192	apolipoprotein A-I	Mus musculus	75-92
25084135-8	2014	Cholesterol transport assays revealed that miR-19b dramatically suppressed apolipoprotein AI-mediated ABCA1-dependent cholesterol efflux, resulting in the increased levels of total cholesterol (TC), free cholesterol (FC) and cholesterol ester (CE) as revealed by HPLC.	Fc(alpha) receptor	217-219	apolipoprotein A-I	Mus musculus	75-92
25084135-8	2014	Cholesterol transport assays revealed that miR-19b dramatically suppressed apolipoprotein AI-mediated ABCA1-dependent cholesterol efflux, resulting in the increased levels of total cholesterol (TC), free cholesterol (FC) and cholesterol ester (CE) as revealed by HPLC.	Cholesterol Esters	225-242	apolipoprotein A-I	Mus musculus	75-92
24729189-3	2014	In this study, a naturally occurring methionine oxidation in the major HDL protein, apolipoprotein (apo) A-I, was exploited as a novel way to target HDL to macrophages.	Methionine	37-47	apolipoprotein A-I	Mus musculus	84-108
25117703-8	2014	The increases in HDL- paraoxonase 1 were translated into decreased plasma malondialdehyde levels depending on the presence of Apolipoprotein A1.	Malondialdehyde	74-89	apolipoprotein A-I	Mus musculus	126-143
24793484-0	2014	ApoA-I or ABCA1 expression suppresses fatty acid synthesis by reducing 27-hydroxycholesterol levels.	Fatty Acids	38-48	apolipoprotein A-I	Mus musculus	0-6
24793484-0	2014	ApoA-I or ABCA1 expression suppresses fatty acid synthesis by reducing 27-hydroxycholesterol levels.	27-hydroxycholesterol	71-92	apolipoprotein A-I	Mus musculus	0-6
24793484-2	2014	The ATP-binding cassette transporter A1 (ABCA1) protein mediates the transport of cholesterol and phospholipids from cells to apolipoprotein A-I (apoA-I) to generate nascent HDL particles.	Cholesterol	82-93	apolipoprotein A-I	Mus musculus	126-144
24793484-2	2014	The ATP-binding cassette transporter A1 (ABCA1) protein mediates the transport of cholesterol and phospholipids from cells to apolipoprotein A-I (apoA-I) to generate nascent HDL particles.	Cholesterol	82-93	apolipoprotein A-I	Mus musculus	146-152
24793484-2	2014	The ATP-binding cassette transporter A1 (ABCA1) protein mediates the transport of cholesterol and phospholipids from cells to apolipoprotein A-I (apoA-I) to generate nascent HDL particles.	Phospholipids	98-111	apolipoprotein A-I	Mus musculus	126-144
24793484-2	2014	The ATP-binding cassette transporter A1 (ABCA1) protein mediates the transport of cholesterol and phospholipids from cells to apolipoprotein A-I (apoA-I) to generate nascent HDL particles.	Phospholipids	98-111	apolipoprotein A-I	Mus musculus	146-152
24793484-4	2014	Here, we examined the effect of apoA-I and ABCA1 overexpression on genes involved in fatty acid synthesis in QSG-7701 hepatocytes and in mice.	Fatty Acids	85-95	apolipoprotein A-I	Mus musculus	32-38
24793484-7	2014	Overexpression of either apoA-I or ABCA1 resulted in an increase in cholesterol efflux and a decrease in cellular cholesterol, fatty acids, and triglycerides.	Cholesterol	68-79	apolipoprotein A-I	Mus musculus	25-31
24793484-7	2014	Overexpression of either apoA-I or ABCA1 resulted in an increase in cholesterol efflux and a decrease in cellular cholesterol, fatty acids, and triglycerides.	Cholesterol	114-125	apolipoprotein A-I	Mus musculus	25-31
24793484-7	2014	Overexpression of either apoA-I or ABCA1 resulted in an increase in cholesterol efflux and a decrease in cellular cholesterol, fatty acids, and triglycerides.	Fatty Acids	127-138	apolipoprotein A-I	Mus musculus	25-31
24793484-7	2014	Overexpression of either apoA-I or ABCA1 resulted in an increase in cholesterol efflux and a decrease in cellular cholesterol, fatty acids, and triglycerides.	Triglycerides	144-157	apolipoprotein A-I	Mus musculus	25-31
24793484-9	2014	Overexpression of apoA-I in mice reduced hepatic lipid levels, 27-hydroxycholesterol levels, and the mRNA levels of fatty acid synthase and acetyl-CoA carboxylase 1.	Hydroxycholesterols	66-84	apolipoprotein A-I	Mus musculus	18-24
24793484-10	2014	These results suggest that expression of apoA-I or ABCA1 can reduce steatosis by decreasing lipid storage and modifying lipid transport in hepatocytes and may also inhibit fatty acid synthesis by decreasing 27-hydroxycholesterol levels.	Fatty Acids	172-182	apolipoprotein A-I	Mus musculus	41-47
24793484-10	2014	These results suggest that expression of apoA-I or ABCA1 can reduce steatosis by decreasing lipid storage and modifying lipid transport in hepatocytes and may also inhibit fatty acid synthesis by decreasing 27-hydroxycholesterol levels.	Hydroxycholesterols	210-228	apolipoprotein A-I	Mus musculus	41-47
24992457-1	2014	PURPOSE OF REVIEW: ATP-binding cassette transporter A1 (ABCA1) facilitates cellular cholesterol efflux to lipid-poor apolipoprotein AI (apoAI) and plays a key role in the formation and function of HDL.	Cholesterol	84-95	apolipoprotein A-I	Mus musculus	117-134
24759932-5	2014	A substantial defect was present at baseline in the electron transport chain of cardiac myocytes from apoA1(-/-) mice localized to the coenzyme Q (CoQ) pool with impaired electron transfer (67% decrease) from complex II to complex III.	Ubiquinone	147-150	apolipoprotein A-I	Mus musculus	102-107
24759932-6	2014	Administration of coenzyme Q10 (CoQ10) to apoA1 null mice normalized the cardiac mitochondrial CoQ pool and reduced infarct size to that observed in WT mice.	Ubiquinone	32-35	apolipoprotein A-I	Mus musculus	42-47
24759932-8	2014	These data identify CoQ pool content leading to impaired mitochondrial function as major contributors to infarct size in the setting of low HDL/apoA1.	Ubiquinone	20-23	apolipoprotein A-I	Mus musculus	144-149
24931346-6	2014	As a consequence, macrophages from the miR-33b KI mice had a reduced cholesterol efflux capacity via apoA-I and HDL-C.	Cholesterol	69-80	apolipoprotein A-I	Mus musculus	101-107
29450188-3	2014	We synthesized a novel 24-amino acid apoA-I mimetic peptide-type5 (FAMP5), which potently removes cholesterol via specific ATP-binding cassette transporter A1 (ABCA1).	Cholesterol	98-109	apolipoprotein A-I	Mus musculus	37-43
24463557-9	2014	PI polyamide also significantly increased apolipoprotein AI-mediated HDL biogenesis in RAW264 cells.	Nylons	3-12	apolipoprotein A-I	Mus musculus	42-59
24463557-10	2014	Cellular cholesterol efflux mediated by apolipoprotein AI was significantly increased by the PI polyamide treatment.	Cholesterol	9-20	apolipoprotein A-I	Mus musculus	40-57
24463557-10	2014	Cellular cholesterol efflux mediated by apolipoprotein AI was significantly increased by the PI polyamide treatment.	pi polyamide	93-105	apolipoprotein A-I	Mus musculus	40-57
24463557-19	2014	PI polyamide increased ABCA1 protein and apolipoprotein AI mediated HDL biogenesis.	Nylons	3-12	apolipoprotein A-I	Mus musculus	41-58
24407029-6	2014	In ApoA-I(-/-) mice, ApoA-I oxidation significantly impaired reverse cholesterol transport in vivo.	Cholesterol	69-80	apolipoprotein A-I	Mus musculus	3-9
24407029-6	2014	In ApoA-I(-/-) mice, ApoA-I oxidation significantly impaired reverse cholesterol transport in vivo.	Cholesterol	69-80	apolipoprotein A-I	Mus musculus	21-27
24442447-0	2014	Single injections of apoA-I acutely improve in vivo glucose tolerance in insulin-resistant mice.	Glucose	52-59	apolipoprotein A-I	Mus musculus	21-27
24442447-1	2014	AIMS/HYPOTHESIS: Apolipoprotein A-I (apoA-I), the main protein constituent of HDL, has a central role in the reverse cholesterol-transport pathway, which together with the anti-inflammatory properties of apoA-I/HDL provide cardioprotection.	Cholesterol	117-128	apolipoprotein A-I	Mus musculus	17-35
24442447-1	2014	AIMS/HYPOTHESIS: Apolipoprotein A-I (apoA-I), the main protein constituent of HDL, has a central role in the reverse cholesterol-transport pathway, which together with the anti-inflammatory properties of apoA-I/HDL provide cardioprotection.	Cholesterol	117-128	apolipoprotein A-I	Mus musculus	37-43
24442447-2	2014	Recent findings of direct stimulation of glucose uptake in muscle by apoA-I/HDL suggest that altered apoA-I and HDL functionality may be a contributing factor to the development of diabetes.	Glucose	41-48	apolipoprotein A-I	Mus musculus	69-75
24442447-2	2014	Recent findings of direct stimulation of glucose uptake in muscle by apoA-I/HDL suggest that altered apoA-I and HDL functionality may be a contributing factor to the development of diabetes.	Glucose	41-48	apolipoprotein A-I	Mus musculus	101-107
24442447-7	2014	RESULTS: ApoA-I treatment significantly improved insulin secretion and blood glucose clearance in the glucose tolerance test, with an efficiency exceeding that of lean control animals, and led to decreased basal glucose during the 3 h incubation.	Glucose	77-84	apolipoprotein A-I	Mus musculus	9-15
24442447-7	2014	RESULTS: ApoA-I treatment significantly improved insulin secretion and blood glucose clearance in the glucose tolerance test, with an efficiency exceeding that of lean control animals, and led to decreased basal glucose during the 3 h incubation.	Glucose	102-109	apolipoprotein A-I	Mus musculus	9-15
24442447-7	2014	RESULTS: ApoA-I treatment significantly improved insulin secretion and blood glucose clearance in the glucose tolerance test, with an efficiency exceeding that of lean control animals, and led to decreased basal glucose during the 3 h incubation.	Glucose	102-109	apolipoprotein A-I	Mus musculus	9-15
24442447-8	2014	Notably, the two apoA-I variants triggered insulin secretion and glucose clearance to the same extent.	Glucose	65-72	apolipoprotein A-I	Mus musculus	17-23
24433070-4	2014	Resveratrol significantly decreased the plasma total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C) concentrations, apoB/apoA-I ratio, hepatic cholesterol, and triglyceride (TG) contents, whereas significantly it increased the plasma HDL-C concentration compared with the control and lovastatin groups.	Resveratrol	0-11	apolipoprotein A-I	Mus musculus	195-201
24567123-10	2014	In cell culture studies, HDL and apoA-I specifically increased catecholamine-induced lipolysis possibly through modulating the adipocyte plasma membrane cholesterol content.	Catecholamines	63-76	apolipoprotein A-I	Mus musculus	33-39
24567123-10	2014	In cell culture studies, HDL and apoA-I specifically increased catecholamine-induced lipolysis possibly through modulating the adipocyte plasma membrane cholesterol content.	Cholesterol	153-164	apolipoprotein A-I	Mus musculus	33-39
24334873-10	2014	ApoA-I deficiency decreased very-LDL/LDL cholesterol in C57BL/6 mice but not in FVB/N mice.	Cholesterol	41-52	apolipoprotein A-I	Mus musculus	0-6
24334873-14	2014	ApoA-I deficiency increased macrophage cholesterol content only in C57BL/6.	Cholesterol	39-50	apolipoprotein A-I	Mus musculus	0-6
24212237-5	2014	Coincubation of AcLDL with 50 mug/ml apoA-I eliminated all extracellular and cell surface-associated cholesterol microdomains, while coincubation with the same concentration of HDL only removed extracellular matrix-associated cholesterol microdomains.	Cholesterol	101-112	apolipoprotein A-I	Mus musculus	37-43
24212237-5	2014	Coincubation of AcLDL with 50 mug/ml apoA-I eliminated all extracellular and cell surface-associated cholesterol microdomains, while coincubation with the same concentration of HDL only removed extracellular matrix-associated cholesterol microdomains.	Cholesterol	226-237	apolipoprotein A-I	Mus musculus	37-43
24196952-2	2013	Telomerase-immortalized Tangier fibroblasts of family 1 (TT1) showed 30% residual cholesterol efflux capacity in response to apolipoprotein A-I, whereas telomerase-immortalized Tangier fibroblasts of family 2 (TT2) showed only 20%.	Cholesterol	82-93	apolipoprotein A-I	Mus musculus	125-143
25278768-2	2013	It has been shown previously that the thieno-TZD Ro 11-1464 increases plasma levels of apoA-I and in vivomacrophage reverse cholesterol transport in mice.	thieno-tzd	38-48	apolipoprotein A-I	Mus musculus	87-93
25278768-2	2013	It has been shown previously that the thieno-TZD Ro 11-1464 increases plasma levels of apoA-I and in vivomacrophage reverse cholesterol transport in mice.	9-methyl-4-phenyl-6H-thieno(3,2-f)(1,2,4)triazolo(4,3-a)(1,4)diazepine	49-59	apolipoprotein A-I	Mus musculus	87-93
23990662-2	2013	Adenovirus-mediated gene transfer of apoA-I[L218A/L219A/V221A/L222A] in apoA-I-/- mice decreased plasma cholesterol and apoA-I levels to 15% of wild-type (WT) control mice and generated pre-beta- and alpha4-HDL particles.	Cholesterol	104-115	apolipoprotein A-I	Mus musculus	37-43
23990662-2	2013	Adenovirus-mediated gene transfer of apoA-I[L218A/L219A/V221A/L222A] in apoA-I-/- mice decreased plasma cholesterol and apoA-I levels to 15% of wild-type (WT) control mice and generated pre-beta- and alpha4-HDL particles.	Cholesterol	104-115	apolipoprotein A-I	Mus musculus	72-78
23990662-2	2013	Adenovirus-mediated gene transfer of apoA-I[L218A/L219A/V221A/L222A] in apoA-I-/- mice decreased plasma cholesterol and apoA-I levels to 15% of wild-type (WT) control mice and generated pre-beta- and alpha4-HDL particles.	Cholesterol	104-115	apolipoprotein A-I	Mus musculus	72-78
23990662-5	2013	The apoA-I[218-222] and apoA-I[E223A/K226A] mutants had 20% and normal capacity, respectively, to promote ABCA1-mediated cholesterol efflux.	Cholesterol	121-132	apolipoprotein A-I	Mus musculus	4-10
23990662-5	2013	The apoA-I[218-222] and apoA-I[E223A/K226A] mutants had 20% and normal capacity, respectively, to promote ABCA1-mediated cholesterol efflux.	Cholesterol	121-132	apolipoprotein A-I	Mus musculus	24-30
24123812-2	2013	Adenovirus-mediated gene transfer of an apoA-I[F225A/V227A/F229A/L230A] mutant in apoA-I-/- mice decreased plasma cholesterol, HDL cholesterol, and apoA-I levels.	Cholesterol	114-125	apolipoprotein A-I	Mus musculus	40-46
24123812-2	2013	Adenovirus-mediated gene transfer of an apoA-I[F225A/V227A/F229A/L230A] mutant in apoA-I-/- mice decreased plasma cholesterol, HDL cholesterol, and apoA-I levels.	Cholesterol	114-125	apolipoprotein A-I	Mus musculus	82-88
24123812-2	2013	Adenovirus-mediated gene transfer of an apoA-I[F225A/V227A/F229A/L230A] mutant in apoA-I-/- mice decreased plasma cholesterol, HDL cholesterol, and apoA-I levels.	Cholesterol	114-125	apolipoprotein A-I	Mus musculus	82-88
24123812-2	2013	Adenovirus-mediated gene transfer of an apoA-I[F225A/V227A/F229A/L230A] mutant in apoA-I-/- mice decreased plasma cholesterol, HDL cholesterol, and apoA-I levels.	Cholesterol	131-142	apolipoprotein A-I	Mus musculus	40-46
24123812-2	2013	Adenovirus-mediated gene transfer of an apoA-I[F225A/V227A/F229A/L230A] mutant in apoA-I-/- mice decreased plasma cholesterol, HDL cholesterol, and apoA-I levels.	Cholesterol	131-142	apolipoprotein A-I	Mus musculus	82-88
24123812-2	2013	Adenovirus-mediated gene transfer of an apoA-I[F225A/V227A/F229A/L230A] mutant in apoA-I-/- mice decreased plasma cholesterol, HDL cholesterol, and apoA-I levels.	Cholesterol	131-142	apolipoprotein A-I	Mus musculus	82-88
24123812-5	2013	Coexpression of the apoA-I mutant and LCAT increased and shifted the-HDL cholesterol peak toward lower densities, created normal alphaHDL subpopulations, and generated spherical-HDL particles.	Cholesterol	73-84	apolipoprotein A-I	Mus musculus	20-26
24123812-7	2013	The mutations also reduced the ability of apoA-I to promote ABCA1-mediated cholesterol efflux and to activate LCAT to 31% and 66%, respectively, of the WT control.	Cholesterol	75-86	apolipoprotein A-I	Mus musculus	42-48
24231102-0	2013	Dietary oleanolic acid mediates circadian clock gene expression in liver independently of diet and animal model but requires apolipoprotein A1.	Oleanolic Acid	8-22	apolipoprotein A-I	Mus musculus	125-142
24170386-5	2013	Mitochondria isolated from gastrocnemius muscle of apoA-I ko mice displayed markedly blunted ATP synthesis.	Adenosine Triphosphate	93-96	apolipoprotein A-I	Mus musculus	51-57
24170386-8	2013	ApoA-I tg mice exhibited lower fasting glucose levels, improved glucose tolerance test, increased lactate levels, reduced fat mass, associated with protection against age-induced decline of endurance capacity compared with wild-type mice.	Glucose	39-46	apolipoprotein A-I	Mus musculus	0-6
24170386-8	2013	ApoA-I tg mice exhibited lower fasting glucose levels, improved glucose tolerance test, increased lactate levels, reduced fat mass, associated with protection against age-induced decline of endurance capacity compared with wild-type mice.	Glucose	64-71	apolipoprotein A-I	Mus musculus	0-6
24170386-8	2013	ApoA-I tg mice exhibited lower fasting glucose levels, improved glucose tolerance test, increased lactate levels, reduced fat mass, associated with protection against age-induced decline of endurance capacity compared with wild-type mice.	Lactic Acid	98-105	apolipoprotein A-I	Mus musculus	0-6
24170386-10	2013	Consistent with an increase in glucose utilization of skeletal muscle, genetically increased HDL and apoA-I levels in mice prevented high-fat diet-induced impairment of glucose homeostasis.	Glucose	31-38	apolipoprotein A-I	Mus musculus	101-107
23754667-3	2013	METHODS AND RESULTS: Methionine-induced HHcy in mice resulted in an approximately 20% decreased concentration of HDL-cholesterol and HDL main protein component, apolipoprotein A-I.	Methionine	21-31	apolipoprotein A-I	Mus musculus	161-179
23889245-0	2013	Apolipoprotein A1 potentiates lipoxin A4 synthesis and recovery of allergen-induced disrupted tight junctions in the airway epithelium.	lipoxin A4	30-40	apolipoprotein A-I	Mus musculus	0-17
23889245-11	2013	ApoA1-induced increases in the TJ proteins were dependent on increased production of lipoxin A4 (LX A4).	lipoxin A4	85-95	apolipoprotein A-I	Mus musculus	0-5
23889245-11	2013	ApoA1-induced increases in the TJ proteins were dependent on increased production of lipoxin A4 (LX A4).	lipoxin A4	97-102	apolipoprotein A-I	Mus musculus	0-5
23874769-0	2013	An apolipoprotein A-I mimetic peptide designed with a reductionist approach stimulates reverse cholesterol transport and reduces atherosclerosis in mice.	Cholesterol	95-106	apolipoprotein A-I	Mus musculus	3-21
23874769-2	2013	An apoA-I mimetic peptide ELK-2A2K2E was designed with a reductionist approach and has shown exceptional activity in supporting cholesterol efflux but modest anti-inflammatory and anti-oxidant properties in vitro.	Cholesterol	128-139	apolipoprotein A-I	Mus musculus	3-9
23725986-4	2013	Single dose administration of rHDL (100 mg apoA-I/kg) resulted in an early (4 h) increase in plasma free cholesterol levels (p &lt; 0.001), without affecting hepatic cholesterol levels or fecal mass sterol excretion.	rhdl	30-34	apolipoprotein A-I	Mus musculus	43-49
23725986-4	2013	Single dose administration of rHDL (100 mg apoA-I/kg) resulted in an early (4 h) increase in plasma free cholesterol levels (p &lt; 0.001), without affecting hepatic cholesterol levels or fecal mass sterol excretion.	Cholesterol	105-116	apolipoprotein A-I	Mus musculus	43-49
23543682-4	2013	Increases in the available cell lipid:apoAI ratio due to either elevated ATP-binding cassette transporter A1 (ABCA1) expression and activity or raised cell density (i.e., increasing numerator) shifted the production of nascent HDL from smaller particles with fewer apoAI molecules per particle and fewer molecules of choline-phospholipid and cholesterol per apoAI molecule to larger particles that contained more apoAI and more lipid per molecule of apoAI.	Choline	317-324	apolipoprotein A-I	Mus musculus	38-43
23543682-4	2013	Increases in the available cell lipid:apoAI ratio due to either elevated ATP-binding cassette transporter A1 (ABCA1) expression and activity or raised cell density (i.e., increasing numerator) shifted the production of nascent HDL from smaller particles with fewer apoAI molecules per particle and fewer molecules of choline-phospholipid and cholesterol per apoAI molecule to larger particles that contained more apoAI and more lipid per molecule of apoAI.	Phospholipids	325-337	apolipoprotein A-I	Mus musculus	38-43
23543682-4	2013	Increases in the available cell lipid:apoAI ratio due to either elevated ATP-binding cassette transporter A1 (ABCA1) expression and activity or raised cell density (i.e., increasing numerator) shifted the production of nascent HDL from smaller particles with fewer apoAI molecules per particle and fewer molecules of choline-phospholipid and cholesterol per apoAI molecule to larger particles that contained more apoAI and more lipid per molecule of apoAI.	Cholesterol	342-353	apolipoprotein A-I	Mus musculus	38-43
23840542-7	2013	Moreover, treatment with both LXRalpha siRNA and PPARgamma siRNA made the up-regulation of DHC on ABCA1, ABCG1, ABCG5, SR-B1, NPC1, CD36, LDLR, HMGCR, apoA1 and apoE expression notably abolished while made the down-regulation of DHC on SRA1 expression markedly compensated.	dihydrocapsaicin	91-94	apolipoprotein A-I	Mus musculus	151-156
23658016-7	2013	In addition, apoA-I-KO mice had less LPS clearance, reduced corticosterone generation, and impaired leukocyte recruitment in sepsis.	Corticosterone	60-74	apolipoprotein A-I	Mus musculus	13-19
23564081-7	2013	In LPS-challenged mice injected with rAAV-apoA-I-GFP, viral particles and human apoA-I were detected in the livers, total plasma human apoA-I levels were grammatically increased; HDL-cholesterol level was significantly increased, TG and TC were slightly increased.	Cholesterol	183-194	apolipoprotein A-I	Mus musculus	42-48
23564081-7	2013	In LPS-challenged mice injected with rAAV-apoA-I-GFP, viral particles and human apoA-I were detected in the livers, total plasma human apoA-I levels were grammatically increased; HDL-cholesterol level was significantly increased, TG and TC were slightly increased.	Thioguanine	230-232	apolipoprotein A-I	Mus musculus	42-48
23564081-7	2013	In LPS-challenged mice injected with rAAV-apoA-I-GFP, viral particles and human apoA-I were detected in the livers, total plasma human apoA-I levels were grammatically increased; HDL-cholesterol level was significantly increased, TG and TC were slightly increased.	Technetium	237-239	apolipoprotein A-I	Mus musculus	42-48
23430591-10	2013	Finally, we also found that E2 enhanced the cholesterol efflux to apoA I in RAW264.7 cells.	Cholesterol	44-55	apolipoprotein A-I	Mus musculus	66-72
23741493-5	2013	Cholesterol efflux to control or glycated lipid-free apoA-I, or discoidal reconstituted HDL containing glycated apoA-I (drHDL), was examined using cholesterol-loaded murine (J774A.1) macrophages treated to increase expression of ATP binding cassette transporters A1 (ABCA1) or G1 (ABCG1).	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	53-59
23741493-5	2013	Cholesterol efflux to control or glycated lipid-free apoA-I, or discoidal reconstituted HDL containing glycated apoA-I (drHDL), was examined using cholesterol-loaded murine (J774A.1) macrophages treated to increase expression of ATP binding cassette transporters A1 (ABCA1) or G1 (ABCG1).	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	112-118
23709562-0	2013	FAMP, a novel apoA-I mimetic peptide, suppresses aortic plaque formation through promotion of biological HDL function in ApoE-deficient mice.	fludarabine phosphate	0-4	apolipoprotein A-I	Mus musculus	14-20
23709562-9	2013	CONCLUSIONS: A newly developed apoA-I mimetic peptide, FAMP, has an antiatherosclerotic effect through the enhancement of the biological function of HDL.	fludarabine phosphate	55-59	apolipoprotein A-I	Mus musculus	31-37
23583377-6	2013	Moreover, EA supplementation upregulated mRNA expression of apoa1, ldlr, cpt1a, and ppara genes in the liver.	Ellagic Acid	10-12	apolipoprotein A-I	Mus musculus	60-65
23501697-3	2013	The anti-inflammatory effects of apolipoprotein AI (apoAI) and high-density lipoprotein (HDL) on macrophages and endothelial cells seem to occur via cholesterol depletion of LRs.	Cholesterol	149-160	apolipoprotein A-I	Mus musculus	33-50
23493286-5	2013	Cholesterol efflux from unloaded cells to apolipoprotein A-I or high-density lipoprotein was similar in the 2 strains.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	42-60
23606429-2	2013	This protein contrast agent was obtained by attaching the thiol-reactive Gd[MTS-ADO3A] label at Cys residues replaced at four distinct positions (52, 55, 76 and 80) in apoA-I.	Sulfhydryl Compounds	58-63	apolipoprotein A-I	Mus musculus	168-174
23606429-6	2013	Consistent with its superior relaxivity measured by NMR, the rHDL-associated apoA-I containing the Gd[MTS-ADO3A] probe attached to position 55 displays favorable dynamic and water accessibility properties as determined by X-band EPR.	Water	174-179	apolipoprotein A-I	Mus musculus	77-83
23471027-0	2013	Discoidal HDL and apoA-I-derived peptides improve glucose uptake in skeletal muscle.	Glucose	50-57	apolipoprotein A-I	Mus musculus	18-24
23471027-1	2013	Lipid-free apoA-I and mature spherical HDL have been shown to induce glucose uptake in skeletal muscle.	Glucose	69-76	apolipoprotein A-I	Mus musculus	11-17
23471027-7	2013	A survey of domain-specific peptides of apoA-I showed that the lipid-free C-terminal 190-243 fragment increases plasma membrane GLUT4, promotes glucose uptake, and activates AMPK signaling but not Akt.	Glucose	144-151	apolipoprotein A-I	Mus musculus	40-46
23471027-9	2013	Discoidal HDL and the 190-243 peptide of apoA-I are potent agonists of glucose uptake in skeletal muscle, and the C-terminal alpha-helical content of apoA-I may be an important determinant of this effect.	Glucose	71-78	apolipoprotein A-I	Mus musculus	41-47
23112124-0	2013	Low dietary folate and methylenetetrahydrofolate reductase deficiency may lead to pregnancy complications through modulation of ApoAI and IFN-gamma in spleen and placenta, and through reduction of methylation potential.	Folic Acid	12-18	apolipoprotein A-I	Mus musculus	128-133
23112124-10	2013	Plasma homocysteine correlated negatively with liver and spleen ApoAI, and positively with IFN-gamma.	Homocysteine	7-19	apolipoprotein A-I	Mus musculus	64-69
23112124-11	2013	CONCLUSION: Low dietary folate or Mthfr deficiency during pregnancy may result in adverse pregnancy outcomes by altering expression of the inflammatory mediators ApoAI and IFN-gamma in spleen and placenta.	Folic Acid	24-30	apolipoprotein A-I	Mus musculus	162-167
23425306-3	2013	The abilities of (14)C-labeled human and mouse apoA-I variants to associate with human HDL and lipid emulsion particles were determined using ultracentrifugation to separate free and bound protein.	Carbon	21-22	apolipoprotein A-I	Mus musculus	47-53
23322769-4	2013	Apolipoprotein A-I (ApoA-I) is the major protein component of HDL-c that mediates reverse cholesterol transport from tissues to the liver for excretion.	Cholesterol	90-101	apolipoprotein A-I	Mus musculus	0-18
23322769-4	2013	Apolipoprotein A-I (ApoA-I) is the major protein component of HDL-c that mediates reverse cholesterol transport from tissues to the liver for excretion.	Cholesterol	90-101	apolipoprotein A-I	Mus musculus	20-26
23322769-11	2013	Repression of farnesyltransferase (FNTA) by siRNA and the enzyme inhibitor manumycin A caused elevation of ApoA-I secretion from hepatocytes and from transgenic mice expressing hApoA-I and cholesterol ester transfer protein transgenes.	manumycin	75-86	apolipoprotein A-I	Mus musculus	107-113
23204275-9	2013	ApoA1 levels, but not diabetes, were strongly correlated with the ability of plasma to efflux cholesterol from macrophages.	Cholesterol	94-105	apolipoprotein A-I	Mus musculus	0-5
24016269-6	2013	-NPC1 cells treated with LXR agonist TO901317 (TO90) displayed a modest increase in cholesterol efflux to apolipoprotein A-I (apoA-I) but not to HDL3, or in the absence of extracellular cholesterol acceptors.	Cholesterol	84-95	apolipoprotein A-I	Mus musculus	106-124
24016269-6	2013	-NPC1 cells treated with LXR agonist TO901317 (TO90) displayed a modest increase in cholesterol efflux to apolipoprotein A-I (apoA-I) but not to HDL3, or in the absence of extracellular cholesterol acceptors.	Cholesterol	84-95	apolipoprotein A-I	Mus musculus	126-132
23132909-4	2013	Gene transfer of apoA-IV in apoA-I(-/-) x apoE(-/-) mice increased plasma cholesterol and triglyceride levels, and 80% of the protein was distributed in the VLDL/IDL/LDL region.	Cholesterol	74-85	apolipoprotein A-I	Mus musculus	17-23
23132909-4	2013	Gene transfer of apoA-IV in apoA-I(-/-) x apoE(-/-) mice increased plasma cholesterol and triglyceride levels, and 80% of the protein was distributed in the VLDL/IDL/LDL region.	Triglycerides	90-102	apolipoprotein A-I	Mus musculus	17-23
23132909-8	2013	Lipid-free apoA-IV and reconstituted HDL-A-IV promoted ABCA1 and scavenger receptor BI (SR-BI)-mediated cholesterol efflux, respectively, as efficiently as apoA-I and apoE.	Cholesterol	104-115	apolipoprotein A-I	Mus musculus	11-17
23409054-7	2013	The level of transforming growth factor-b1 decreased in the bronchoalveolar lavage fluid, whereas lipoxin A4 was increased in the ApoA1_D7 and D15 groups compared with the silica-treated ApoA1 non-overexpressing mice.	Silicon Dioxide	172-178	apolipoprotein A-I	Mus musculus	187-192
23409054-8	2013	The silica-induced increase in the number of apoptotic cells was significantly reduced in the lungs of mice overexpressing ApoA1.	Silicon Dioxide	4-10	apolipoprotein A-I	Mus musculus	123-128
23409054-9	2013	Overexpression of ApoA1 decreased silica-induced lung inflammation and fibrotic nodule formation.	Silicon Dioxide	34-40	apolipoprotein A-I	Mus musculus	18-23
23409054-10	2013	The restoration of lipoxin A4 may contribute to the protective effect of ApoA1 overexpression against silica-induced lung fibrosis.	Silicon Dioxide	102-108	apolipoprotein A-I	Mus musculus	73-78
22977169-8	2013	The decrease in serum CHOL was consistent with the induction of hepatic reverse CHOL transport genes Lcat (2.0-fold), Apoa1 (1.7-fold), and Ldlr (3.6-fold), and the repression of CHOL biosynthesis genes Hmgcs1 (-2.1-fold) and Hmgcr (-2.3-fold).	Cholesterol	22-26	apolipoprotein A-I	Mus musculus	118-123
23227865-6	2012	RESULTS: The positive control, resveratrol (24 h), significantly enhanced cholesterol efflux to apoA-I at concentrations &gt;=30 muM.	Resveratrol	31-42	apolipoprotein A-I	Mus musculus	96-102
23227865-6	2012	RESULTS: The positive control, resveratrol (24 h), significantly enhanced cholesterol efflux to apoA-I at concentrations &gt;=30 muM.	Cholesterol	74-85	apolipoprotein A-I	Mus musculus	96-102
23227865-7	2012	By contrast, cholesterol efflux to apoA-I was significantly inhibited by nigericin (45%; p&lt;0.01) and oligomycin (55%; p&lt;0.01), under conditions (10 muM, 3 h) which did not induce cellular toxicity or deplete total cellular ATP content.	Cholesterol	13-24	apolipoprotein A-I	Mus musculus	35-41
23227865-7	2012	By contrast, cholesterol efflux to apoA-I was significantly inhibited by nigericin (45%; p&lt;0.01) and oligomycin (55%; p&lt;0.01), under conditions (10 muM, 3 h) which did not induce cellular toxicity or deplete total cellular ATP content.	Nigericin	73-82	apolipoprotein A-I	Mus musculus	35-41
23227865-7	2012	By contrast, cholesterol efflux to apoA-I was significantly inhibited by nigericin (45%; p&lt;0.01) and oligomycin (55%; p&lt;0.01), under conditions (10 muM, 3 h) which did not induce cellular toxicity or deplete total cellular ATP content.	Oligomycins	104-114	apolipoprotein A-I	Mus musculus	35-41
23227865-7	2012	By contrast, cholesterol efflux to apoA-I was significantly inhibited by nigericin (45%; p&lt;0.01) and oligomycin (55%; p&lt;0.01), under conditions (10 muM, 3 h) which did not induce cellular toxicity or deplete total cellular ATP content.	Adenosine Triphosphate	229-232	apolipoprotein A-I	Mus musculus	35-41
23227865-11	2012	CONCLUSIONS: Acute loss of mitochondrial function, and in particular Deltapsim, reduces cholesterol efflux to apoA-I and dysregulates macrophage cholesterol homeostasis mechanisms.	Cholesterol	88-99	apolipoprotein A-I	Mus musculus	110-116
23316322-1	2012	BACKGROUND: Cholesterol efflux from cells to apolipoprotein A-I (apoA-I) acceptors via the ATP-binding cassette transporters ABCA1 and ABCG1 is thought to be central in the antiatherogenic mechanism.	Cholesterol	12-23	apolipoprotein A-I	Mus musculus	45-63
23316322-1	2012	BACKGROUND: Cholesterol efflux from cells to apolipoprotein A-I (apoA-I) acceptors via the ATP-binding cassette transporters ABCA1 and ABCG1 is thought to be central in the antiatherogenic mechanism.	Cholesterol	12-23	apolipoprotein A-I	Mus musculus	65-71
23046066-8	2012	The expressions of several proteins with important biological functions-such as cysteine sulfinic acid decarboxylase, aldehyde dehydrogenase, and apolipoprotein A-I, also correlated with PFOS exposure.	perfluorooctane sulfonic acid	187-191	apolipoprotein A-I	Mus musculus	146-164
23259564-5	2012	Moreover, studies using gene-targeted mice have indicated that genetic modifications leading to a similar increase of HDL cholesterol levels can either reduce (i.e. apoA1 transgene overexpression) or accelerate (i.e. SR-B1 deficiency) atherosclerosis, depending on the molecular target.	Cholesterol	122-133	apolipoprotein A-I	Mus musculus	165-170
23239437-6	2012	Realtime polymerase chain reaction detection disclosed that the expression of several transporters involved in reverse cholesterol transport was induced by THPA, and the expression of hepatic ABCA1 and apoA-I, which play roles in the maturation of HDL-C, was also elevated in the THPA-treated groups.	triacetyl-3-hydroxyphenyladenosine	280-284	apolipoprotein A-I	Mus musculus	202-208
22845860-1	2012	BACKGROUND/AIMS: Apolipoprotein (apo)A-I(M) (ilano), is a molecular variant of apoA-I(wild-type), associated with dramatically low HDL-cholesterol levels, but no increased risk for cardiovascular disease.	Cholesterol	135-146	apolipoprotein A-I	Mus musculus	79-85
22845860-2	2012	In view of the present uncertainties on the role of apoA-I in liver cholesterol removal by way of bile acids and neutral sterols, and of the greater capacity of apoA-I(M) (ilano) to remove arterial cholesterol, biliary sterol metabolism was evaluated in transgenic mice expressing apoA-I(M) (ilano).	Cholesterol	198-209	apolipoprotein A-I	Mus musculus	161-167
22845860-2	2012	In view of the present uncertainties on the role of apoA-I in liver cholesterol removal by way of bile acids and neutral sterols, and of the greater capacity of apoA-I(M) (ilano) to remove arterial cholesterol, biliary sterol metabolism was evaluated in transgenic mice expressing apoA-I(M) (ilano).	Cholesterol	198-209	apolipoprotein A-I	Mus musculus	161-167
22845860-7	2012	ApoA-I(M) (ilano) mice showed lower cholesterol output from the liver compared with apoA-I(wild-type) mice, in the absence of liver sterol accumulation.	Cholesterol	36-47	apolipoprotein A-I	Mus musculus	0-6
22845860-7	2012	ApoA-I(M) (ilano) mice showed lower cholesterol output from the liver compared with apoA-I(wild-type) mice, in the absence of liver sterol accumulation.	Sterols	41-47	apolipoprotein A-I	Mus musculus	0-6
22576368-2	2012	We investigated the involvement of apoA-I in diet-induced accumulation of triglycerides in hepatocytes and its potential role in the treatment of nonalcoholic fatty liver disease (NAFLD).	Triglycerides	74-87	apolipoprotein A-I	Mus musculus	35-41
22576368-3	2012	ApoA-I-deficient (apoA-I(-/-)) mice showed increased diet-induced hepatic triglyceride deposition and disturbed hepatic histology while they exhibited reduced glucose tolerance and insulin sensitivity.	Triglycerides	74-86	apolipoprotein A-I	Mus musculus	0-6
22576368-3	2012	ApoA-I-deficient (apoA-I(-/-)) mice showed increased diet-induced hepatic triglyceride deposition and disturbed hepatic histology while they exhibited reduced glucose tolerance and insulin sensitivity.	Triglycerides	74-86	apolipoprotein A-I	Mus musculus	18-29
22576368-7	2012	In agreement with these findings, adenovirus-mediated gene transfer of apoA-I(Milano) in apoA-I(-/-) mice fed a Western-type diet for 12 wks resulted in a significant reduction in hepatic triglyceride content and an improvement of hepatic histology and architecture.	Triglycerides	188-200	apolipoprotein A-I	Mus musculus	71-77
22576368-7	2012	In agreement with these findings, adenovirus-mediated gene transfer of apoA-I(Milano) in apoA-I(-/-) mice fed a Western-type diet for 12 wks resulted in a significant reduction in hepatic triglyceride content and an improvement of hepatic histology and architecture.	Triglycerides	188-200	apolipoprotein A-I	Mus musculus	89-95
22308547-1	2012	OBJECTIVE: Synthetic class A amphipathic helical peptide analogs of apolipoprotein-AI (apoAI; with varied phenylalanine residues) are emerging therapeutic approaches under investigation for atherosclerosis.	Phenylalanine	106-119	apolipoprotein A-I	Mus musculus	68-85
22633282-5	2012	Conflicting reports exist in the literature concerning the relative influence of homocysteine and cysteine upon apoA-I expression.	Homocysteine	81-93	apolipoprotein A-I	Mus musculus	112-118
22633282-5	2012	Conflicting reports exist in the literature concerning the relative influence of homocysteine and cysteine upon apoA-I expression.	Cysteine	85-93	apolipoprotein A-I	Mus musculus	112-118
22633282-11	2012	Our results indicate that plasma apoA-I levels in HCU are inversely related to homocysteine and are consistent with a plausible role for decreased expression of apoA-I as a contributory factor for both cardiovascular disease and cognitive impairment in HCU.	Homocysteine	79-91	apolipoprotein A-I	Mus musculus	33-39
22427535-1	2012	Apolipoprotein A-I (apoA-I) is a key component of high-density lipoproteins that mediates reverse cholesterol transport from cells and reduces vascular inflammation.	Cholesterol	98-109	apolipoprotein A-I	Mus musculus	0-18
22427535-1	2012	Apolipoprotein A-I (apoA-I) is a key component of high-density lipoproteins that mediates reverse cholesterol transport from cells and reduces vascular inflammation.	Cholesterol	98-109	apolipoprotein A-I	Mus musculus	20-26
22427535-3	2012	We found that apoA-I expression was significantly reduced in the lungs of OVA-challenged, compared with saline-challenged, wild-type (WT) mice.	Sodium Chloride	104-110	apolipoprotein A-I	Mus musculus	14-20
22652597-8	2012	Intravenous apoA-I infusion abolished histamine-induced platelet-endothelial interactions, which are important for DVT initiation.	Histamine	38-47	apolipoprotein A-I	Mus musculus	12-18
22850721-5	2012	In this study, we investigated mimetic lipoprotein particle prepared from recombinant apolipoprotein A1 (apoA) and apolipoprotein E3 (apoE) as a delivery vehicle for chol-siRNAs.	chol	166-170	apolipoprotein A-I	Mus musculus	86-110
22345306-5	2012	Intimal SMCs accumulate excess amounts of cholesteryl esters when compared with medial layer SMCs, possibly explained by reduced ATP-binding cassette transporter A1 expression and ApoA-I binding to intimal-type SMCs.	Cholesterol Esters	42-60	apolipoprotein A-I	Mus musculus	180-186
22499994-6	2012	Transfusion of [(3)H]cholesterol-labeled RBCs led to robust delivery of the labeled cholesterol to the feces in apolipoprotein AI-deficient hosts.	Cholesterol	21-32	apolipoprotein A-I	Mus musculus	112-129
22499994-6	2012	Transfusion of [(3)H]cholesterol-labeled RBCs led to robust delivery of the labeled cholesterol to the feces in apolipoprotein AI-deficient hosts.	Cholesterol	84-95	apolipoprotein A-I	Mus musculus	112-129
22431312-3	2012	Studies in gene-targeted mice, however, have also indicated that increasing HDL-cholesterol plasma levels can either limit (e.g. apolipoprotein A-I) or accelerate (e.g. Scavenger receptor class B type I) atherosclerosis.	Cholesterol	80-91	apolipoprotein A-I	Mus musculus	129-147
22287724-10	2012	The peptibody and apoA-I may work cooperatively to generate larger HDL particles in vivo, either at the cholesterol efflux stage and/or via fusion of HDL particles that were generated by the peptibody and apoA-I individually.	Cholesterol	104-115	apolipoprotein A-I	Mus musculus	18-24
22799025-6	2012	Studies also showed that the 2030421B could induce apoA-I-mediated cholesterol efflux and inhibit lipids uptake into mouse peritoneal macrophages RAW264.7.	Cholesterol	67-78	apolipoprotein A-I	Mus musculus	51-57
21889608-0	2012	The LXR agonist GW3965 increases apoA-I protein levels in the central nervous system independent of ABCA1.	GW 3965	16-22	apolipoprotein A-I	Mus musculus	33-39
21889608-7	2012	Additionally, treatment of symptomatic AD mice with GW3965, an LXR agonist that stimulates ABCA1 expression, increases apoA-I more dramatically in the CNS compared to the periphery.	GW 3965	52-58	apolipoprotein A-I	Mus musculus	119-125
21889608-8	2012	Furthermore, GW3965-mediated up-regulation of CNS apoA-I is independent of ABCA1.	GW 3965	13-19	apolipoprotein A-I	Mus musculus	50-56
21944998-11	2012	Taken together these data suggest that the presence of large apoE enriched HDL particles containing apoA-I L159R lack the normal cholesterol efflux promoting properties of HDL, rendering them dysfunctional and pro-atherogenic.	Cholesterol	129-140	apolipoprotein A-I	Mus musculus	100-106
22020260-6	2012	Mouse macrophages deficient in ACSL1 exhibited reduced sensitivity to oleate- and linoleate-mediated ABCA1 degradation, which resulted in increased ABCA1 levels and increased apolipoprotein A-I-dependent cholesterol efflux in the presence of these fatty acids, as compared with wildtype mouse macrophages.	Oleic Acid	70-76	apolipoprotein A-I	Mus musculus	175-193
22020260-6	2012	Mouse macrophages deficient in ACSL1 exhibited reduced sensitivity to oleate- and linoleate-mediated ABCA1 degradation, which resulted in increased ABCA1 levels and increased apolipoprotein A-I-dependent cholesterol efflux in the presence of these fatty acids, as compared with wildtype mouse macrophages.	Linoleic Acid	82-91	apolipoprotein A-I	Mus musculus	175-193
22020260-6	2012	Mouse macrophages deficient in ACSL1 exhibited reduced sensitivity to oleate- and linoleate-mediated ABCA1 degradation, which resulted in increased ABCA1 levels and increased apolipoprotein A-I-dependent cholesterol efflux in the presence of these fatty acids, as compared with wildtype mouse macrophages.	Cholesterol	204-215	apolipoprotein A-I	Mus musculus	175-193
22020260-6	2012	Mouse macrophages deficient in ACSL1 exhibited reduced sensitivity to oleate- and linoleate-mediated ABCA1 degradation, which resulted in increased ABCA1 levels and increased apolipoprotein A-I-dependent cholesterol efflux in the presence of these fatty acids, as compared with wildtype mouse macrophages.	Fatty Acids	248-259	apolipoprotein A-I	Mus musculus	175-193
22237709-2	2012	While cholesterol acceptors such as high-density lipoproteins (HDL) and apolipoproteins A-I (apoA-I) and J (Apo J) have been found in male and female reproductive tracts, transporters that mediate cholesterol efflux from plasma membranes of spermatozoa to acceptors are not well defined.	Cholesterol	6-17	apolipoprotein A-I	Mus musculus	72-91
22237709-2	2012	While cholesterol acceptors such as high-density lipoproteins (HDL) and apolipoproteins A-I (apoA-I) and J (Apo J) have been found in male and female reproductive tracts, transporters that mediate cholesterol efflux from plasma membranes of spermatozoa to acceptors are not well defined.	Cholesterol	6-17	apolipoprotein A-I	Mus musculus	93-106
22237709-2	2012	While cholesterol acceptors such as high-density lipoproteins (HDL) and apolipoproteins A-I (apoA-I) and J (Apo J) have been found in male and female reproductive tracts, transporters that mediate cholesterol efflux from plasma membranes of spermatozoa to acceptors are not well defined.	Cholesterol	197-208	apolipoprotein A-I	Mus musculus	93-106
22237709-7	2012	Moreover, ABCA17 antibody interferes with cholesterol efflux from spermatozoa to lipid acceptors apoA-I.	Cholesterol	42-53	apolipoprotein A-I	Mus musculus	97-103
22190590-2	2012	Under basal conditions, in WT hepatocytes, cholesterol efflux to exogenous apoA-I was accompanied by conversion of apoA-I to HDL-sized particles.	Cholesterol	43-54	apolipoprotein A-I	Mus musculus	75-81
22190590-2	2012	Under basal conditions, in WT hepatocytes, cholesterol efflux to exogenous apoA-I was accompanied by conversion of apoA-I to HDL-sized particles.	Cholesterol	43-54	apolipoprotein A-I	Mus musculus	115-121
22190590-3	2012	LXR activation by T0901317 markedly enhanced the formation of larger HDL-sized particles as well as cellular cholesterol efflux to apoA-I.	Cholesterol	109-120	apolipoprotein A-I	Mus musculus	131-137
22190590-6	2012	ABCG1-deficient cells showed similar capacity to efflux cholesterol to apoA-I and to form nascent HDL particles compared with WT cells.	Cholesterol	56-67	apolipoprotein A-I	Mus musculus	71-77
22190590-7	2012	Cholesterol efflux to apoA-I and nascent HDL formation were slightly but significantly enhanced in SR-BI-deficient cells compared with WT cells under basal but not LXR activated conditions.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	22-28
22259189-0	2012	Disturbed one-carbon metabolism causing adverse reproductive outcomes in mice is associated with altered expression of apolipoprotein AI and inflammatory mediators PPARalpha, interferon-gamma, and interleukin-10.	Carbon	14-20	apolipoprotein A-I	Mus musculus	119-136
22171091-0	2012	Apolipoprotein A-I (ApoA-I) mimetic peptide P2a by restoring cholesterol esterification unmasks ApoA-I anti-inflammatory endogenous activity in vivo.	Cholesterol	61-72	apolipoprotein A-I	Mus musculus	0-18
22171091-0	2012	Apolipoprotein A-I (ApoA-I) mimetic peptide P2a by restoring cholesterol esterification unmasks ApoA-I anti-inflammatory endogenous activity in vivo.	Cholesterol	61-72	apolipoprotein A-I	Mus musculus	20-26
22171091-8	2012	CEs significantly decreased in carrageenan-treated mice during edema development and negatively correlated with the Hpt/ApoA-I ratio.	Cholesterol Esters	0-3	apolipoprotein A-I	Mus musculus	120-126
22171091-8	2012	CEs significantly decreased in carrageenan-treated mice during edema development and negatively correlated with the Hpt/ApoA-I ratio.	Carrageenan	31-42	apolipoprotein A-I	Mus musculus	120-126
22053073-9	2012	Apoe(h/h)Ldlr(-/-) mice displayed increased levels of apoA1-rich HDL that were potent in promoting cellular cholesterol efflux.	Cholesterol	108-119	apolipoprotein A-I	Mus musculus	54-59
22095982-8	2012	LDN treatment increased macrophage ABCA1 and ABCG1 expression, significantly raised cholesterol efflux to ApoA-1, and decreased foam cell formation.	LDN	0-3	apolipoprotein A-I	Mus musculus	106-112
22039582-4	2012	ApoA-I-mediated cholesterol efflux from aortic EC was 2.6-fold higher (P &lt; 0.0001) for cells from transgenic versus control mice.	Cholesterol	16-27	apolipoprotein A-I	Mus musculus	0-6
22178419-5	2012	Results obtained from SR-BI-enriched Fu5AH and ABCA1-enriched J774 cells revealed that AD impaired the interaction of HDL and apoA-I with both the ABCA1 transporter and SR-BI receptor.	fu5ah	37-42	apolipoprotein A-I	Mus musculus	126-132
23285013-1	2012	Apolipoprotein A-I (Apo A-I) is a major component of high density lipoproteins (HDL) that transport cholesterol in circulation.	Cholesterol	100-111	apolipoprotein A-I	Mus musculus	0-18
23285013-1	2012	Apolipoprotein A-I (Apo A-I) is a major component of high density lipoproteins (HDL) that transport cholesterol in circulation.	Cholesterol	100-111	apolipoprotein A-I	Mus musculus	20-27
23133551-2	2012	It mediates the efflux of cellular cholesterol to lipid-poor apolipoprotein A-I.	Cholesterol	35-46	apolipoprotein A-I	Mus musculus	61-79
22479476-0	2012	Apolipoprotein A-I attenuates palmitate-mediated NF-kappaB activation by reducing Toll-like receptor-4 recruitment into lipid rafts.	Palmitates	30-39	apolipoprotein A-I	Mus musculus	0-18
22479476-3	2012	In this study, we used endothelial cells to demonstrate that while palmitic acid activates NF-kappaB signaling, apolipoprotein A-I, (apoA-I), the major protein component of HDL, attenuates palmitate-induced NF-kappaB activation.	Palmitates	189-198	apolipoprotein A-I	Mus musculus	112-130
22479476-3	2012	In this study, we used endothelial cells to demonstrate that while palmitic acid activates NF-kappaB signaling, apolipoprotein A-I, (apoA-I), the major protein component of HDL, attenuates palmitate-induced NF-kappaB activation.	Palmitates	189-198	apolipoprotein A-I	Mus musculus	133-139
22479476-7	2012	Finally, we show that in endothelial cells TLR4 is recruited into lipid rafts in response to palmitate, and that apoA-I prevents palmitate-induced TLR4 trafficking into lipid rafts, thereby blocking NF-kappaB activation.	Palmitates	129-138	apolipoprotein A-I	Mus musculus	113-119
22129452-0	2011	13-hydroxy linoleic acid increases expression of the cholesterol transporters ABCA1, ABCG1 and SR-BI and stimulates apoA-I-dependent cholesterol efflux in RAW264.7 macrophages.	13-hydroxylinoleic acid	0-24	apolipoprotein A-I	Mus musculus	116-122
22129452-5	2011	In addition, 13-HODE enhanced cholesterol concentration in the medium but decreased cellular cholesterol concentration during incubation of cells with the extracellular lipid acceptor apolipoprotein A-I (P &lt; 0.05).	13-hydroxy-9,11-octadecadienoic acid	13-20	apolipoprotein A-I	Mus musculus	184-202
21885853-8	2011	In mouse cells, miR-758 reduced cellular cholesterol efflux to apolipoprotein A1 (apoA1), and anti-miR-758 increased it.	Cholesterol	41-52	apolipoprotein A-I	Mus musculus	63-80
21885853-8	2011	In mouse cells, miR-758 reduced cellular cholesterol efflux to apolipoprotein A1 (apoA1), and anti-miR-758 increased it.	Cholesterol	41-52	apolipoprotein A-I	Mus musculus	82-87
21885853-11	2011	CONCLUSION: We identified miR-758 as a novel miRNA that posttranscriptionally controls ABCA1 levels in different cells and regulates macrophage cellular cholesterol efflux to apoA1, opening new avenues to increase apoA1 and raise high-density lipoprotein levels.	Cholesterol	153-164	apolipoprotein A-I	Mus musculus	175-180
21885853-11	2011	CONCLUSION: We identified miR-758 as a novel miRNA that posttranscriptionally controls ABCA1 levels in different cells and regulates macrophage cellular cholesterol efflux to apoA1, opening new avenues to increase apoA1 and raise high-density lipoprotein levels.	Cholesterol	153-164	apolipoprotein A-I	Mus musculus	214-219
21449977-7	2011	KEY RESULTS: Treatment with Ro 11-1464 300 mg kg(-1)  day(-1) resulted in a nearly 2-fold increase in plasma apoA-I, a 2- to 3-fold increase in the level of large sized-pre-beta high-density lipoprotein and a 3-fold selective up-regulation of hepatic apoA-I mRNA, but a marked decrease in all plasma lipids and LCAT activity.	9-methyl-4-phenyl-6H-thieno(3,2-f)(1,2,4)triazolo(4,3-a)(1,4)diazepine	28-38	apolipoprotein A-I	Mus musculus	109-115
21449977-7	2011	KEY RESULTS: Treatment with Ro 11-1464 300 mg kg(-1)  day(-1) resulted in a nearly 2-fold increase in plasma apoA-I, a 2- to 3-fold increase in the level of large sized-pre-beta high-density lipoprotein and a 3-fold selective up-regulation of hepatic apoA-I mRNA, but a marked decrease in all plasma lipids and LCAT activity.	9-methyl-4-phenyl-6H-thieno(3,2-f)(1,2,4)triazolo(4,3-a)(1,4)diazepine	28-38	apolipoprotein A-I	Mus musculus	251-257
21486287-3	2011	The aim of the present study was to investigate in vivo the effect of rosuvastatin on apoA-I expression and secretion in a transgenic mouse model for human apoA-I.	Rosuvastatin Calcium	70-82	apolipoprotein A-I	Mus musculus	86-92
21869747-1	2011	The ATP-binding cassette transporter A1 (ABCA1) mediates the cellular efflux of excess cholesterol and phospholipids to lipid-poor apolipoprotein A-I (apoA-I).	Cholesterol	87-98	apolipoprotein A-I	Mus musculus	131-149
21869747-1	2011	The ATP-binding cassette transporter A1 (ABCA1) mediates the cellular efflux of excess cholesterol and phospholipids to lipid-poor apolipoprotein A-I (apoA-I).	Cholesterol	87-98	apolipoprotein A-I	Mus musculus	151-157
21869747-1	2011	The ATP-binding cassette transporter A1 (ABCA1) mediates the cellular efflux of excess cholesterol and phospholipids to lipid-poor apolipoprotein A-I (apoA-I).	Phospholipids	103-116	apolipoprotein A-I	Mus musculus	131-149
21869747-1	2011	The ATP-binding cassette transporter A1 (ABCA1) mediates the cellular efflux of excess cholesterol and phospholipids to lipid-poor apolipoprotein A-I (apoA-I).	Phospholipids	103-116	apolipoprotein A-I	Mus musculus	151-157
21869747-8	2011	This compound stimulated ApoA-I-mediated cellular cholesterol efflux from RAW 264.7 cells.	Cholesterol	50-61	apolipoprotein A-I	Mus musculus	25-31
21838883-2	2011	Homocysteine influences the liver expression of ApoA-I and decreases its blood level and HDL in genetic mice model.	Homocysteine	0-12	apolipoprotein A-I	Mus musculus	48-54
21622630-5	2011	Apoa1-/- mice showed the expected significant reduction in total cholesterol (TC), HDL cholesterol (HDL-C), and triglyceride (TG) plasma levels.	Cholesterol	65-76	apolipoprotein A-I	Mus musculus	0-5
21622630-5	2011	Apoa1-/- mice showed the expected significant reduction in total cholesterol (TC), HDL cholesterol (HDL-C), and triglyceride (TG) plasma levels.	Technetium	78-80	apolipoprotein A-I	Mus musculus	0-5
21622630-5	2011	Apoa1-/- mice showed the expected significant reduction in total cholesterol (TC), HDL cholesterol (HDL-C), and triglyceride (TG) plasma levels.	Cholesterol	87-98	apolipoprotein A-I	Mus musculus	0-5
21622630-5	2011	Apoa1-/- mice showed the expected significant reduction in total cholesterol (TC), HDL cholesterol (HDL-C), and triglyceride (TG) plasma levels.	Triglycerides	112-124	apolipoprotein A-I	Mus musculus	0-5
21622630-5	2011	Apoa1-/- mice showed the expected significant reduction in total cholesterol (TC), HDL cholesterol (HDL-C), and triglyceride (TG) plasma levels.	Triglycerides	126-128	apolipoprotein A-I	Mus musculus	0-5
21504968-3	2011	Functional studies using adenovirus-mediated gene transfer of two apoA-I mutants in apoA-I-deficient mice showed that apoA-I[D89A/E91A/E92A] increased plasma cholesterol and caused severe hypertriglyceridemia.	Cholesterol	158-169	apolipoprotein A-I	Mus musculus	66-72
21504968-3	2011	Functional studies using adenovirus-mediated gene transfer of two apoA-I mutants in apoA-I-deficient mice showed that apoA-I[D89A/E91A/E92A] increased plasma cholesterol and caused severe hypertriglyceridemia.	Cholesterol	158-169	apolipoprotein A-I	Mus musculus	84-90
21504968-3	2011	Functional studies using adenovirus-mediated gene transfer of two apoA-I mutants in apoA-I-deficient mice showed that apoA-I[D89A/E91A/E92A] increased plasma cholesterol and caused severe hypertriglyceridemia.	Cholesterol	158-169	apolipoprotein A-I	Mus musculus	84-90
21520143-1	2011	Apolipoprotein A-I (ApoA-I) is the major protein component of high density lipoprotein (HDL) particles in serum, and participates in the reverse transport of cholesterol from tissues to the liver for excretion.	Cholesterol	158-169	apolipoprotein A-I	Mus musculus	20-26
21600874-4	2011	This elevated level of apolipoprotein A-I was coupled with an elevated level of H-ras12V protein and ROS.	ros	101-104	apolipoprotein A-I	Mus musculus	23-41
21464203-1	2011	It is claimed that apoA-I expression is repressed in mice by cholic acid (CA) and its taurine conjugate, taurocholic acid (TCA) via farnesoid X receptor (FXR) activation.	Cholic Acid	61-72	apolipoprotein A-I	Mus musculus	19-25
21464203-1	2011	It is claimed that apoA-I expression is repressed in mice by cholic acid (CA) and its taurine conjugate, taurocholic acid (TCA) via farnesoid X receptor (FXR) activation.	Taurine	86-93	apolipoprotein A-I	Mus musculus	19-25
21464203-1	2011	It is claimed that apoA-I expression is repressed in mice by cholic acid (CA) and its taurine conjugate, taurocholic acid (TCA) via farnesoid X receptor (FXR) activation.	Taurocholic Acid	105-121	apolipoprotein A-I	Mus musculus	19-25
21464203-1	2011	It is claimed that apoA-I expression is repressed in mice by cholic acid (CA) and its taurine conjugate, taurocholic acid (TCA) via farnesoid X receptor (FXR) activation.	Taurocholic Acid	123-126	apolipoprotein A-I	Mus musculus	19-25
21464203-2	2011	We measured apoA-I expression in mice, hamsters, and rats treated with highly potent and selective synthetic FXR agonists or with TCA.	Taurocholic Acid	130-133	apolipoprotein A-I	Mus musculus	12-18
21283904-7	2011	In conclusion, our data that L-5F inhibits angiogenesis suggests that apoA-I mimetic peptides may serve as novel anti-angiogenesis agents for the treatment of angiogenesis-associated diseases, including cancer.	l-5f	29-33	apolipoprotein A-I	Mus musculus	70-76
21288012-0	2011	Enhanced binding of apolipoprotein A-I variants associated with hypertriglyceridemia to triglyceride-rich particles.	Triglycerides	69-81	apolipoprotein A-I	Mus musculus	20-38
21288012-8	2011	We found that the apoA-I[E110A/E111A] and apoA-I[Delta(61-78)] mutations lead to enhanced binding of apoA-I to TG-rich particles, destabilization, and greater exposure of the hydrophobic surface of the protein.	Triglycerides	111-113	apolipoprotein A-I	Mus musculus	18-24
21288012-8	2011	We found that the apoA-I[E110A/E111A] and apoA-I[Delta(61-78)] mutations lead to enhanced binding of apoA-I to TG-rich particles, destabilization, and greater exposure of the hydrophobic surface of the protein.	Triglycerides	111-113	apolipoprotein A-I	Mus musculus	42-48
21288012-8	2011	We found that the apoA-I[E110A/E111A] and apoA-I[Delta(61-78)] mutations lead to enhanced binding of apoA-I to TG-rich particles, destabilization, and greater exposure of the hydrophobic surface of the protein.	Triglycerides	111-113	apolipoprotein A-I	Mus musculus	42-48
21257755-4	2011	LDL also induced an ~2-fold increase in macrophage surface expression of ABCA1 and a 14-fold-increase in apolipoprotein AI-mediated cholesterol efflux.	Cholesterol	132-143	apolipoprotein A-I	Mus musculus	105-122
21219878-0	2011	Tributyltin chloride induces ABCA1 expression and apolipoprotein A-I-mediated cellular cholesterol efflux by activating LXRalpha/RXR.	tributyltin	0-20	apolipoprotein A-I	Mus musculus	50-68
21219878-0	2011	Tributyltin chloride induces ABCA1 expression and apolipoprotein A-I-mediated cellular cholesterol efflux by activating LXRalpha/RXR.	Cholesterol	87-98	apolipoprotein A-I	Mus musculus	50-68
21219878-8	2011	TBTC augmented ABCA1 protein levels and apolipoprotein A-I-dependent cellular cholesterol efflux (HDL generation).	tributyltin	0-4	apolipoprotein A-I	Mus musculus	40-58
21219878-8	2011	TBTC augmented ABCA1 protein levels and apolipoprotein A-I-dependent cellular cholesterol efflux (HDL generation).	Cholesterol	78-89	apolipoprotein A-I	Mus musculus	40-58
21212401-8	2011	The ability of intraperitoneally administered phospholipid vesicles to promote RCT in wild-type mice was not blocked by 48/80, supporting the notion that mast cell-dependent proteolysis of the intraperitoneally administered apoA-I was responsible for RCT inhibition.	Phospholipids	46-58	apolipoprotein A-I	Mus musculus	224-230
21419084-10	2011	After treatment, GXK decoction and simvastatin improved the dyslipidemia by increasing the concentrations of ApoA I and HDL-C and decreasing the concentrations of TC, TAG, LDL-C, ApoB, CRP, SAA and Fbg (P&lt;0.05).	Simvastatin	35-46	apolipoprotein A-I	Mus musculus	109-115
21071688-0	2011	Influence of apolipoprotein A-I domain structure on macrophage reverse cholesterol transport in mice.	Cholesterol	71-82	apolipoprotein A-I	Mus musculus	13-31
21071688-3	2011	METHODS AND RESULTS: The different apoA-I variants were expressed in apoA-I-null mice that were injected with [H(3)]cholesterol-labeled J774 mouse macrophages to measure RCT.	HS 3	111-115	apolipoprotein A-I	Mus musculus	35-41
21071688-3	2011	METHODS AND RESULTS: The different apoA-I variants were expressed in apoA-I-null mice that were injected with [H(3)]cholesterol-labeled J774 mouse macrophages to measure RCT.	Cholesterol	116-127	apolipoprotein A-I	Mus musculus	35-41
21071688-4	2011	Significantly more cholesterol was removed from the macrophages and deposited in the feces via the RCT pathway in mice expressing mouse-H apoA-I compared with all other groups.	Cholesterol	19-30	apolipoprotein A-I	Mus musculus	138-144
21071688-5	2011	Analysis of the individual components of the RCT pathway demonstrated that mouse-H apoA-I promoted ATP-binding cassette transporter A1-mediated cholesterol efflux more efficiently than all other variants, as well as increasing the rate of cholesterol uptake into liver cells.	Cholesterol	144-155	apolipoprotein A-I	Mus musculus	83-89
21071688-5	2011	Analysis of the individual components of the RCT pathway demonstrated that mouse-H apoA-I promoted ATP-binding cassette transporter A1-mediated cholesterol efflux more efficiently than all other variants, as well as increasing the rate of cholesterol uptake into liver cells.	Cholesterol	239-250	apolipoprotein A-I	Mus musculus	83-89
21130455-3	2011	As compared to family controls mutations in the genes for apolipoprotein A-I, ATP binding cassette transporter (ABC) A1 and lecithin:cholesterol acylstransferase (LCAT) were associated with reduced concentrations of both HDL-cholesterol and HDL-27OHC whereas mutations in the genes for cholesterylester transfer protein (CETP), scavenger receptor type BI and hepatic lipase were associated with elevated HDL concentrations of either sterol.	Cholesterol	133-144	apolipoprotein A-I	Mus musculus	58-76
21130455-3	2011	As compared to family controls mutations in the genes for apolipoprotein A-I, ATP binding cassette transporter (ABC) A1 and lecithin:cholesterol acylstransferase (LCAT) were associated with reduced concentrations of both HDL-cholesterol and HDL-27OHC whereas mutations in the genes for cholesterylester transfer protein (CETP), scavenger receptor type BI and hepatic lipase were associated with elevated HDL concentrations of either sterol.	Sterols	138-144	apolipoprotein A-I	Mus musculus	58-76
21156318-3	2011	Homocysteine influences the liver expression of ApoA-I and decreases its blood level and HDL in genetic mice models.	Homocysteine	0-12	apolipoprotein A-I	Mus musculus	48-54
21134113-1	2011	BACKGROUND/AIMS: Apolipoprotein A-I (apo A-I) is the main protein component of plasma high-density lipoproteins (HDL) and a key determinant of HDL cholesterol levels and metabolism.	Cholesterol	147-158	apolipoprotein A-I	Mus musculus	17-35
21134113-1	2011	BACKGROUND/AIMS: Apolipoprotein A-I (apo A-I) is the main protein component of plasma high-density lipoproteins (HDL) and a key determinant of HDL cholesterol levels and metabolism.	Cholesterol	147-158	apolipoprotein A-I	Mus musculus	37-44
21134113-6	2011	RESULTS: Bile acid pool size and faecal excretion were within the normal range in chow- and cholesterol-fed apo A-I knockout (KO) mice.	Cholesterol	92-103	apolipoprotein A-I	Mus musculus	108-115
21134113-8	2011	Lithogenic diet-fed apo A-I KO mice exhibited an impaired hypercholesterolaemic response owing to a lower increase in cholesterol levels transported in large lipoproteins.	Cholesterol	63-74	apolipoprotein A-I	Mus musculus	20-27
21241519-5	2011	Plasma analysis by enzymatic method or ELISA showed that high-density lipoprotein-cholesterol (HDL-C) and apolipoprotein A-I (apoA-I) contents were remarkably increased by treatment with simvastatin.	Simvastatin	187-198	apolipoprotein A-I	Mus musculus	106-124
21241519-5	2011	Plasma analysis by enzymatic method or ELISA showed that high-density lipoprotein-cholesterol (HDL-C) and apolipoprotein A-I (apoA-I) contents were remarkably increased by treatment with simvastatin.	Simvastatin	187-198	apolipoprotein A-I	Mus musculus	126-132
21241519-7	2011	Real-time PCR detection disclosed that the expression of several transporters involved in reverse cholesterol transport, including macrophage scavenger receptor class B type I, hepatic ATP-binding cassette (ABC) transporters ABCG5, and ABCB4 were induced by simvastatin treatment, the expression of hepatic ABCA1 and apoA-I, which play roles in the maturation of HDL-C, were also elevated in simvastatin treated groups.	Cholesterol	98-109	apolipoprotein A-I	Mus musculus	317-323
21241519-7	2011	Real-time PCR detection disclosed that the expression of several transporters involved in reverse cholesterol transport, including macrophage scavenger receptor class B type I, hepatic ATP-binding cassette (ABC) transporters ABCG5, and ABCB4 were induced by simvastatin treatment, the expression of hepatic ABCA1 and apoA-I, which play roles in the maturation of HDL-C, were also elevated in simvastatin treated groups.	Simvastatin	258-269	apolipoprotein A-I	Mus musculus	317-323
21241519-9	2011	We confirmed here for the first time simvastatin increased the expression of hepatic ABCB4 and ABCG5, which involved in secretion of cholesterol and bile acids into the bile, besides upregulated ABCA1 and apoA-I.	Simvastatin	37-48	apolipoprotein A-I	Mus musculus	205-211
21636950-6	2011	RESULTS: High dose (500microM) of glibenclamide inhibited ABCA1 function and apolipoprotein A-I (apoA-I)-mediated cholesterol efflux, and attenuated ABCA1 expression.	Glyburide	34-47	apolipoprotein A-I	Mus musculus	77-95
21636950-6	2011	RESULTS: High dose (500microM) of glibenclamide inhibited ABCA1 function and apolipoprotein A-I (apoA-I)-mediated cholesterol efflux, and attenuated ABCA1 expression.	Glyburide	34-47	apolipoprotein A-I	Mus musculus	97-103
21636950-6	2011	RESULTS: High dose (500microM) of glibenclamide inhibited ABCA1 function and apolipoprotein A-I (apoA-I)-mediated cholesterol efflux, and attenuated ABCA1 expression.	Cholesterol	114-125	apolipoprotein A-I	Mus musculus	77-95
21636950-6	2011	RESULTS: High dose (500microM) of glibenclamide inhibited ABCA1 function and apolipoprotein A-I (apoA-I)-mediated cholesterol efflux, and attenuated ABCA1 expression.	Cholesterol	114-125	apolipoprotein A-I	Mus musculus	97-103
21636950-7	2011	Although glimepiride maintained apoA-I-mediated cholesterol efflux from RAW264.7 cells, like glibenclamide, it inhibited ABCA1-mediated cholesterol efflux from transfected HEK293 cells.	glimepiride	9-20	apolipoprotein A-I	Mus musculus	32-38
21115733-2	2011	Apolipoprotein A-I (apoA-I), the major structural protein of high-density lipoproteins, mediates reverse cholesterol transport and has atheroprotective and anti-inflammatory effects.	Cholesterol	105-116	apolipoprotein A-I	Mus musculus	0-18
21115733-2	2011	Apolipoprotein A-I (apoA-I), the major structural protein of high-density lipoproteins, mediates reverse cholesterol transport and has atheroprotective and anti-inflammatory effects.	Cholesterol	105-116	apolipoprotein A-I	Mus musculus	20-26
22022523-2	2011	In contrast to apoA-I, apoE is secreted by macrophages and can, like apoA-I, induce ABCA1-mediated cholesterol efflux.	Cholesterol	99-110	apolipoprotein A-I	Mus musculus	69-75
21858084-7	2011	Our results indicate that there are at least two independent lipid binding sites for apoA-I; Cav1-mediated apoA-I surface binding and uptake is not linked to cholesterol efflux, indicating that membrane domains other than caveolae regulate ABCA1-mediated cholesterol efflux.	Cholesterol	255-266	apolipoprotein A-I	Mus musculus	107-113
21311139-0	2011	[Effect of apolipoprotein A-I mimetic peptides on cholesterol efflux in RAW264.7 cells].	Cholesterol	50-61	apolipoprotein A-I	Mus musculus	11-29
21115285-0	2010	ApoA-I mimetic peptides promote pre-beta HDL formation in vivo causing remodeling of HDL and triglyceride accumulation at higher dose.	Triglycerides	93-105	apolipoprotein A-I	Mus musculus	0-6
21115285-1	2010	Reverse cholesterol transport promoted by HDL-apoA-I is an important mechanism of protection against atherosclerosis.	Cholesterol	8-19	apolipoprotein A-I	Mus musculus	46-52
20817832-0	2010	Inhibition of collar-induced carotid atherosclerosis by recombinant apoA-I cysteine mutants in apoE-deficient mice.	Cysteine	75-83	apolipoprotein A-I	Mus musculus	68-74
20817832-1	2010	The previous studies in our laboratory revealed that seven cysteine mutants of apolipoprotein A-I (apoA-I) have different structural features and biological activities in vitro and in vivo.	Cysteine	59-67	apolipoprotein A-I	Mus musculus	79-97
20817832-1	2010	The previous studies in our laboratory revealed that seven cysteine mutants of apolipoprotein A-I (apoA-I) have different structural features and biological activities in vitro and in vivo.	Cysteine	59-67	apolipoprotein A-I	Mus musculus	99-105
20817832-6	2010	In summary, intravenous injection with rHDL74 reconstituted with apoA-I cysteine mutant apoA-I (N74C) dramatically delays the development of atherosclerosis induced by perivascular carotid collar placement and reduces vascular remodeling in the carotid artery in apoE-/- mice.	Cysteine	72-80	apolipoprotein A-I	Mus musculus	65-71
20817832-6	2010	In summary, intravenous injection with rHDL74 reconstituted with apoA-I cysteine mutant apoA-I (N74C) dramatically delays the development of atherosclerosis induced by perivascular carotid collar placement and reduces vascular remodeling in the carotid artery in apoE-/- mice.	Cysteine	72-80	apolipoprotein A-I	Mus musculus	88-94
21041624-4	2010	Serum levels of lysophosphatidic acid, a well-characterized modulator of tumor cell proliferation, were significantly reduced (&gt;50% compared with control mice, P &lt; 0.05) in mice that received apoA-I mimetic peptides (administered either subcutaneously or orally), suggesting that binding and removal of lysophosphatidic acid is a potential mechanism for the inhibition of tumor development by apoA-I mimetic peptides, which may serve as a previously unexplored class of anticancer agents.	lysophosphatidic acid	16-37	apolipoprotein A-I	Mus musculus	198-204
21041624-4	2010	Serum levels of lysophosphatidic acid, a well-characterized modulator of tumor cell proliferation, were significantly reduced (&gt;50% compared with control mice, P &lt; 0.05) in mice that received apoA-I mimetic peptides (administered either subcutaneously or orally), suggesting that binding and removal of lysophosphatidic acid is a potential mechanism for the inhibition of tumor development by apoA-I mimetic peptides, which may serve as a previously unexplored class of anticancer agents.	lysophosphatidic acid	16-37	apolipoprotein A-I	Mus musculus	399-405
21041624-4	2010	Serum levels of lysophosphatidic acid, a well-characterized modulator of tumor cell proliferation, were significantly reduced (&gt;50% compared with control mice, P &lt; 0.05) in mice that received apoA-I mimetic peptides (administered either subcutaneously or orally), suggesting that binding and removal of lysophosphatidic acid is a potential mechanism for the inhibition of tumor development by apoA-I mimetic peptides, which may serve as a previously unexplored class of anticancer agents.	lysophosphatidic acid	309-330	apolipoprotein A-I	Mus musculus	198-204
20723893-4	2010	METHODS AND RESULTS: We observed that treatment of THP-1 macrophages, human monocyte-derived macrophages, and RAW264.7 cells with cilostazol increased ABCA1 and ABCG1 expression in a concentration-dependent manner, translating into enhanced apoA-I- and HDL-mediated cholesterol efflux from the macrophages.	Cilostazol	130-140	apolipoprotein A-I	Mus musculus	241-247
20655299-7	2010	Overexpression of GPR109A reduced primary hepatocyte free cholesterol efflux to apoA-I; conversely, GPR109A deficient hepatocytes had increased ABCA1-mediated cholesterol efflux.	Cholesterol	58-69	apolipoprotein A-I	Mus musculus	80-86
20655299-8	2010	These data support the concept that the HDL-C lowering effect of niacin in wild-type mice is mediated through stimulation of GPR109A in hepatocytes; such an effect then leads to reduced hepatocyte ABCA1 expression and activity, decreased cholesterol efflux to nascent apoA-I, and reduced HDL-C levels.	Niacin	65-71	apolipoprotein A-I	Mus musculus	268-274
20463180-8	2010	In bleomycin-treated mice, Apo A-I protein in BALF was lower than that in sham-treated control animals.	Bleomycin	3-12	apolipoprotein A-I	Mus musculus	27-34
20463180-10	2010	Intranasal treatment with Apo A-I protein reduced the bleomycin-induced increases in number of inflammatory cells and collagen deposition in sham-treated mice in a dose-dependent manner.	Bleomycin	54-63	apolipoprotein A-I	Mus musculus	26-33
20537649-5	2010	However, plasma cholesterol, glucose and APOA1 were significantly decreased in homozygous Cbs-deficient mice when they received the cysteine and glycine-enriched beverage.	Cysteine	132-140	apolipoprotein A-I	Mus musculus	41-46
20537649-7	2010	A significant, inverse relationship was observed between plasma and hepatic APOA1 concentrations while a positive one was found between plasma levels of cysteine and APOA1.	Cysteine	153-161	apolipoprotein A-I	Mus musculus	166-171
20498409-3	2010	ApoA-I null (apoA-I(-/-)) mice had reduced total and HDL cholesterol but increased pro-inflammatory HDL compared with C57BL/6J mice.	Cholesterol	57-68	apolipoprotein A-I	Mus musculus	0-6
20498409-3	2010	ApoA-I null (apoA-I(-/-)) mice had reduced total and HDL cholesterol but increased pro-inflammatory HDL compared with C57BL/6J mice.	Cholesterol	57-68	apolipoprotein A-I	Mus musculus	13-19
20498409-8	2010	Inflammatory cells, collagen deposition, 3-nitrotyrosine, and 4-hydroxy-2-nonenal were increased in apoA-I(-/-) lungs but not oxidized phospholipids.	3-nitrotyrosine	41-56	apolipoprotein A-I	Mus musculus	100-106
20498409-8	2010	Inflammatory cells, collagen deposition, 3-nitrotyrosine, and 4-hydroxy-2-nonenal were increased in apoA-I(-/-) lungs but not oxidized phospholipids.	4-hydroxy-2-nonenal	62-81	apolipoprotein A-I	Mus musculus	100-106
20498409-9	2010	Colocalization of 4-hydroxy-2-nonenal with transforming growth factor beta-1 (TGFbeta-1 was increased in apoA-I(-/-) lungs.	4-hydroxy-2-nonenal	18-37	apolipoprotein A-I	Mus musculus	105-116
20498409-11	2010	Dichlorodihydrofluorescein-detectable oxidants were increased in bronchoalveolar lavage fluid (BALF) in apoA-I(-/-) mice.	dichlorodihydrofluorescein	0-26	apolipoprotein A-I	Mus musculus	104-110
20498409-12	2010	In contrast, BALF nitrite+nitrate levels were decreased in apoA-I(-/-) mice.	Nitrites	18-25	apolipoprotein A-I	Mus musculus	59-65
20498409-12	2010	In contrast, BALF nitrite+nitrate levels were decreased in apoA-I(-/-) mice.	Nitrates	26-33	apolipoprotein A-I	Mus musculus	59-65
20735223-2	2010	MATERIALS &amp; METHODS: Apolipoprotein A-I, a major component protein of HDL, was genetically fused to TAT peptide, a protein transduction domain.	Adenosine Monophosphate	11-14	apolipoprotein A-I	Mus musculus	25-43
20460831-6	2010	Plasma levels of HDL cholesterol and apolipoproteins related to these lipoparticles, such as apoA-I, apoA-II, apoA-IV, apoA-V and apoJ, were significantly different between these two strains and there were sex-related differences in some of these apolipoproteins.	Cholesterol	21-32	apolipoprotein A-I	Mus musculus	93-99
20431058-2	2010	The ATP-binding cassette transporters ABCA1 and ABCG1 have a major role in promoting cholesterol efflux from macrophages to apolipoprotein A-1 and HDL and are upregulated during the phagocytosis of apoptotic cells (efferocytosis).	Cholesterol	85-96	apolipoprotein A-I	Mus musculus	124-142
20488992-3	2010	Transplantation of Abca1(-/-) Abcg1(-/-) bone marrow into apolipoprotein A-1 transgenic mice with elevated levels of high-density lipoprotein (HDL) suppressed the LSK population, reduced leukocytosis, reversed the myeloproliferative disorder, and accelerated atherosclerosis.	lsk	163-166	apolipoprotein A-I	Mus musculus	58-76
20979886-0	2010	[Anti-inflammatory action of lipid-bound apoA-I cysteine mutants].	Cysteine	48-56	apolipoprotein A-I	Mus musculus	41-47
20979886-1	2010	OBJECTIVE: To determine the anti-inflammatory functions of different cysteine mutants of apolipoprotein A-I recombinant HDLs.	Cysteine	69-77	apolipoprotein A-I	Mus musculus	89-107
20083572-0	2010	Overexpression of steroidogenic acute regulatory protein increases macrophage cholesterol efflux to apolipoprotein AI.	Cholesterol	78-89	apolipoprotein A-I	Mus musculus	100-117
20083572-1	2010	AIMS: In this study, we investigated the impact of enhancing cholesterol delivery to mitochondrial sterol 27-hydroxylase, via steroidogenic acute regulatory protein (StAR), on the expression of genes involved in macrophage cholesterol homeostasis and efflux of cholesterol to apolipoprotein (apo) AI.	Cholesterol	61-72	apolipoprotein A-I	Mus musculus	276-299
20083572-1	2010	AIMS: In this study, we investigated the impact of enhancing cholesterol delivery to mitochondrial sterol 27-hydroxylase, via steroidogenic acute regulatory protein (StAR), on the expression of genes involved in macrophage cholesterol homeostasis and efflux of cholesterol to apolipoprotein (apo) AI.	Cholesterol	223-234	apolipoprotein A-I	Mus musculus	276-299
20083572-1	2010	AIMS: In this study, we investigated the impact of enhancing cholesterol delivery to mitochondrial sterol 27-hydroxylase, via steroidogenic acute regulatory protein (StAR), on the expression of genes involved in macrophage cholesterol homeostasis and efflux of cholesterol to apolipoprotein (apo) AI.	Cholesterol	223-234	apolipoprotein A-I	Mus musculus	276-299
19949424-1	2010	We have used a new ApoA-I transgenic mouse model to identify by global gene expression profiling, candidate genes that affect lipid and lipoprotein metabolism in response to fenofibrate treatment.	Fenofibrate	174-185	apolipoprotein A-I	Mus musculus	19-25
20214958-10	2010	Agarose gel electrophoresis and sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-SPAGE) patterns indicated that TA-NLC could bind to apolipoprotein A-I (apoA-I) specifically in vitro.	polyacrylamide	55-69	apolipoprotein A-I	Mus musculus	147-165
19913791-2	2010	Tumor necrosis factor-alpha (TNF) induces macrophage ATP-binding cassette transporter A1 (ABCA1), a cardioprotective transmembrane protein that exports cellular cholesterol to apolipoprotein A-I.	Cholesterol	161-172	apolipoprotein A-I	Mus musculus	176-194
20102334-0	2010	Myriocin-mediated up-regulation of hepatocyte apoA-I synthesis is associated with ERK inhibition.	thermozymocidin	0-8	apolipoprotein A-I	Mus musculus	46-52
20102334-3	2010	Interestingly, hepatic apoA-I (apolipoprotein A-I) synthesis and plasma HDL (high-density lipoprotein)-cholesterol levels were also increased in apoE-null mice treated with myriocin.	thermozymocidin	173-181	apolipoprotein A-I	Mus musculus	23-29
20102334-3	2010	Interestingly, hepatic apoA-I (apolipoprotein A-I) synthesis and plasma HDL (high-density lipoprotein)-cholesterol levels were also increased in apoE-null mice treated with myriocin.	thermozymocidin	173-181	apolipoprotein A-I	Mus musculus	31-49
20102334-4	2010	Since myriocin is a known inhibitor of ERK (extracellular-signal-related kinase) phosphorylation, we assessed the possibility that myriocin may be acting to increase hepatic apoA-I production via this pathway.	thermozymocidin	131-139	apolipoprotein A-I	Mus musculus	174-180
20102334-5	2010	To address this, HepG2 cells and primary mouse hepatocytes were treated with 200 muM myriocin for up to 48 h. Myriocin increased apoA-I mRNA and protein levels by approx.	thermozymocidin	85-93	apolipoprotein A-I	Mus musculus	129-135
20102334-5	2010	To address this, HepG2 cells and primary mouse hepatocytes were treated with 200 muM myriocin for up to 48 h. Myriocin increased apoA-I mRNA and protein levels by approx.	thermozymocidin	110-118	apolipoprotein A-I	Mus musculus	129-135
20102334-7	2010	Myriocin also increased apoA-I secretion up to 3.5-fold and decreased ERK phosphorylation by approx.	thermozymocidin	0-8	apolipoprotein A-I	Mus musculus	24-30
20102334-10	2010	Further experiments revealed that the MEK (mitogen-activated protein kinase/ERK kinase) inhibitor PD98059 potently inhibited ERK phosphorylation, as expected, and increased primary hepatocyte apoA-I production by 3-fold.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	98-105	apolipoprotein A-I	Mus musculus	192-198
20102334-11	2010	These results indicate that ERK phosphorylation plays a role in regulating hepatic apoA-I expression and suggest that the anti-atherogenic mechanism of action for myriocin may be linked to this pathway.	thermozymocidin	163-171	apolipoprotein A-I	Mus musculus	83-89
20212278-4	2010	METHODS AND RESULTS: Cholesterol efflux from wild-type, ABCA1(-/-), SR-BI(-/-), and ABCG1(-/-) adipocytes to apolipoprotein A-I (apoA-I) and HDL3 were measured in vitro.	Cholesterol	21-32	apolipoprotein A-I	Mus musculus	109-127
20212278-4	2010	METHODS AND RESULTS: Cholesterol efflux from wild-type, ABCA1(-/-), SR-BI(-/-), and ABCG1(-/-) adipocytes to apolipoprotein A-I (apoA-I) and HDL3 were measured in vitro.	Cholesterol	21-32	apolipoprotein A-I	Mus musculus	129-135
20212278-8	2010	Cholesterol efflux to apoA-I and HDL3 was impaired in ABCA1(-/-) and SR-BI(-/-) adipocytes, respectively, with no effect observed in ABCG1(-/-) adipocytes.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	22-28
20212278-9	2010	Intraperitoneal injection of labeled 3T3L1 adipocytes resulted in increased HDL-associated (3)H-cholesterol in apoA-I transgenic mice but reduced levels in apoA-I(-/-) animals.	Cholesterol	96-107	apolipoprotein A-I	Mus musculus	111-117
20208418-0	2010	D-4F, an apolipoprotein A-I mimetic peptide, promotes cholesterol efflux from macrophages via ATP-binding cassette transporter A1.	Cholesterol	54-65	apolipoprotein A-I	Mus musculus	9-27
19679305-7	2010	This inhibitory effect was related to mast cell-dependent proteolytic degradation of apoA-I, apoA-IV, and apoE, i.e., the HDL-associated apolipoproteins that are efficient inducers of cholesterol efflux.	Cholesterol	184-195	apolipoprotein A-I	Mus musculus	85-91
21088444-0	2010	Aspirin increases apolipoprotein-A-I-mediated cholesterol efflux via enhancing expression of ATP-binding cassette transporter A1.	Aspirin	0-7	apolipoprotein A-I	Mus musculus	18-36
21088444-0	2010	Aspirin increases apolipoprotein-A-I-mediated cholesterol efflux via enhancing expression of ATP-binding cassette transporter A1.	Cholesterol	46-57	apolipoprotein A-I	Mus musculus	18-36
21088444-5	2010	RESULTS: 0.5 mmol/l aspirin increased apoA-I-mediated cholesterol efflux and increased the expression of ABCA1.	Aspirin	20-27	apolipoprotein A-I	Mus musculus	38-44
21088444-5	2010	RESULTS: 0.5 mmol/l aspirin increased apoA-I-mediated cholesterol efflux and increased the expression of ABCA1.	Cholesterol	54-65	apolipoprotein A-I	Mus musculus	38-44
21088444-7	2010	In cells transfected with a specific peroxisome proliferator-activated receptor (PPAR)-alpha small interfering RNA, the induction of ABCA1 expression and apoA-I-mediated 3H-cholesterol efflux by aspirin were substantially suppressed.	Tritium	170-172	apolipoprotein A-I	Mus musculus	154-160
21088444-7	2010	In cells transfected with a specific peroxisome proliferator-activated receptor (PPAR)-alpha small interfering RNA, the induction of ABCA1 expression and apoA-I-mediated 3H-cholesterol efflux by aspirin were substantially suppressed.	Cholesterol	173-184	apolipoprotein A-I	Mus musculus	154-160
21088444-7	2010	In cells transfected with a specific peroxisome proliferator-activated receptor (PPAR)-alpha small interfering RNA, the induction of ABCA1 expression and apoA-I-mediated 3H-cholesterol efflux by aspirin were substantially suppressed.	Aspirin	195-202	apolipoprotein A-I	Mus musculus	154-160
21088444-8	2010	CONCLUSIONS: The data demonstrate that low-dose aspirin increases ABCA1 expression via a PPAR-alpha-dependent mechanism and increases apoA-I-mediated cholesterol efflux.	Aspirin	48-55	apolipoprotein A-I	Mus musculus	134-140
21088444-8	2010	CONCLUSIONS: The data demonstrate that low-dose aspirin increases ABCA1 expression via a PPAR-alpha-dependent mechanism and increases apoA-I-mediated cholesterol efflux.	Cholesterol	150-161	apolipoprotein A-I	Mus musculus	134-140
19729076-8	2009	Expression of hepatic mRNA of the sterol-related genes reflected the cellular cholesterol increase, such as decrease in SREBP2 and HMG-CoA reductase and increase in apoA-I, apoE, and ABCG1.	Sterols	34-40	apolipoprotein A-I	Mus musculus	165-171
19729076-8	2009	Expression of hepatic mRNA of the sterol-related genes reflected the cellular cholesterol increase, such as decrease in SREBP2 and HMG-CoA reductase and increase in apoA-I, apoE, and ABCG1.	Cholesterol	78-89	apolipoprotein A-I	Mus musculus	165-171
20193280-1	2009	OBJECTIVE: To determine the anti-inflammatory functions of different cysteine mutants of apolipoprotein A-I recombinant HDLs.	Cysteine	69-77	apolipoprotein A-I	Mus musculus	89-107
19661486-0	2009	Macrophage reverse cholesterol transport in mice expressing ApoA-I Milano.	Cholesterol	19-30	apolipoprotein A-I	Mus musculus	60-66
19661486-4	2009	Analysis of the individual components of the RCT pathway demonstrated that the apoA-I(M)-expressing mice promoted ATP-binding cassette transporter A1 (ABCA1)-mediated cholesterol efflux as efficiently as WT apoA-I but that apoA-I(M) had a reduced ability to promote cholesterol esterification via lecithin cholesterol-acyltransferase (LCAT).	Cholesterol	167-178	apolipoprotein A-I	Mus musculus	79-85
19661486-4	2009	Analysis of the individual components of the RCT pathway demonstrated that the apoA-I(M)-expressing mice promoted ATP-binding cassette transporter A1 (ABCA1)-mediated cholesterol efflux as efficiently as WT apoA-I but that apoA-I(M) had a reduced ability to promote cholesterol esterification via lecithin cholesterol-acyltransferase (LCAT).	Cholesterol	266-277	apolipoprotein A-I	Mus musculus	79-85
19661486-5	2009	This resulted in reduced cholesteryl ester (CE) and increased free cholesterol (FC) levels in the plasma of mice expressing apoA-I(M) compared to WT apoA-I.	Cholesterol Esters	25-42	apolipoprotein A-I	Mus musculus	124-130
19661486-5	2009	This resulted in reduced cholesteryl ester (CE) and increased free cholesterol (FC) levels in the plasma of mice expressing apoA-I(M) compared to WT apoA-I.	Fc(alpha) receptor	80-82	apolipoprotein A-I	Mus musculus	124-130
19884767-3	2009	By comparing control with EPS-fed mice, we found that at least six proteins were significantly altered in ob/ob mice, including Apo A-I, IV, C-III, E, retinol-binding protein 4, and transferrin, and their levels were interestingly normalized after EPS treatment.	eps	26-29	apolipoprotein A-I	Mus musculus	128-149
19433476-0	2009	An apoA-I mimetic peptide containing a proline residue has greater in vivo HDL binding and anti-inflammatory ability than the 4F peptide.	Proline	39-46	apolipoprotein A-I	Mus musculus	3-9
19433476-1	2009	Modifying apolipoprotein (apo) A-I mimetic peptides to include a proline-punctuated alpha-helical repeat increases their anti-inflammatory properties as well as allows better mimicry of full-length apoA-I function.	Proline	65-72	apolipoprotein A-I	Mus musculus	198-204
19377069-4	2009	METHODS AND RESULTS: [3H]-Cholesterol- and [3H]-methylcholine chloride-labelled murine macrophages treated with EP 80317 showed a significant increase in cholesterol and phospholipid efflux to both apolipoprotein A-I and high-density lipoprotein in a CD36-dependent manner.	Tritium	22-24	apolipoprotein A-I	Mus musculus	198-216
19377069-4	2009	METHODS AND RESULTS: [3H]-Cholesterol- and [3H]-methylcholine chloride-labelled murine macrophages treated with EP 80317 showed a significant increase in cholesterol and phospholipid efflux to both apolipoprotein A-I and high-density lipoprotein in a CD36-dependent manner.	methylcholine chloride	48-70	apolipoprotein A-I	Mus musculus	198-216
19729862-7	2009	As the dietary ratio of n-6/n-3 fatty acids increased, so did mRNA levels of hepatic apoA-I, scavenger receptor B class-1 (SR-B1), LCAT, ATP binding cassette transporter A1 (ABCA1), ABCG1 and liver X receptor alpha (LXRalpha).	n-6	24-27	apolipoprotein A-I	Mus musculus	85-91
19729862-7	2009	As the dietary ratio of n-6/n-3 fatty acids increased, so did mRNA levels of hepatic apoA-I, scavenger receptor B class-1 (SR-B1), LCAT, ATP binding cassette transporter A1 (ABCA1), ABCG1 and liver X receptor alpha (LXRalpha).	Fatty Acids, Omega-3	28-43	apolipoprotein A-I	Mus musculus	85-91
19571140-4	2009	Chronic activation of the heterologous Ap oa(1) by its natural ligand evoked antidepressant-like behaviors, accompanied by enhanced phosphorylation of cAMP response element-binding protein and transcription of VEGF in hippocampal dentate gyrus (DG) neurons.	Cyclic AMP	151-155	apolipoprotein A-I	Mus musculus	39-47
19286630-6	2009	Both LN enlargement and cellular cholesterol expansion were "prevented" when diet-fed DKO mice were treated with helper dependent adenovirus expressing apoA-I.	Cholesterol	33-44	apolipoprotein A-I	Mus musculus	152-158
19286630-8	2009	CONCLUSIONS: ApoA-I prevented cholesterol-associated lymphocyte activation and proliferation in peripheral LN of diet-fed DKO mice.	Cholesterol	30-41	apolipoprotein A-I	Mus musculus	13-19
19215022-8	2009	Folate-deficient placentae had decreased ApoA-I expression, and there was a trend toward a negative correlation between ApoA-I expression with maternal homocysteine concentrations.	Folic Acid	0-6	apolipoprotein A-I	Mus musculus	41-47
19215022-8	2009	Folate-deficient placentae had decreased ApoA-I expression, and there was a trend toward a negative correlation between ApoA-I expression with maternal homocysteine concentrations.	Folic Acid	0-6	apolipoprotein A-I	Mus musculus	120-126
19215022-8	2009	Folate-deficient placentae had decreased ApoA-I expression, and there was a trend toward a negative correlation between ApoA-I expression with maternal homocysteine concentrations.	Homocysteine	152-164	apolipoprotein A-I	Mus musculus	120-126
19638715-2	2009	V156E of apoA-I (apoA-Ioita) shows unique structural and functional properties and more potent antioxidant activity against copper-mediated low-density lipoprotein (LDL) oxidation in vitro.	Copper	124-130	apolipoprotein A-I	Mus musculus	9-15
19638715-2	2009	V156E of apoA-I (apoA-Ioita) shows unique structural and functional properties and more potent antioxidant activity against copper-mediated low-density lipoprotein (LDL) oxidation in vitro.	Copper	124-130	apolipoprotein A-I	Mus musculus	17-27
20559986-5	2009	Clenbuterol treatment in MLP(-/-) mice was associated with significant changes in the following circulating factors: tissue inhibitor of metalloproteinase-type 1, leukemia inhibitory factor 1, C-reactive protein, apolipoprotein A1, fibroblast growth factor 2, serum glutamic oxaloacetic transaminase, macrophage-derived chemokine, and monocyte chemoattractant protein-3.	Clenbuterol	0-11	apolipoprotein A-I	Mus musculus	213-230
19138167-1	2009	Besides functioning as the plasma transporter of retinol and thyroxine, TTR (transthyretin) is a protease, cleaving apoA-I (apolipoprotein A-I) after a phenylalanine residue.	Vitamin A	49-56	apolipoprotein A-I	Mus musculus	116-122
19138167-1	2009	Besides functioning as the plasma transporter of retinol and thyroxine, TTR (transthyretin) is a protease, cleaving apoA-I (apolipoprotein A-I) after a phenylalanine residue.	Vitamin A	49-56	apolipoprotein A-I	Mus musculus	124-142
19138167-1	2009	Besides functioning as the plasma transporter of retinol and thyroxine, TTR (transthyretin) is a protease, cleaving apoA-I (apolipoprotein A-I) after a phenylalanine residue.	Thyroxine	61-70	apolipoprotein A-I	Mus musculus	116-122
19138167-1	2009	Besides functioning as the plasma transporter of retinol and thyroxine, TTR (transthyretin) is a protease, cleaving apoA-I (apolipoprotein A-I) after a phenylalanine residue.	Thyroxine	61-70	apolipoprotein A-I	Mus musculus	124-142
19138167-1	2009	Besides functioning as the plasma transporter of retinol and thyroxine, TTR (transthyretin) is a protease, cleaving apoA-I (apolipoprotein A-I) after a phenylalanine residue.	Phenylalanine	152-165	apolipoprotein A-I	Mus musculus	116-122
19138167-1	2009	Besides functioning as the plasma transporter of retinol and thyroxine, TTR (transthyretin) is a protease, cleaving apoA-I (apolipoprotein A-I) after a phenylalanine residue.	Phenylalanine	152-165	apolipoprotein A-I	Mus musculus	124-142
19138167-3	2009	By using both P-diverse libraries and a library of phosphonate inhibitors, a TTR preference for a lysine residue in P1 was determined, suggesting that TTR might have a dual specificity and that, in addition to apoA-I, other TTR substrates might exist.	Lysine	98-104	apolipoprotein A-I	Mus musculus	210-216
19150509-6	2009	Analysis of the hepatic expression of genes involved in HDL metabolism showed that PCN decreased expression of genes involved in HDL synthesis (Abca1, Apoa1), maturation (Lcat, Pltp) and clearance (Sr-b1).	PREGNENOLONE CARBONITRILE	83-86	apolipoprotein A-I	Mus musculus	151-156
19056557-5	2009	RESULTS: A substantial efflux of alpha- and gamma-tocopherol, but not of retinyl esters, was induced by the presence of apolipoprotein A-I at the basolateral side of Caco-2 monolayers.	alpha- and gamma-tocopherol	33-60	apolipoprotein A-I	Mus musculus	120-138
20084185-1	2009	Anti-atherogenic effects of high density lipoprotein (HDL) and its major protein component apolipoprotein A-I (apoA-I) are principally thought to be due to their ability to mediate reverse cholesterol transport.	Cholesterol	189-200	apolipoprotein A-I	Mus musculus	91-109
20084185-1	2009	Anti-atherogenic effects of high density lipoprotein (HDL) and its major protein component apolipoprotein A-I (apoA-I) are principally thought to be due to their ability to mediate reverse cholesterol transport.	Cholesterol	189-200	apolipoprotein A-I	Mus musculus	111-117
19075690-5	2008	Mice fed with TO901317 for six days showed a downregulation of apoM and apoAI in the liver to 40 % and 60 % respectively and an upregulation of Cyp7A1 to 280 %.	T0901317	14-22	apolipoprotein A-I	Mus musculus	72-77
18789348-8	2008	Apolipoprotein A-I (apoA-I) contents of hepatic lipoprotein-rich and microsomal fractions of CD-treated mice are higher than controls.	Chlordecone	93-95	apolipoprotein A-I	Mus musculus	0-18
18789348-8	2008	Apolipoprotein A-I (apoA-I) contents of hepatic lipoprotein-rich and microsomal fractions of CD-treated mice are higher than controls.	Chlordecone	93-95	apolipoprotein A-I	Mus musculus	20-26
18789348-10	2008	At 14 days after 15 mg CD/kg apoA-I and apoB-100 proteins but not CYP3A11 protein in hepatic microsomes are similar to controls.	Chlordecone	23-25	apolipoprotein A-I	Mus musculus	29-35
18793613-2	2008	While acceptors such as high-density lipoproteins (HDL) and apolipoproteins A-I (apoA-I) and J have been found in male and female reproductive tracts, transporters that mediate cholesterol efflux from plasma membranes of spermatozoa to such acceptors have not yet been defined.	Cholesterol	177-188	apolipoprotein A-I	Mus musculus	81-87
18793613-5	2008	Moreover, we show that ABCA1, ABCA7, and ABCG1 antibodies decrease cholesterol efflux from spermatozoa to lipid acceptors apoA-I and albumin and inhibit in vitro fertilization.	Cholesterol	67-78	apolipoprotein A-I	Mus musculus	122-128
18775511-7	2008	A protein lacking its best lipid-binding region (ApoA-I Delta 10) did not stimulate any changes in the lin(-)BMCs indicating that ApoA-I may mediate its effects by regulating cholesterol efflux.	Cholesterol	175-186	apolipoprotein A-I	Mus musculus	130-136
18622028-0	2008	Enhancing apolipoprotein A-I-dependent cholesterol efflux elevates cholesterol export from macrophages in vivo.	Cholesterol	39-50	apolipoprotein A-I	Mus musculus	10-28
18622028-0	2008	Enhancing apolipoprotein A-I-dependent cholesterol efflux elevates cholesterol export from macrophages in vivo.	Cholesterol	67-78	apolipoprotein A-I	Mus musculus	10-28
18622028-7	2008	We conclude that pathways of cholesterol efflux using apoA-I as an acceptor make a predominant contribution to cholesterol export from macrophages in vivo.	Cholesterol	29-40	apolipoprotein A-I	Mus musculus	54-60
18622028-7	2008	We conclude that pathways of cholesterol efflux using apoA-I as an acceptor make a predominant contribution to cholesterol export from macrophages in vivo.	Cholesterol	111-122	apolipoprotein A-I	Mus musculus	54-60
18060750-1	2008	BACKGROUND AND AIM: Monounsaturated fatty acids in diets are beneficial for the plasma lipoprotein profile, but studies in cell culture point out that they may also be detrimental by inhibiting cholesterol efflux to apo AI.	Fatty Acids, Monounsaturated	20-47	apolipoprotein A-I	Mus musculus	216-222
18060750-1	2008	BACKGROUND AND AIM: Monounsaturated fatty acids in diets are beneficial for the plasma lipoprotein profile, but studies in cell culture point out that they may also be detrimental by inhibiting cholesterol efflux to apo AI.	Cholesterol	194-205	apolipoprotein A-I	Mus musculus	216-222
18852364-11	2008	CONCLUSIONS: The results suggest that high-density lipoprotein and apolipoprotein A-1 exert anti-inflammatory effects by promoting cholesterol efflux via ABCG1 and ABCA1 with consequent attenuation of signaling via Toll-like receptors.	Cholesterol	131-142	apolipoprotein A-I	Mus musculus	67-85
18703020-10	2008	In APN-KO mice, the expression of ABCA1, LXRalpha, PPARgamma, and apoA-I-mediated cholesterol efflux was decreased compared with wild-type mice.	Cholesterol	82-93	apolipoprotein A-I	Mus musculus	66-72
18540024-0	2008	Homocysteine modulates the effect of simvastatin on expression of ApoA-I and NF-kappaB/iNOS.	Homocysteine	0-12	apolipoprotein A-I	Mus musculus	66-72
18540024-0	2008	Homocysteine modulates the effect of simvastatin on expression of ApoA-I and NF-kappaB/iNOS.	Simvastatin	37-48	apolipoprotein A-I	Mus musculus	66-72
18540024-2	2008	In earlier work, we showed that homocysteine (Hcy) reduced synthesis of apolipoprotein A-I (ApoA-I).	Homocysteine	32-44	apolipoprotein A-I	Mus musculus	72-90
18540024-2	2008	In earlier work, we showed that homocysteine (Hcy) reduced synthesis of apolipoprotein A-I (ApoA-I).	Homocysteine	32-44	apolipoprotein A-I	Mus musculus	92-98
18540024-2	2008	In earlier work, we showed that homocysteine (Hcy) reduced synthesis of apolipoprotein A-I (ApoA-I).	Homocysteine	46-49	apolipoprotein A-I	Mus musculus	72-90
18540024-2	2008	In earlier work, we showed that homocysteine (Hcy) reduced synthesis of apolipoprotein A-I (ApoA-I).	Homocysteine	46-49	apolipoprotein A-I	Mus musculus	92-98
18540024-3	2008	Our goal in this study was to determine whether Hcy could interfere with the ability of simvastatin to increase ApoA-I synthesis or to modify statin-dependent regulation of inflammatory factors.	Homocysteine	48-51	apolipoprotein A-I	Mus musculus	112-118
18540024-3	2008	Our goal in this study was to determine whether Hcy could interfere with the ability of simvastatin to increase ApoA-I synthesis or to modify statin-dependent regulation of inflammatory factors.	Simvastatin	88-99	apolipoprotein A-I	Mus musculus	112-118
18519978-0	2008	Induction of paraoxonase 1 and apolipoprotein A-I gene expression by aspirin.	Aspirin	69-76	apolipoprotein A-I	Mus musculus	31-49
18519978-4	2008	Mice treated with aspirin also showed a 2-fold increase in plasma PON1 activity and a significant induction of both PON1 and apoA-I gene expression in the liver.	Aspirin	18-25	apolipoprotein A-I	Mus musculus	125-131
18823548-7	2008	We found that activation of Ap oa1 by octopamine enhanced glutamatergic synaptic transmission in the ACC by increasing presynaptic glutamate release in vitro.	Octopamine	38-48	apolipoprotein A-I	Mus musculus	28-34
18823548-7	2008	We found that activation of Ap oa1 by octopamine enhanced glutamatergic synaptic transmission in the ACC by increasing presynaptic glutamate release in vitro.	Glutamic Acid	58-67	apolipoprotein A-I	Mus musculus	28-34
18779669-6	2008	RESULTS: Significant reductions of staining scores and higher corneal epithelial thickness values were observed in both ApoA-1- and ApoA-1 + DP-treated groups compared with untreated dry-eye mouse and phosphate-buffered saline-treated group.	pantethine	141-143	apolipoprotein A-I	Mus musculus	132-138
18779669-6	2008	RESULTS: Significant reductions of staining scores and higher corneal epithelial thickness values were observed in both ApoA-1- and ApoA-1 + DP-treated groups compared with untreated dry-eye mouse and phosphate-buffered saline-treated group.	Phosphate-Buffered Saline	201-226	apolipoprotein A-I	Mus musculus	120-126
18779669-6	2008	RESULTS: Significant reductions of staining scores and higher corneal epithelial thickness values were observed in both ApoA-1- and ApoA-1 + DP-treated groups compared with untreated dry-eye mouse and phosphate-buffered saline-treated group.	Phosphate-Buffered Saline	201-226	apolipoprotein A-I	Mus musculus	132-138
18497309-6	2008	Expression of apoAI significantly increased cholesterol efflux in wild-type and apoE(-/-) macrophages.	Cholesterol	44-55	apolipoprotein A-I	Mus musculus	14-19
18497309-9	2008	Expression of apoAI in macrophages improves cholesterol trafficking in wild-type apoE-producing macrophages and causes upregulation of ABCA1 and ABCG1.	Cholesterol	44-55	apolipoprotein A-I	Mus musculus	14-19
18497309-10	2008	These novel observations set the stage for a cell therapy approach to atherosclerosis regression, exploiting the cooperation between apoE and apoAI to maximize cholesterol exit from the plaque.	Cholesterol	160-171	apolipoprotein A-I	Mus musculus	142-147
17643522-4	2008	Cholesterol efflux rate was determined through measuring release of radioactivity from (3)H-cholesterol prelabeled cells into medium containing apolipoprotein A-I (apoA-I).	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	144-162
17643522-4	2008	Cholesterol efflux rate was determined through measuring release of radioactivity from (3)H-cholesterol prelabeled cells into medium containing apolipoprotein A-I (apoA-I).	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	164-170
17643522-5	2008	RESULTS: Low concentrations of oxLDL caused a significant increase in apoA-I-mediated cholesterol efflux via enhancement of ATP binding cassette transporter A1 (ABCA1) pathway, whereas higher concentrations were incapable.	Cholesterol	86-97	apolipoprotein A-I	Mus musculus	70-76
17643522-6	2008	In adipocytes preincubated with 25 microg/mL oxLDL for 24 h, 22(R)-hydroxycholesterol could increase ABCA1 and LXR* mRNA levels and apoA-I-mediated cholesterol efflux.	22-hydroxycholesterol	61-85	apolipoprotein A-I	Mus musculus	132-138
17643522-6	2008	In adipocytes preincubated with 25 microg/mL oxLDL for 24 h, 22(R)-hydroxycholesterol could increase ABCA1 and LXR* mRNA levels and apoA-I-mediated cholesterol efflux.	Cholesterol	74-85	apolipoprotein A-I	Mus musculus	132-138
18501625-0	2008	Apolipoprotein A-I diminishes acute lung injury and sepsis in mice induced by lipoteichoic acid.	lipoteichoic acid	78-95	apolipoprotein A-I	Mus musculus	0-18
18501625-4	2008	We found that ApoA-I could attenuate LTA-induced acute lung injury and inflammation and significantly inhibit LTA-induced IL-1beta and TNF-alpha accumulation in the serum (P&lt;0.01 and P&lt;0.05, respectively), as well as in bronchoalveolar lavage (BAL) fluid (P&lt;0.01 and P&lt;0.05, respectively).	lipoteichoic acid	37-40	apolipoprotein A-I	Mus musculus	14-20
18418863-6	2008	Moreover, the apo-AI mRNA levels were increased in a BPA dose-dependent manner in 3- and 7-week-old female mice.	bisphenol A	53-56	apolipoprotein A-I	Mus musculus	14-20
18418863-8	2008	Our study, which is based on proteome analyses, suggests that apo-AI, DPPIII, and VAT represent protein biomarkers for BPA and provide useful mechanistic clues for BPA-induced endocrine disruption.	bisphenol A	119-122	apolipoprotein A-I	Mus musculus	62-68
18323574-11	2008	In addition, apoA-I mimetic peptides may increase reverse cholesterol transport through both ABCA1 as well as ABCG1 pathways.	Cholesterol	58-69	apolipoprotein A-I	Mus musculus	13-19
18498712-3	2008	Peroxisome proliferator-activated receptor alpha (PPARalpha) can increase expression of liver X receptor alpha (LXRalpha) in macrophages and thereby promote the expression of ABCA1, which, in turn, mediates cholesterol efflux to apoA1.	Cholesterol	207-218	apolipoprotein A-I	Mus musculus	229-234
18056684-3	2008	ApoA-I mimetic peptides have been proposed to stimulate the formation of prebeta1 HDL and increase reverse cholesterol transport in apoE-null mice.	Cholesterol	107-118	apolipoprotein A-I	Mus musculus	0-6
18224302-0	2008	Simvastatin reverses the hypertension of heterozygous mice lacking cystathionine beta-synthase and apolipoprotein A-I.	Simvastatin	0-11	apolipoprotein A-I	Mus musculus	99-117
18224302-9	2008	In conclusion, the results of this study demonstrate that the use of simvastatin can improve blood pressure control in mice with elevated homocysteinemia and low levels of apoA-I, and this effect is mediated by mechanisms independent of plasma lipids and related to nitric oxide levels.	Simvastatin	69-80	apolipoprotein A-I	Mus musculus	172-178
18287885-5	2008	Trimeric apoA-I was biologically active in terms of promoting cholesterol efflux, stimulation of lecithin cholesterol acyltransferase-mediated cholesterol esterification, and reducing progression of atherosclerosis in cholesterol-fed low-density lipoprotein receptor-deficient mice.	Cholesterol	62-73	apolipoprotein A-I	Mus musculus	9-15
18287885-5	2008	Trimeric apoA-I was biologically active in terms of promoting cholesterol efflux, stimulation of lecithin cholesterol acyltransferase-mediated cholesterol esterification, and reducing progression of atherosclerosis in cholesterol-fed low-density lipoprotein receptor-deficient mice.	Cholesterol	106-117	apolipoprotein A-I	Mus musculus	9-15
18246469-2	2008	To this point, five discrete categories of apoA-I mutants have been characterized that may affect the interactions of apoA-I with ATP-binding cassette superfamily A, member 1 (ABCA1) or lecithin:cholesterol acyl transferase (LCAT) or may influence the plasma phospholipid transfer protein activity or may cause various forms of dyslipidemia.	Phospholipids	259-271	apolipoprotein A-I	Mus musculus	43-49
18246469-2	2008	To this point, five discrete categories of apoA-I mutants have been characterized that may affect the interactions of apoA-I with ATP-binding cassette superfamily A, member 1 (ABCA1) or lecithin:cholesterol acyl transferase (LCAT) or may influence the plasma phospholipid transfer protein activity or may cause various forms of dyslipidemia.	Phospholipids	259-271	apolipoprotein A-I	Mus musculus	118-124
18209963-6	2008	RESULTS: The mean reduction in DAI scores from day 7 to day 14 for anti-TNFalpha group, simvastatin and atorvastatin group were 74 %, 76 % and 64 %, respectively as compared to 41 % reduction in vehicle and anti-apolipoprotein A-I antibody-treated groups.	Atorvastatin	104-116	apolipoprotein A-I	Mus musculus	212-230
17689540-8	2007	Betaine did not affect staining of nitrotyrosine but increased ApoA-I staining.	Betaine	0-7	apolipoprotein A-I	Mus musculus	63-69
17689540-9	2007	A significant negative correlation was observed between plasma homocysteine and liver ApoA-I.	Homocysteine	63-75	apolipoprotein A-I	Mus musculus	86-92
17689540-11	2007	Betaine has a lipotropic effect, which is associated with a reduction in homocysteine, an increase in ApoA-I and an amelioration of the atherogenic risk profile.	Betaine	0-7	apolipoprotein A-I	Mus musculus	102-108
17693625-0	2007	ApoA-I cleaved by transthyretin has reduced ability to promote cholesterol efflux and increased amyloidogenicity.	Cholesterol	63-74	apolipoprotein A-I	Mus musculus	0-6
17693625-9	2007	Our results show that apoA-I cleavage by TTR may affect HDL biology and the development of atherosclerosis by reducing cholesterol efflux and increasing the apoA-I amyloidogenic potential.	Cholesterol	119-130	apolipoprotein A-I	Mus musculus	22-28
17824618-9	2007	Plasma of carrageenan-treated mice was analyzed by ELISA for the levels of haptoglobin and ApoA-I, and used to isolate HDL for MS analysis.	Carrageenan	10-21	apolipoprotein A-I	Mus musculus	91-97
17711302-0	2007	LCAT can rescue the abnormal phenotype produced by the natural ApoA-I mutations (Leu141Arg)Pisa and (Leu159Arg)FIN.	leu141arg	81-90	apolipoprotein A-I	Mus musculus	63-69
17711302-1	2007	To explain the etiology and find a mode of therapy of genetically determined low levels of high-density lipoprotein (HDL), we have generated recombinant adenoviruses expressing apolipoprotein A-I (apoA-I)(Leu141Arg)Pisa and apoA-I(Leu159Arg)FIN and studied their properties in vitro and in vivo.	leu141arg	205-214	apolipoprotein A-I	Mus musculus	177-195
17711302-1	2007	To explain the etiology and find a mode of therapy of genetically determined low levels of high-density lipoprotein (HDL), we have generated recombinant adenoviruses expressing apolipoprotein A-I (apoA-I)(Leu141Arg)Pisa and apoA-I(Leu159Arg)FIN and studied their properties in vitro and in vivo.	leu141arg	205-214	apolipoprotein A-I	Mus musculus	197-203
17711302-3	2007	Adenovirus-mediated gene transfer of either of the two mutants in apoA-I-deficient (apoA-I-/-) mice resulted in greatly decreased total plasma cholesterol, apoA-I, and HDL cholesterol levels.	Cholesterol	143-154	apolipoprotein A-I	Mus musculus	66-72
17711302-3	2007	Adenovirus-mediated gene transfer of either of the two mutants in apoA-I-deficient (apoA-I-/-) mice resulted in greatly decreased total plasma cholesterol, apoA-I, and HDL cholesterol levels.	Cholesterol	143-154	apolipoprotein A-I	Mus musculus	84-90
17711302-3	2007	Adenovirus-mediated gene transfer of either of the two mutants in apoA-I-deficient (apoA-I-/-) mice resulted in greatly decreased total plasma cholesterol, apoA-I, and HDL cholesterol levels.	Cholesterol	143-154	apolipoprotein A-I	Mus musculus	84-90
17711302-3	2007	Adenovirus-mediated gene transfer of either of the two mutants in apoA-I-deficient (apoA-I-/-) mice resulted in greatly decreased total plasma cholesterol, apoA-I, and HDL cholesterol levels.	Cholesterol	172-183	apolipoprotein A-I	Mus musculus	66-72
17711302-3	2007	Adenovirus-mediated gene transfer of either of the two mutants in apoA-I-deficient (apoA-I-/-) mice resulted in greatly decreased total plasma cholesterol, apoA-I, and HDL cholesterol levels.	Cholesterol	172-183	apolipoprotein A-I	Mus musculus	84-90
17711302-3	2007	Adenovirus-mediated gene transfer of either of the two mutants in apoA-I-deficient (apoA-I-/-) mice resulted in greatly decreased total plasma cholesterol, apoA-I, and HDL cholesterol levels.	Cholesterol	172-183	apolipoprotein A-I	Mus musculus	84-90
17711302-6	2007	The study establishes that apoA-I(Leu141Arg)Pisa and apoA-I(Leu159Arg)FIN inhibit an early step in the biogenesis of HDL due to inefficient esterification of the cholesterol of the prebeta1-HDL particles by the endogenous LCAT.	leu141arg	34-43	apolipoprotein A-I	Mus musculus	27-33
17711302-6	2007	The study establishes that apoA-I(Leu141Arg)Pisa and apoA-I(Leu159Arg)FIN inhibit an early step in the biogenesis of HDL due to inefficient esterification of the cholesterol of the prebeta1-HDL particles by the endogenous LCAT.	Cholesterol	162-173	apolipoprotein A-I	Mus musculus	27-33
17711302-6	2007	The study establishes that apoA-I(Leu141Arg)Pisa and apoA-I(Leu159Arg)FIN inhibit an early step in the biogenesis of HDL due to inefficient esterification of the cholesterol of the prebeta1-HDL particles by the endogenous LCAT.	Cholesterol	162-173	apolipoprotein A-I	Mus musculus	53-59
17639303-0	2007	Apolipoprotein A-I stimulates AMP-activated protein kinase and improves glucose metabolism.	Glucose	72-79	apolipoprotein A-I	Mus musculus	0-18
17639303-6	2007	RESULTS: APOA-I was able to stimulate the phosphorylation of AMPK and ACC, and elevated glucose uptake in C2C12 myocytes.	Glucose	88-95	apolipoprotein A-I	Mus musculus	9-15
17639303-10	2007	In addition, the Apoa-I (-/-) mice had increased fat content and compromised glucose tolerance.	Glucose	77-84	apolipoprotein A-I	Mus musculus	17-23
17582142-9	2007	In vivo absorption of [(3)H]alpha-tocopherol by mice after poloxamer 407 injection to inhibit lipoprotein lipase revealed that vitamin E was associated with triglyceride-rich lipoproteins and small HDLs containing apoB-48 and apoA-I.	Vitamin E	127-136	apolipoprotein A-I	Mus musculus	226-232
17665897-3	2007	Despite its selectivity and modest potency, the compound can induce APO-AI-dependent cholesterol efflux from macrophages with full efficacy.	Cholesterol	85-96	apolipoprotein A-I	Mus musculus	68-74
17615369-1	2007	Apolipoprotein A-I (apoA-I), the major protein constituent within high-density lipoprotein (HDL), has been associated with antiatherogenic protection by mechanisms that include reverse cholesterol transport and antiinflammatory functions.	Cholesterol	185-196	apolipoprotein A-I	Mus musculus	0-18
17615369-1	2007	Apolipoprotein A-I (apoA-I), the major protein constituent within high-density lipoprotein (HDL), has been associated with antiatherogenic protection by mechanisms that include reverse cholesterol transport and antiinflammatory functions.	Cholesterol	185-196	apolipoprotein A-I	Mus musculus	20-26
17615369-7	2007	Another consequence of the augmented levels of nitrated proteins was the induction of humoral responses documented by the increased circulating immunoglobulins that recognize nitrotyrosine in LA-apoA-I(-/-) as compared with the LA mice.	3-nitrotyrosine	175-188	apolipoprotein A-I	Mus musculus	195-201
17506726-5	2007	The total plasma cholesterol of mice expressing the apoA-I(R160L)Oslo, apoA-I(R149A) and apoA-I(R151C)Paris mutants was reduced by 78, 59 and 61% and the apoA-I levels were reduced by 68, 64 and 55% respectively, as compared with mice expressing the WT apoA-I.	Cholesterol	17-28	apolipoprotein A-I	Mus musculus	52-58
17553802-3	2007	Here we show that, whereas lipid efflux to apoA-I in Npc1-null macrophages is impaired, the lipidation of endogenously synthesized apoA-I by low density lipoprotein-derived cholesterol or de novo synthesized cholesterol or phospholipids in Npc1-null hepatocytes is significantly increased by about 1-, 3-, and 8-fold, respectively.	low density lipoprotein-derived cholesterol	141-184	apolipoprotein A-I	Mus musculus	131-137
17553802-3	2007	Here we show that, whereas lipid efflux to apoA-I in Npc1-null macrophages is impaired, the lipidation of endogenously synthesized apoA-I by low density lipoprotein-derived cholesterol or de novo synthesized cholesterol or phospholipids in Npc1-null hepatocytes is significantly increased by about 1-, 3-, and 8-fold, respectively.	Cholesterol	173-184	apolipoprotein A-I	Mus musculus	131-137
17553802-3	2007	Here we show that, whereas lipid efflux to apoA-I in Npc1-null macrophages is impaired, the lipidation of endogenously synthesized apoA-I by low density lipoprotein-derived cholesterol or de novo synthesized cholesterol or phospholipids in Npc1-null hepatocytes is significantly increased by about 1-, 3-, and 8-fold, respectively.	Phospholipids	223-236	apolipoprotein A-I	Mus musculus	131-137
17541020-1	2007	BACKGROUND: ATP-binding cassette transporter A1 (ABCA1) is a key mediator of cholesterol efflux to apoA-I in cholesterol loaded macrophages, a first step of reverse cholesterol transport (RCT) in vivo.	Cholesterol	77-88	apolipoprotein A-I	Mus musculus	99-105
17541020-1	2007	BACKGROUND: ATP-binding cassette transporter A1 (ABCA1) is a key mediator of cholesterol efflux to apoA-I in cholesterol loaded macrophages, a first step of reverse cholesterol transport (RCT) in vivo.	Cholesterol	109-120	apolipoprotein A-I	Mus musculus	99-105
17541020-1	2007	BACKGROUND: ATP-binding cassette transporter A1 (ABCA1) is a key mediator of cholesterol efflux to apoA-I in cholesterol loaded macrophages, a first step of reverse cholesterol transport (RCT) in vivo.	Cholesterol	109-120	apolipoprotein A-I	Mus musculus	99-105
17767055-5	2007	Cholesterol efflux mediated by apolipoprotein A-I (apoA-I) was determined using liquid scintillator.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	31-49
17767055-5	2007	Cholesterol efflux mediated by apolipoprotein A-I (apoA-I) was determined using liquid scintillator.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	51-57
17767055-7	2007	In adipocytes preincubated with 25 microg/mL ox-LDL for 24 hours, 22(R)-hydroxycholesterol could increase ABCA1 and LXRalpha mRNA and apoA-I-mediated cholesterol efflux, but had no effect on the SR-BI mRNA expression.	22-hydroxycholesterol	66-90	apolipoprotein A-I	Mus musculus	134-140
17767055-7	2007	In adipocytes preincubated with 25 microg/mL ox-LDL for 24 hours, 22(R)-hydroxycholesterol could increase ABCA1 and LXRalpha mRNA and apoA-I-mediated cholesterol efflux, but had no effect on the SR-BI mRNA expression.	Cholesterol	79-90	apolipoprotein A-I	Mus musculus	134-140
19636841-2	2007	Lipid-free apoAI specifically binds to phospholipids, triggering HDL formation.	Phospholipids	39-52	apolipoprotein A-I	Mus musculus	11-16
17321001-6	2007	RESULTS: In both genotypes ethanol markedly reduced serum cholesterol, apolipoprotein A-I, phospholipid transfer protein activity and hepatic mRNA levels of fatty acid-binding proteins and fatty acid beta-oxidation enzymes.	Ethanol	27-34	apolipoprotein A-I	Mus musculus	71-89
16554055-6	2007	However, the apoA-I secreted by PLTP-KO hepatocytes contained less choline PL, differing also in phosphatidylcholine/sphingomyelin ratio and fatty acyl species composition when compared to apoA-I from WT hepatocytes.	Choline	67-74	apolipoprotein A-I	Mus musculus	13-19
16554055-6	2007	However, the apoA-I secreted by PLTP-KO hepatocytes contained less choline PL, differing also in phosphatidylcholine/sphingomyelin ratio and fatty acyl species composition when compared to apoA-I from WT hepatocytes.	Phosphatidylcholines	97-116	apolipoprotein A-I	Mus musculus	13-19
16554055-6	2007	However, the apoA-I secreted by PLTP-KO hepatocytes contained less choline PL, differing also in phosphatidylcholine/sphingomyelin ratio and fatty acyl species composition when compared to apoA-I from WT hepatocytes.	Sphingomyelins	117-130	apolipoprotein A-I	Mus musculus	13-19
16554055-7	2007	Furthermore, the PLTP-KO-derived PL-deficient apoA-I was less stable in the hepatocyte culture medium than that produced by WT cells.	Phospholipids	17-19	apolipoprotein A-I	Mus musculus	46-52
18020970-4	2007	Severe HHcy (plasma Hcy 210 micromol/L) accelerates spontaneous arthrosclerosis in the CBS(-/-)/apoE(-/-) mice, reduces the concentration of circulating HDL, apoA-I, and large HDL particles, inhibits HDL function, and enhances HDL-C clearance.	Homocysteine	8-11	apolipoprotein A-I	Mus musculus	158-164
18020970-5	2007	We have demonstrated further that Hcy (0.5-2 mmol/L) reduces apoA-I protein synthesis and secretion, but not RNA transcription in mouse primary hepatocytes.	Homocysteine	34-37	apolipoprotein A-I	Mus musculus	61-67
18020970-7	2007	These studies suggest that Hcy-induced HDL-C and apoA-I inhibition represent a novel mechanism by which Hcy induces atherosclerotic CVD.	Homocysteine	27-30	apolipoprotein A-I	Mus musculus	49-55
18020970-7	2007	These studies suggest that Hcy-induced HDL-C and apoA-I inhibition represent a novel mechanism by which Hcy induces atherosclerotic CVD.	Homocysteine	104-107	apolipoprotein A-I	Mus musculus	49-55
17071966-0	2007	Inflammation and skin cholesterol in LDLr-/-, apoA-I-/- mice: link between cholesterol homeostasis and self-tolerance?	Cholesterol	22-33	apolipoprotein A-I	Mus musculus	46-52
17071966-1	2007	Diet-fed low density lipoprotein receptor-deficient/apolipoprotein A-I-deficient (LDLr-/-, apoA-I-/-) mice accumulate a 10-fold greater mass of cholesterol in their skin despite a 1.5- to 2-fold lower plasma cholesterol concentration compared with diet-fed LDLr-/- mice.	Cholesterol	144-155	apolipoprotein A-I	Mus musculus	52-70
17071966-1	2007	Diet-fed low density lipoprotein receptor-deficient/apolipoprotein A-I-deficient (LDLr-/-, apoA-I-/-) mice accumulate a 10-fold greater mass of cholesterol in their skin despite a 1.5- to 2-fold lower plasma cholesterol concentration compared with diet-fed LDLr-/- mice.	Cholesterol	144-155	apolipoprotein A-I	Mus musculus	91-97
17071966-4	2007	After 4 weeks of diet, LDLr-/-, apoA-I-/- mice showed a significant increase in skin cholesterol mass compared with LDLr-/- mice.	Cholesterol	85-96	apolipoprotein A-I	Mus musculus	32-38
17071966-7	2007	In summary, the use of hypercholesterolemic LDLr-/-, apoA-I-/- mice may provide a useful tool to investigate the role that apoA-I plays in maintaining cholesterol homeostasis and its relationship to inflammation.	Cholesterol	28-39	apolipoprotein A-I	Mus musculus	123-129
17822335-2	2007	The increase in HDL-cholesterol concentration can be also due to an ethanol-enhanced synthesis and secretion of apolipoprotein A-I (apo A-I) from hepatocytes.	Cholesterol	20-31	apolipoprotein A-I	Mus musculus	112-130
17822335-2	2007	The increase in HDL-cholesterol concentration can be also due to an ethanol-enhanced synthesis and secretion of apolipoprotein A-I (apo A-I) from hepatocytes.	Cholesterol	20-31	apolipoprotein A-I	Mus musculus	132-139
17822335-2	2007	The increase in HDL-cholesterol concentration can be also due to an ethanol-enhanced synthesis and secretion of apolipoprotein A-I (apo A-I) from hepatocytes.	Ethanol	68-75	apolipoprotein A-I	Mus musculus	112-130
17822335-2	2007	The increase in HDL-cholesterol concentration can be also due to an ethanol-enhanced synthesis and secretion of apolipoprotein A-I (apo A-I) from hepatocytes.	Ethanol	68-75	apolipoprotein A-I	Mus musculus	132-139
17822335-3	2007	Therefore, the hypothesis that ethanol consumption affects the LPL and apo A-I gene (LPL and APOA1, respectively) expression was tested in male C57BL/6 mice drinking 5 % ethanol or water and fed a standard chow or high-fat (HF) diet for 4 weeks.	Ethanol	31-38	apolipoprotein A-I	Mus musculus	71-78
17822335-3	2007	Therefore, the hypothesis that ethanol consumption affects the LPL and apo A-I gene (LPL and APOA1, respectively) expression was tested in male C57BL/6 mice drinking 5 % ethanol or water and fed a standard chow or high-fat (HF) diet for 4 weeks.	Ethanol	31-38	apolipoprotein A-I	Mus musculus	93-98
18154121-0	2007	[Effect of apolipoprotein A-1 containing steroid hormones on DNA and protein biosynthesis in cells of ascitic hepatoma HA-1].	Steroids	41-57	apolipoprotein A-I	Mus musculus	11-29
18154121-2	2007	That was demonstrated for apolipoprotein A-1 complexes with dehydroepiandrosterone, dehydroepiandrosterone sulfate and tetrahydrocortisol.	Dehydroepiandrosterone	60-82	apolipoprotein A-I	Mus musculus	26-44
18154121-2	2007	That was demonstrated for apolipoprotein A-1 complexes with dehydroepiandrosterone, dehydroepiandrosterone sulfate and tetrahydrocortisol.	Dehydroepiandrosterone Sulfate	84-114	apolipoprotein A-I	Mus musculus	26-44
18154121-2	2007	That was demonstrated for apolipoprotein A-1 complexes with dehydroepiandrosterone, dehydroepiandrosterone sulfate and tetrahydrocortisol.	Tetrahydrocortisol	119-137	apolipoprotein A-I	Mus musculus	26-44
18154121-3	2007	Apolipoprotein A-1 complexes serve as a vehicle for steroids penetration into cells to influence protein biosynthesis.	Steroids	52-60	apolipoprotein A-I	Mus musculus	0-18
17082477-3	2006	Oxidative modification of the apolipoprotein A-I inhibits reverse cholesterol transport.	Cholesterol	66-77	apolipoprotein A-I	Mus musculus	30-48
16902247-2	2006	ABCA1 mediates the transport of cholesterol and phospholipids from cells to lipid-poor apolipoprotein A-I (apoA-I), whereas ABCG1 and ABCG4 mediate the transport of cholesterol from cells to lipidated lipoproteins.	Cholesterol	32-43	apolipoprotein A-I	Mus musculus	87-105
16902247-2	2006	ABCA1 mediates the transport of cholesterol and phospholipids from cells to lipid-poor apolipoprotein A-I (apoA-I), whereas ABCG1 and ABCG4 mediate the transport of cholesterol from cells to lipidated lipoproteins.	Cholesterol	32-43	apolipoprotein A-I	Mus musculus	107-113
16902247-2	2006	ABCA1 mediates the transport of cholesterol and phospholipids from cells to lipid-poor apolipoprotein A-I (apoA-I), whereas ABCG1 and ABCG4 mediate the transport of cholesterol from cells to lipidated lipoproteins.	Phospholipids	48-61	apolipoprotein A-I	Mus musculus	87-105
16902247-2	2006	ABCA1 mediates the transport of cholesterol and phospholipids from cells to lipid-poor apolipoprotein A-I (apoA-I), whereas ABCG1 and ABCG4 mediate the transport of cholesterol from cells to lipidated lipoproteins.	Phospholipids	48-61	apolipoprotein A-I	Mus musculus	107-113
16902247-4	2006	Here, we show that the lipidated particles generated by incubating cells overexpressing ABCA1 with apoA-I are efficient acceptors for cholesterol released from cells overexpressing either ABCG1 or ABCG4.	Cholesterol	134-145	apolipoprotein A-I	Mus musculus	99-105
16902247-6	2006	ABCA1 cells incubated with apoA-I generated two major populations of cholesterol- and phospholipid-rich lipoprotein particles that were converted by ABCG1 or ABCG4 cells to one major particle population that was highly enriched in cholesterol.	Cholesterol	69-80	apolipoprotein A-I	Mus musculus	27-33
16902247-6	2006	ABCA1 cells incubated with apoA-I generated two major populations of cholesterol- and phospholipid-rich lipoprotein particles that were converted by ABCG1 or ABCG4 cells to one major particle population that was highly enriched in cholesterol.	Cholesterol	231-242	apolipoprotein A-I	Mus musculus	27-33
17010811-8	2006	Apolipoprotein A-I Milano was more effective than wild-type apoA-I in promoting macrophage cholesterol efflux.	Cholesterol	91-102	apolipoprotein A-I	Mus musculus	0-18
17010811-8	2006	Apolipoprotein A-I Milano was more effective than wild-type apoA-I in promoting macrophage cholesterol efflux.	Cholesterol	91-102	apolipoprotein A-I	Mus musculus	60-66
16825483-6	2006	Cholesterol-efflux studies verify that LXRbeta can drive apoA1-dependent cholesterol mobilization from macrophages.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	57-62
16825483-6	2006	Cholesterol-efflux studies verify that LXRbeta can drive apoA1-dependent cholesterol mobilization from macrophages.	Cholesterol	73-84	apolipoprotein A-I	Mus musculus	57-62
16931800-5	2006	Moreover, Hcy (0.5 to 2 mmol/L) reduced the levels of apoA-I protein but not mRNA and inhibited apoA-1 protein synthesis in mouse primary hepatocytes.	Homocysteine	10-13	apolipoprotein A-I	Mus musculus	54-60
16931800-5	2006	Moreover, Hcy (0.5 to 2 mmol/L) reduced the levels of apoA-I protein but not mRNA and inhibited apoA-1 protein synthesis in mouse primary hepatocytes.	Homocysteine	10-13	apolipoprotein A-I	Mus musculus	96-102
16873395-7	2006	However, hydroxytyrosol administration decreased apolipoprotein A-I and increased total cholesterol, atherosclerotic lesion areas and circulating monocytes expressing Mac-1.	3,4-dihydroxyphenylethanol	9-23	apolipoprotein A-I	Mus musculus	49-67
16603689-12	2006	Cellular cholesterol efflux to apolipoprotein A-I was not significantly reduced in Cav-1(-/-) MPMs compared with wild-type MPMs.	Cholesterol	9-20	apolipoprotein A-I	Mus musculus	31-49
16832169-3	2006	Administration of D-4F to low-density lipoprotein receptor null mice fed a Western diet reduced the association of myeloperoxidase with apoA-I and reduced the 3-nitrotyrosine content of apoA-I.	3-nitrotyrosine	161-174	apolipoprotein A-I	Mus musculus	186-192
16832169-9	2006	SUMMARY: Peptides that sequester lipoprotein lipid hydroperoxides release a series of high-density lipoprotein-associated antioxidant enzymes such as paraoxonase from inhibition and protect apoA-I from oxidative damage that would impair cholesterol efflux.	Lipid Peroxides	45-65	apolipoprotein A-I	Mus musculus	190-196
16832169-9	2006	SUMMARY: Peptides that sequester lipoprotein lipid hydroperoxides release a series of high-density lipoprotein-associated antioxidant enzymes such as paraoxonase from inhibition and protect apoA-I from oxidative damage that would impair cholesterol efflux.	Cholesterol	237-248	apolipoprotein A-I	Mus musculus	190-196
16687660-6	2006	After cAMP treatment, which upregulated the expression of ABCA1, cholesterol efflux from PLTP-KO foam cells to apoA-I increased markedly and reached a level similar to that observed in cAMP-treated WT foam cells, restoring the decreased cholesterol efflux associated with PLTP deficiency.	Cyclic AMP	6-10	apolipoprotein A-I	Mus musculus	111-117
16687660-6	2006	After cAMP treatment, which upregulated the expression of ABCA1, cholesterol efflux from PLTP-KO foam cells to apoA-I increased markedly and reached a level similar to that observed in cAMP-treated WT foam cells, restoring the decreased cholesterol efflux associated with PLTP deficiency.	Cholesterol	65-76	apolipoprotein A-I	Mus musculus	111-117
16687660-6	2006	After cAMP treatment, which upregulated the expression of ABCA1, cholesterol efflux from PLTP-KO foam cells to apoA-I increased markedly and reached a level similar to that observed in cAMP-treated WT foam cells, restoring the decreased cholesterol efflux associated with PLTP deficiency.	Cyclic AMP	185-189	apolipoprotein A-I	Mus musculus	111-117
16687660-6	2006	After cAMP treatment, which upregulated the expression of ABCA1, cholesterol efflux from PLTP-KO foam cells to apoA-I increased markedly and reached a level similar to that observed in cAMP-treated WT foam cells, restoring the decreased cholesterol efflux associated with PLTP deficiency.	Cholesterol	237-248	apolipoprotein A-I	Mus musculus	111-117
16723084-6	2006	When given at daily doses of 0.25 and 1 g/kg for 4 d, bifendate increased serum TG levels (56%-79%), with concomitant elevations in apolipoprotein A-I and apolipoprotein B levels at 24 h after the last dosing.	bifendate	54-63	apolipoprotein A-I	Mus musculus	132-150
16497661-6	2006	When fed a high-fat Western-type (HFW) diet, Apoa1/c3/a4(-/-) mice showed a further decrease in HDLc concentration and a moderate increase in TC, essentially in non-HDL fraction.	Technetium	142-144	apolipoprotein A-I	Mus musculus	45-50
16497661-7	2006	The capacity of Apoa1/c3/a4(-/-) plasma to promote cholesterol efflux in vitro was decreased to 75% (P &lt; 0.001), and LCAT activity was decreased by 38% (P &lt; 0.01).	Cholesterol	51-62	apolipoprotein A-I	Mus musculus	16-21
16456089-5	2006	Peritoneal macrophages isolated from the ABCA1 BAC --&gt; LDLr-/- chimeras exhibited a 60% (P=0.0006) increase in cholesterol efflux to apolipoprotein AI.	Cholesterol	114-125	apolipoprotein A-I	Mus musculus	136-153
16543947-2	2006	The ATP-binding cassette, subfamily A, member 1 (ABCA1) mediates the rate-controlling step in HDL particle formation, the assembly of free cholesterol and phospholipids with apoA-I.	Cholesterol	139-150	apolipoprotein A-I	Mus musculus	174-180
16543947-2	2006	The ATP-binding cassette, subfamily A, member 1 (ABCA1) mediates the rate-controlling step in HDL particle formation, the assembly of free cholesterol and phospholipids with apoA-I.	Phospholipids	155-168	apolipoprotein A-I	Mus musculus	174-180
16418537-1	2006	The nascent HDL created by ABCA1-mediated efflux of cellular phospholipid (PL) and free (unesterified) cholesterol (FC) to apolipoprotein A-I (apoA-I) has not been defined.	Phospholipids	61-73	apolipoprotein A-I	Mus musculus	143-149
16418537-1	2006	The nascent HDL created by ABCA1-mediated efflux of cellular phospholipid (PL) and free (unesterified) cholesterol (FC) to apolipoprotein A-I (apoA-I) has not been defined.	Phospholipids	75-77	apolipoprotein A-I	Mus musculus	143-149
16439690-0	2006	Elevated homocysteine reduces apolipoprotein A-I expression in hyperhomocysteinemic mice and in males with coronary artery disease.	Homocysteine	9-21	apolipoprotein A-I	Mus musculus	30-48
16439690-6	2006	We also performed Western analysis for plasma ApoA-I protein levels in 60 males with coronary artery disease and identified a significant (P&lt;0.01) negative correlation (-0.33) between ApoA-I and plasma homocysteine levels.	Homocysteine	205-217	apolipoprotein A-I	Mus musculus	46-52
16439690-6	2006	We also performed Western analysis for plasma ApoA-I protein levels in 60 males with coronary artery disease and identified a significant (P&lt;0.01) negative correlation (-0.33) between ApoA-I and plasma homocysteine levels.	Homocysteine	205-217	apolipoprotein A-I	Mus musculus	187-193
16477221-4	2006	When normalized to apoA-I content, non-ABCA1-dependent cholesterol efflux from RAW 264.7 macrophage cells to plasma from high HDL patients was 33% lower when compared to plasma from patients with low HDL, whereas ABCA1-dependent cholesterol efflux was not impaired.	Cholesterol	55-66	apolipoprotein A-I	Mus musculus	19-25
16314670-2	2006	Addition of apolipoprotein A-I to a multilamellar phospholipid vesicle dispersion containing 20% (w/w) AMB induces the formation of reconstituted high density lipoprotein (rHDL), with solubilization of the antibiotic.	Amphotericin B	103-106	apolipoprotein A-I	Mus musculus	12-30
16424111-5	2006	Plasma apoA-I and paraoxonase concentrations were significantly lower in the trans-10, cis-12-CLA group than in the cis-9, trans-11-CLA group.	trans-10, cis-12-cla	77-97	apolipoprotein A-I	Mus musculus	7-13
16424111-5	2006	Plasma apoA-I and paraoxonase concentrations were significantly lower in the trans-10, cis-12-CLA group than in the cis-9, trans-11-CLA group.	cis-9	116-121	apolipoprotein A-I	Mus musculus	7-13
16424111-5	2006	Plasma apoA-I and paraoxonase concentrations were significantly lower in the trans-10, cis-12-CLA group than in the cis-9, trans-11-CLA group.	trans-11-cla	123-135	apolipoprotein A-I	Mus musculus	7-13
16226489-7	2005	Fenofibrate stimulated liver fatty acid beta-oxidation, increased the transcriptional expression of carnitine palmitoyltransferase 1 and phospholipid transfer protein, and decreased expression of apoA-I and apoC-III.	Fenofibrate	0-11	apolipoprotein A-I	Mus musculus	196-202
16204232-2	2005	Here we have characterized the intracellular lipidation of newly synthesized apoA-I, in primary hepatocytes cultured with [3H]choline to label choline-phospholipids, low density lipoprotein-[3H]cholesterol to label the cell surface, or [3H]mevalonate to label de novo synthesized cholesterol.	Tritium	123-125	apolipoprotein A-I	Mus musculus	77-83
16204232-2	2005	Here we have characterized the intracellular lipidation of newly synthesized apoA-I, in primary hepatocytes cultured with [3H]choline to label choline-phospholipids, low density lipoprotein-[3H]cholesterol to label the cell surface, or [3H]mevalonate to label de novo synthesized cholesterol.	Choline	126-133	apolipoprotein A-I	Mus musculus	77-83
16204232-2	2005	Here we have characterized the intracellular lipidation of newly synthesized apoA-I, in primary hepatocytes cultured with [3H]choline to label choline-phospholipids, low density lipoprotein-[3H]cholesterol to label the cell surface, or [3H]mevalonate to label de novo synthesized cholesterol.	Choline	143-150	apolipoprotein A-I	Mus musculus	77-83
16204232-2	2005	Here we have characterized the intracellular lipidation of newly synthesized apoA-I, in primary hepatocytes cultured with [3H]choline to label choline-phospholipids, low density lipoprotein-[3H]cholesterol to label the cell surface, or [3H]mevalonate to label de novo synthesized cholesterol.	Phospholipids	151-164	apolipoprotein A-I	Mus musculus	77-83
16204232-2	2005	Here we have characterized the intracellular lipidation of newly synthesized apoA-I, in primary hepatocytes cultured with [3H]choline to label choline-phospholipids, low density lipoprotein-[3H]cholesterol to label the cell surface, or [3H]mevalonate to label de novo synthesized cholesterol.	Tritium	191-193	apolipoprotein A-I	Mus musculus	77-83
16204232-2	2005	Here we have characterized the intracellular lipidation of newly synthesized apoA-I, in primary hepatocytes cultured with [3H]choline to label choline-phospholipids, low density lipoprotein-[3H]cholesterol to label the cell surface, or [3H]mevalonate to label de novo synthesized cholesterol.	Cholesterol	194-205	apolipoprotein A-I	Mus musculus	77-83
16204232-2	2005	Here we have characterized the intracellular lipidation of newly synthesized apoA-I, in primary hepatocytes cultured with [3H]choline to label choline-phospholipids, low density lipoprotein-[3H]cholesterol to label the cell surface, or [3H]mevalonate to label de novo synthesized cholesterol.	[3h]mevalonate	236-250	apolipoprotein A-I	Mus musculus	77-83
16204232-2	2005	Here we have characterized the intracellular lipidation of newly synthesized apoA-I, in primary hepatocytes cultured with [3H]choline to label choline-phospholipids, low density lipoprotein-[3H]cholesterol to label the cell surface, or [3H]mevalonate to label de novo synthesized cholesterol.	Cholesterol	280-291	apolipoprotein A-I	Mus musculus	77-83
16204232-4	2005	In the presence of cycloheximide, endogenous apoA-I is substantially phospholipidated intracellularly but acquires some additional lipid after export out of the cell.	Cycloheximide	19-32	apolipoprotein A-I	Mus musculus	45-51
16204232-5	2005	In cells labeled with low density lipoprotein-[3H]cholesterol, intracellular cholesterol lipidation of apoA-I is entirely absent, but the secreted apoA-I rapidly accumulates cholesterol after secretion from the cell in the media.	low density lipoprotein-[3h]cholesterol	22-61	apolipoprotein A-I	Mus musculus	103-109
16204232-5	2005	In cells labeled with low density lipoprotein-[3H]cholesterol, intracellular cholesterol lipidation of apoA-I is entirely absent, but the secreted apoA-I rapidly accumulates cholesterol after secretion from the cell in the media.	Cholesterol	50-61	apolipoprotein A-I	Mus musculus	103-109
16204232-5	2005	In cells labeled with low density lipoprotein-[3H]cholesterol, intracellular cholesterol lipidation of apoA-I is entirely absent, but the secreted apoA-I rapidly accumulates cholesterol after secretion from the cell in the media.	Cholesterol	50-61	apolipoprotein A-I	Mus musculus	147-153
16204232-5	2005	In cells labeled with low density lipoprotein-[3H]cholesterol, intracellular cholesterol lipidation of apoA-I is entirely absent, but the secreted apoA-I rapidly accumulates cholesterol after secretion from the cell in the media.	Cholesterol	77-88	apolipoprotein A-I	Mus musculus	103-109
16204232-6	2005	On the other hand, de novo synthesized cholesterol can lipidate apoA-I intracellularly.	Cholesterol	39-50	apolipoprotein A-I	Mus musculus	64-70
16204232-10	2005	Thus, we demonstrated that apoA-I phospholipidation starts early in the ER and is partially dependent on ABCA1, with the bulk of lipidation by phospholipids and cholesterol occurring in the Golgi and at the plasma membrane, respectively.	Cholesterol	161-172	apolipoprotein A-I	Mus musculus	27-33
16224061-6	2005	D-4F had no effect on plasma myeloperoxidase concentrations but reduced myeloperoxidase association with apoA-I as well as 3-nitrotyrosine in apoA-I.	3-nitrotyrosine	123-138	apolipoprotein A-I	Mus musculus	142-148
16274238-2	2005	The primary function of apoAI is to recruit phospholipid and cholesterol for assembly of HDL particles.	Phospholipids	44-56	apolipoprotein A-I	Mus musculus	24-29
16274238-2	2005	The primary function of apoAI is to recruit phospholipid and cholesterol for assembly of HDL particles.	Cholesterol	61-72	apolipoprotein A-I	Mus musculus	24-29
16245952-3	2005	Following adenovirus-mediated gene transfer in apoA-I deficient mice, the level of plasma HDL cholesterol was greatly reduced in helix 6P and helix 6Delta mutants.	Cholesterol	94-105	apolipoprotein A-I	Mus musculus	47-53
16151025-0	2005	Increased atherosclerosis in mice lacking apolipoprotein A-I attributable to both impaired reverse cholesterol transport and increased inflammation.	Cholesterol	99-110	apolipoprotein A-I	Mus musculus	42-60
16151025-5	2005	Compared with LA-apoA-I+/+ mice, serum from LA-apoA-I-/- mice had a significantly reduced capacity to function as an acceptor of ABCA1- and SR-BI-mediated cellular cholesterol efflux, and also had markedly reduced lecithin cholesterol acyltransferase activity.	Cholesterol	164-175	apolipoprotein A-I	Mus musculus	47-53
16151025-6	2005	In addition, LA-apoA-I-/- mice had significantly reduced macrophage-derived cholesterol esterification and reverse cholesterol transport in vivo.	Cholesterol	76-87	apolipoprotein A-I	Mus musculus	16-22
16151025-6	2005	In addition, LA-apoA-I-/- mice had significantly reduced macrophage-derived cholesterol esterification and reverse cholesterol transport in vivo.	Cholesterol	115-126	apolipoprotein A-I	Mus musculus	16-22
16151025-9	2005	We conclude that apoA-I inhibits atherosclerosis by promoting both macrophage reverse cholesterol transport and HDL antiinflammatory function, and that these anti-atherogenic functions of apoA-I are largely independent of the plasma level of HDL-C in this mouse model.	Cholesterol	86-97	apolipoprotein A-I	Mus musculus	17-23
16123326-4	2005	Cholic acid produced significant decreases in high-density lipoprotein (HDL) cholesterol, plasma apolipoprotein (apo)A-I and hepatic apoA-I mRNA in wild-type mice.	Cholic Acid	0-11	apolipoprotein A-I	Mus musculus	133-139
16123326-6	2005	Reciprocally, changes in HDL/apoA-I profiles were abolished in Pxr-null SXR-Tg mice in which PXR-responsive genes, particularly those involved in bile acid detoxification were readily activated after cholic acid treatment.	Bile Acids and Salts	146-155	apolipoprotein A-I	Mus musculus	29-35
16123326-7	2005	CONCLUSIONS: PXR expression in mice antagonizes the cholic acid-mediated downregulation of plasma HDL cholesterol and apoA-I, and magnification of PXR/SXR-mediated changes may constitute a new mean to counteract the effects of bile acids on plasma lipoproteins.	Cholic Acid	52-63	apolipoprotein A-I	Mus musculus	118-124
15995171-9	2005	Moreover, the presence of large HDLs without apoA-I provides evidence for an apoA-I-independent pathway of cholesterol efflux, possibly sustained by apoE.	Cholesterol	107-118	apolipoprotein A-I	Mus musculus	77-83
15834127-3	2005	Cholesterol secretion by the HDLs, but not by the apoB pathway, was significantly reduced in primary enterocytes isolated from chow- and cholesterol-fed apoA-I(-/-) mice.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	153-159
15834127-3	2005	Cholesterol secretion by the HDLs, but not by the apoB pathway, was significantly reduced in primary enterocytes isolated from chow- and cholesterol-fed apoA-I(-/-) mice.	Cholesterol	137-148	apolipoprotein A-I	Mus musculus	153-159
15834127-4	2005	These enterocytes were capable of cholesterol efflux when apoA-I was provided extracellularly.	Cholesterol	34-45	apolipoprotein A-I	Mus musculus	58-64
15834127-6	2005	However, short-term studies revealed that cholesterol absorption was occurring over longer lengths of the intestine, and cholesterol but not triglyceride transport to the plasma and liver in chow- and cholesterol-fed apoA-I(-/-) mice was significantly reduced.	Cholesterol	121-132	apolipoprotein A-I	Mus musculus	217-223
15834127-6	2005	However, short-term studies revealed that cholesterol absorption was occurring over longer lengths of the intestine, and cholesterol but not triglyceride transport to the plasma and liver in chow- and cholesterol-fed apoA-I(-/-) mice was significantly reduced.	Cholesterol	121-132	apolipoprotein A-I	Mus musculus	217-223
15834127-7	2005	These studies indicate that in apoA-I deficiency, there is a delay in cholesterol absorption, but cholesterol is eventually absorbed because of the compensatory apoB pathway.	Cholesterol	70-81	apolipoprotein A-I	Mus musculus	31-37
15834127-7	2005	These studies indicate that in apoA-I deficiency, there is a delay in cholesterol absorption, but cholesterol is eventually absorbed because of the compensatory apoB pathway.	Cholesterol	98-109	apolipoprotein A-I	Mus musculus	31-37
15850779-3	2005	MPO, expressed in foam cell macrophages, was recently shown to oxidize the ApoA-1 component of HDL, impairing ABCA-1 mediated cholesterol efflux.	Cholesterol	126-137	apolipoprotein A-I	Mus musculus	75-81
15797865-6	2005	The transfer of de novo synthesized cholesterol to apoA-I was decreased at all time points, but that of exogenously delivered cholesterol was independent of ABCA1 activity at the early time points.	Cholesterol	36-47	apolipoprotein A-I	Mus musculus	51-57
15797865-7	2005	Progesterone does not affect apoA-I synthesis or its lipidation but inhibited the early phase of apoA-I cholesterol lipidation in both wild type and ABCA1-null hepatocytes.	Progesterone	0-12	apolipoprotein A-I	Mus musculus	97-103
15797865-7	2005	Progesterone does not affect apoA-I synthesis or its lipidation but inhibited the early phase of apoA-I cholesterol lipidation in both wild type and ABCA1-null hepatocytes.	Cholesterol	104-115	apolipoprotein A-I	Mus musculus	97-103
15797865-10	2005	ApoA-I lipidation with newly synthesized cholesterol in ABCA1-null hepatocytes was significantly decreased by brefeldin A and monensin.	Cholesterol	41-52	apolipoprotein A-I	Mus musculus	0-6
15797865-11	2005	In conclusion, we demonstrate that: (i) whereas most hepatic phospholipidation of apoA-I is mediated by ABCA1, acquisition of cholesterol depends on active transfer from intracellular compartments by ABCA1-dependent and -independent pathways, both sensitive to progesterone and (ii) there is separate regulation of phospholipid and cholesterol lipidation of apoA-I in hepatocytes.	Phospholipids	61-73	apolipoprotein A-I	Mus musculus	82-88
15628972-5	2005	In cholesteryl ester-loaded macrophages from Pctp(-/-) mice, the apolipoprotein AI-mediated efflux of phospholipids and cholesterol was decreased.	Cholesterol Esters	3-20	apolipoprotein A-I	Mus musculus	65-82
15628972-5	2005	In cholesteryl ester-loaded macrophages from Pctp(-/-) mice, the apolipoprotein AI-mediated efflux of phospholipids and cholesterol was decreased.	Phospholipids	102-115	apolipoprotein A-I	Mus musculus	65-82
15628972-5	2005	In cholesteryl ester-loaded macrophages from Pctp(-/-) mice, the apolipoprotein AI-mediated efflux of phospholipids and cholesterol was decreased.	Cholesterol	120-131	apolipoprotein A-I	Mus musculus	65-82
15851589-7	2005	Cholesterol efflux to apoA-I was significantly reduced (30% to 40%; P&lt;0.001) in ACAT1-/- peritoneal macrophages compared with ACAT1+/+ controls regardless of apoE expression.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	22-28
15841208-2	2005	ABCA1 controls the rate-limiting step in HDL particle assembly by mediating efflux of cholesterol and phospholipid from cells to lipid-free apoA-I, which forms nascent HDL particles.	Cholesterol	86-97	apolipoprotein A-I	Mus musculus	140-146
16099381-7	2005	In mice and monkeys, the administration of an apoA-I-mimetic peptide renders pro-inflammatory HDL anti-inflammatory, improves HDL-mediated cellular cholesterol efflux; in mice, it dramatically inhibits atherosclerosis.	Cholesterol	148-159	apolipoprotein A-I	Mus musculus	46-52
15751988-2	2005	Adenovirus-mediated gene transfer showed that the apoA-I[Delta(89-99)] deletion mutant caused hypercholesterolemia, characterized by increased plasma cholesterol and phospholipids, that were distributed in the very low density/intermediate density/low-density lipoprotein (VLDL/IDL/LDL) region, and normal triglycerides.	Cholesterol	99-110	apolipoprotein A-I	Mus musculus	50-56
15751988-2	2005	Adenovirus-mediated gene transfer showed that the apoA-I[Delta(89-99)] deletion mutant caused hypercholesterolemia, characterized by increased plasma cholesterol and phospholipids, that were distributed in the very low density/intermediate density/low-density lipoprotein (VLDL/IDL/LDL) region, and normal triglycerides.	Phospholipids	166-179	apolipoprotein A-I	Mus musculus	50-56
15751988-2	2005	Adenovirus-mediated gene transfer showed that the apoA-I[Delta(89-99)] deletion mutant caused hypercholesterolemia, characterized by increased plasma cholesterol and phospholipids, that were distributed in the very low density/intermediate density/low-density lipoprotein (VLDL/IDL/LDL) region, and normal triglycerides.	Triglycerides	306-319	apolipoprotein A-I	Mus musculus	50-56
15751988-5	2005	Similar analysis showed that the apoA-I[Delta(62-78)] deletion mutant in apoA-I-deficient mice caused combined hyperlipidemia characterized by increased triglycerides, cholesterol, and phospholipids in the VLDL/IDL region.	Triglycerides	153-166	apolipoprotein A-I	Mus musculus	33-39
15751988-5	2005	Similar analysis showed that the apoA-I[Delta(62-78)] deletion mutant in apoA-I-deficient mice caused combined hyperlipidemia characterized by increased triglycerides, cholesterol, and phospholipids in the VLDL/IDL region.	Triglycerides	153-166	apolipoprotein A-I	Mus musculus	73-79
15751988-5	2005	Similar analysis showed that the apoA-I[Delta(62-78)] deletion mutant in apoA-I-deficient mice caused combined hyperlipidemia characterized by increased triglycerides, cholesterol, and phospholipids in the VLDL/IDL region.	Cholesterol	168-179	apolipoprotein A-I	Mus musculus	33-39
15751988-5	2005	Similar analysis showed that the apoA-I[Delta(62-78)] deletion mutant in apoA-I-deficient mice caused combined hyperlipidemia characterized by increased triglycerides, cholesterol, and phospholipids in the VLDL/IDL region.	Cholesterol	168-179	apolipoprotein A-I	Mus musculus	73-79
15751988-5	2005	Similar analysis showed that the apoA-I[Delta(62-78)] deletion mutant in apoA-I-deficient mice caused combined hyperlipidemia characterized by increased triglycerides, cholesterol, and phospholipids in the VLDL/IDL region.	Phospholipids	185-198	apolipoprotein A-I	Mus musculus	33-39
15751988-5	2005	Similar analysis showed that the apoA-I[Delta(62-78)] deletion mutant in apoA-I-deficient mice caused combined hyperlipidemia characterized by increased triglycerides, cholesterol, and phospholipids in the VLDL/IDL region.	Phospholipids	185-198	apolipoprotein A-I	Mus musculus	73-79
15751988-9	2005	We conclude that alterations in apoA-I not only may have adverse effects on HDL biosynthesis but also may promote dyslipidemia due to interference of the apoA-I mutants on the overall cholesterol and triglycerides homeostasis.	Cholesterol	184-195	apolipoprotein A-I	Mus musculus	32-38
15751988-9	2005	We conclude that alterations in apoA-I not only may have adverse effects on HDL biosynthesis but also may promote dyslipidemia due to interference of the apoA-I mutants on the overall cholesterol and triglycerides homeostasis.	Cholesterol	184-195	apolipoprotein A-I	Mus musculus	154-160
15751988-9	2005	We conclude that alterations in apoA-I not only may have adverse effects on HDL biosynthesis but also may promote dyslipidemia due to interference of the apoA-I mutants on the overall cholesterol and triglycerides homeostasis.	Triglycerides	200-213	apolipoprotein A-I	Mus musculus	32-38
15751988-9	2005	We conclude that alterations in apoA-I not only may have adverse effects on HDL biosynthesis but also may promote dyslipidemia due to interference of the apoA-I mutants on the overall cholesterol and triglycerides homeostasis.	Triglycerides	200-213	apolipoprotein A-I	Mus musculus	154-160
15721011-8	2005	Similarly, macrophage loading with LPC (by either adding LPC, or PON1 or phospholipase A(2)) significantly increased apolipoprotein A-I (apoA-I) mediated cholesterol efflux by 104, 65 and 56%, respectively, in ABCA1 overexpressing macrophages.	Cholesterol	154-165	apolipoprotein A-I	Mus musculus	117-135
15721011-8	2005	Similarly, macrophage loading with LPC (by either adding LPC, or PON1 or phospholipase A(2)) significantly increased apolipoprotein A-I (apoA-I) mediated cholesterol efflux by 104, 65 and 56%, respectively, in ABCA1 overexpressing macrophages.	Cholesterol	154-165	apolipoprotein A-I	Mus musculus	137-143
15557325-4	2005	T0901317 applied to a variety of in vitro models, including immortalized fibroblasts from Tangier patients, and primary embryonic mouse neurons caused a concentration-dependent decrease in Abeta secretion, and this effect was increased by the addition of apolipoprotein A-I.	T0901317	0-8	apolipoprotein A-I	Mus musculus	255-273
15550377-6	2005	Cholesterol and phospholipid efflux stimulated by apolipoprotein A-I from macrophages isolated from wild type and Abca7-/- mice did not differ, suggesting that these activities may not be central to the physiological role of the transporter in vivo.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	50-68
15550377-6	2005	Cholesterol and phospholipid efflux stimulated by apolipoprotein A-I from macrophages isolated from wild type and Abca7-/- mice did not differ, suggesting that these activities may not be central to the physiological role of the transporter in vivo.	Phospholipids	16-28	apolipoprotein A-I	Mus musculus	50-68
15684336-3	2005	Forty-three of 48 formalin-fixed paraffin-embedded heart specimens with various forms of systemic amyloidosis reacted immunohistochemically with anti-human apoAI antibody.	Formaldehyde	18-26	apolipoprotein A-I	Mus musculus	156-161
15684336-4	2005	ApoAI was also detected in water-extracted amyloid material by immunoblotting.	Water	27-32	apolipoprotein A-I	Mus musculus	0-5
15654758-2	2005	Cholesterol esterification rate (CER) in apoA-I(-)(/)(-) apoE(-)(/)(-) mouse plasma was &lt;7% that of C57Bl/6 (B6) mouse plasma, even though apoA-I(-)(/)(-) apoE(-)(/)(-) plasma retained (1)/(3) the amount of B6 LCAT activity.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	41-47
15654758-2	2005	Cholesterol esterification rate (CER) in apoA-I(-)(/)(-) apoE(-)(/)(-) mouse plasma was &lt;7% that of C57Bl/6 (B6) mouse plasma, even though apoA-I(-)(/)(-) apoE(-)(/)(-) plasma retained (1)/(3) the amount of B6 LCAT activity.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	142-148
16116948-2	2005	After incubation with apoA-I for 24 h, RAW264.7 cells effluxed 37.65% cholesterol loaded by acetyl LDL (ac-LDL), and 9.78% cholesterol in ox-LDL group.	Cholesterol	70-81	apolipoprotein A-I	Mus musculus	22-28
16116948-2	2005	After incubation with apoA-I for 24 h, RAW264.7 cells effluxed 37.65% cholesterol loaded by acetyl LDL (ac-LDL), and 9.78% cholesterol in ox-LDL group.	Cholesterol	123-134	apolipoprotein A-I	Mus musculus	22-28
15520449-1	2005	ABCA7 is homologous to ABCA1 and has recently been shown in cell culture to bind apolipoprotein A-I (apoA-I) and to promote the efflux of phospholipids.	Phospholipids	138-151	apolipoprotein A-I	Mus musculus	81-99
15520449-3	2005	When expressed in HEK293 cells, both human and mouse ABCA7 promoted phospholipid efflux to apoA-I but no detectable cholesterol efflux.	Phospholipids	68-80	apolipoprotein A-I	Mus musculus	91-97
15529023-6	2004	An apoA-I mimetic peptide, namely 4F synthesized from D-amino acids (D-4F), administered orally to mice did not raise HDL-cholesterol concentrations but promoted the formation of pre-beta HDL containing increased paraoxonase activity, resulting in significant improvements in HDL"s anti-inflammatory properties and ability to promote cholesterol efflux from macrophages in vitro.	Cholesterol	334-345	apolipoprotein A-I	Mus musculus	3-9
15358601-0	2004	Cyclosporin A traps ABCA1 at the plasma membrane and inhibits ABCA1-mediated lipid efflux to apolipoprotein A-I.	Cyclosporine	0-13	apolipoprotein A-I	Mus musculus	93-111
15358601-1	2004	OBJECTIVE: ABCA1 mediates cellular cholesterol and phospholipid efflux to apolipoprotein A-I and other apolipoprotein acceptors.	Cholesterol	35-46	apolipoprotein A-I	Mus musculus	74-92
15358601-1	2004	OBJECTIVE: ABCA1 mediates cellular cholesterol and phospholipid efflux to apolipoprotein A-I and other apolipoprotein acceptors.	Phospholipids	51-63	apolipoprotein A-I	Mus musculus	74-92
15358601-4	2004	Using the RAW264.7 mouse macrophage cell line, in which ABCA1 and its associated cholesterol efflux activity are inducible by cAMP analogues, cyclosporin A inhibition of cholesterol efflux to apolipoprotein A-I was rapidly reversible after its removal from the culture media, implying that ABCA1 levels were not drastically reduced by cyclosporin A.	Cyclosporine	142-155	apolipoprotein A-I	Mus musculus	192-210
15292375-1	2004	Differential regulation has been suggested for cellular cholesterol and phospholipid release mediated by apolipoprotein A-I (apoA-I)/ABCA1.	Cholesterol	56-67	apolipoprotein A-I	Mus musculus	105-123
15292375-1	2004	Differential regulation has been suggested for cellular cholesterol and phospholipid release mediated by apolipoprotein A-I (apoA-I)/ABCA1.	Cholesterol	56-67	apolipoprotein A-I	Mus musculus	125-131
15292375-1	2004	Differential regulation has been suggested for cellular cholesterol and phospholipid release mediated by apolipoprotein A-I (apoA-I)/ABCA1.	Phospholipids	72-84	apolipoprotein A-I	Mus musculus	105-123
15292375-1	2004	Differential regulation has been suggested for cellular cholesterol and phospholipid release mediated by apolipoprotein A-I (apoA-I)/ABCA1.	Phospholipids	72-84	apolipoprotein A-I	Mus musculus	125-131
15292375-3	2004	ApoA-I induced a rapid decrease of the cellular cholesterol compartment that is in equilibrium with the ACAT-accessible pool in cells that generate cholesterol-rich HDL.	Cholesterol	48-59	apolipoprotein A-I	Mus musculus	0-6
15292375-3	2004	ApoA-I induced a rapid decrease of the cellular cholesterol compartment that is in equilibrium with the ACAT-accessible pool in cells that generate cholesterol-rich HDL.	Cholesterol	148-159	apolipoprotein A-I	Mus musculus	0-6
15292375-4	2004	Pharmacological and genetic inactivation of ACAT enhanced the apoA-I-mediated cholesterol release through upregulation of ABCA1 and through cholesterol enrichment in the HDL generated.	Cholesterol	78-89	apolipoprotein A-I	Mus musculus	62-68
15292375-4	2004	Pharmacological and genetic inactivation of ACAT enhanced the apoA-I-mediated cholesterol release through upregulation of ABCA1 and through cholesterol enrichment in the HDL generated.	Cholesterol	140-151	apolipoprotein A-I	Mus musculus	62-68
15292375-6	2004	In L929 cells, the PKC activation caused an increase in apoA-I-mediated cholesterol release without detectable change in phospholipid release and in ABCA1 expression.	Cholesterol	72-83	apolipoprotein A-I	Mus musculus	56-62
15292375-7	2004	These results indicate that apoA-I mobilizes intracellular cholesterol for the ABCA1-mediated release from the compartment that is under the control of ACAT.	Cholesterol	59-70	apolipoprotein A-I	Mus musculus	28-34
15292375-8	2004	The cholesterol mobilization process is presumably related to PKC activation by apoA-I.	Cholesterol	4-15	apolipoprotein A-I	Mus musculus	80-86
15269218-6	2004	Here we demonstrate that glial ABCA1 is required for cholesterol efflux to apoA-I and plays a key role in facilitating cholesterol efflux to apoE, which is the major apolipoprotein in the brain.	Cholesterol	53-64	apolipoprotein A-I	Mus musculus	75-81
15353488-8	2004	CONCLUSIONS: Oral and intraperitoneal administration of the apoA-I-mimetic peptide D4F significantly reduced rapidly evolving atherosclerotic lesions in vein grafts but not established atherosclerotic lesions in aortic sinus.	D4F	83-86	apolipoprotein A-I	Mus musculus	60-66
15364338-0	2004	Rapid reversal of endothelial dysfunction in hypercholesterolemic apolipoprotein E-null mice by recombinant apolipoprotein A-I(Milano)-phospholipid complex.	Phospholipids	135-147	apolipoprotein A-I	Mus musculus	108-134
15231854-8	2004	Changes of cAMP-stimulated cholesterol efflux correlated (r = 0.65, P &lt; 0.05) with changes of apoA-I but not with changes of prebeta-HDL (r = 0.30, P = 0.18).	Cyclic AMP	11-15	apolipoprotein A-I	Mus musculus	97-103
15231854-8	2004	Changes of cAMP-stimulated cholesterol efflux correlated (r = 0.65, P &lt; 0.05) with changes of apoA-I but not with changes of prebeta-HDL (r = 0.30, P = 0.18).	Cholesterol	27-38	apolipoprotein A-I	Mus musculus	97-103
15060083-0	2004	Quality control in the apoA-I secretory pathway: deletion of apoA-I helix 6 leads to the formation of cytosolic phospholipid inclusions.	Phospholipids	112-124	apolipoprotein A-I	Mus musculus	23-29
15060083-0	2004	Quality control in the apoA-I secretory pathway: deletion of apoA-I helix 6 leads to the formation of cytosolic phospholipid inclusions.	Phospholipids	112-124	apolipoprotein A-I	Mus musculus	61-67
15060083-8	2004	These data suggest that alterations in native apoA-I conformation can lead to aberrant trafficking and accumulation of apolipoprotein-phospholipid structures.	Phospholipids	134-146	apolipoprotein A-I	Mus musculus	46-52
15188057-9	2004	We also carried out in vitro binding study to investigate the binding capacity of ApoA-I and ApoA-I+LFF to fluorescence labeled LPS (FITC-LPS).	fitc-lps	133-141	apolipoprotein A-I	Mus musculus	82-88
15188057-9	2004	We also carried out in vitro binding study to investigate the binding capacity of ApoA-I and ApoA-I+LFF to fluorescence labeled LPS (FITC-LPS).	fitc-lps	133-141	apolipoprotein A-I	Mus musculus	93-99
15188057-10	2004	It was shown that both ApoA-I and ApoA-I+LFF could bind with FITC-LPS, however, the binding capacity of ApoA-I+LFF to FITC-LPS (64.47 +/- 8.06) was significantly higher than that of ApoA-I alone (24.35 +/- 3.70) (P&lt;0.01).	fitc-lps	61-69	apolipoprotein A-I	Mus musculus	23-29
15188057-10	2004	It was shown that both ApoA-I and ApoA-I+LFF could bind with FITC-LPS, however, the binding capacity of ApoA-I+LFF to FITC-LPS (64.47 +/- 8.06) was significantly higher than that of ApoA-I alone (24.35 +/- 3.70) (P&lt;0.01).	fitc-lps	61-69	apolipoprotein A-I	Mus musculus	34-40
15188057-10	2004	It was shown that both ApoA-I and ApoA-I+LFF could bind with FITC-LPS, however, the binding capacity of ApoA-I+LFF to FITC-LPS (64.47 +/- 8.06) was significantly higher than that of ApoA-I alone (24.35 +/- 3.70) (P&lt;0.01).	fitc-lps	61-69	apolipoprotein A-I	Mus musculus	34-40
15188057-10	2004	It was shown that both ApoA-I and ApoA-I+LFF could bind with FITC-LPS, however, the binding capacity of ApoA-I+LFF to FITC-LPS (64.47 +/- 8.06) was significantly higher than that of ApoA-I alone (24.35 +/- 3.70) (P&lt;0.01).	fitc-lps	61-69	apolipoprotein A-I	Mus musculus	34-40
15188057-10	2004	It was shown that both ApoA-I and ApoA-I+LFF could bind with FITC-LPS, however, the binding capacity of ApoA-I+LFF to FITC-LPS (64.47 +/- 8.06) was significantly higher than that of ApoA-I alone (24.35 +/- 3.70) (P&lt;0.01).	fitc-lps	118-126	apolipoprotein A-I	Mus musculus	23-29
15188057-10	2004	It was shown that both ApoA-I and ApoA-I+LFF could bind with FITC-LPS, however, the binding capacity of ApoA-I+LFF to FITC-LPS (64.47 +/- 8.06) was significantly higher than that of ApoA-I alone (24.35 +/- 3.70) (P&lt;0.01).	fitc-lps	118-126	apolipoprotein A-I	Mus musculus	34-40
15188057-10	2004	It was shown that both ApoA-I and ApoA-I+LFF could bind with FITC-LPS, however, the binding capacity of ApoA-I+LFF to FITC-LPS (64.47 +/- 8.06) was significantly higher than that of ApoA-I alone (24.35 +/- 3.70) (P&lt;0.01).	fitc-lps	118-126	apolipoprotein A-I	Mus musculus	34-40
15188057-10	2004	It was shown that both ApoA-I and ApoA-I+LFF could bind with FITC-LPS, however, the binding capacity of ApoA-I+LFF to FITC-LPS (64.47 +/- 8.06) was significantly higher than that of ApoA-I alone (24.35 +/- 3.70) (P&lt;0.01).	fitc-lps	118-126	apolipoprotein A-I	Mus musculus	34-40
14993246-3	2004	Exogenous apoA-I stimulated cholesterol efflux to the medium from wild-type hepatocytes, but not from ABCA1-deficient (abca1(-/-)) hepatocytes.	Cholesterol	28-39	apolipoprotein A-I	Mus musculus	10-16
14993246-5	2004	ABCA1-dependent cholesterol mobilization to apoA-I increased new cholesterol synthesis, indicating depletion of the regulatory pool of hepatocyte cholesterol during HDL formation.	Cholesterol	16-27	apolipoprotein A-I	Mus musculus	44-50
14993246-5	2004	ABCA1-dependent cholesterol mobilization to apoA-I increased new cholesterol synthesis, indicating depletion of the regulatory pool of hepatocyte cholesterol during HDL formation.	Cholesterol	65-76	apolipoprotein A-I	Mus musculus	44-50
14993246-5	2004	ABCA1-dependent cholesterol mobilization to apoA-I increased new cholesterol synthesis, indicating depletion of the regulatory pool of hepatocyte cholesterol during HDL formation.	Cholesterol	65-76	apolipoprotein A-I	Mus musculus	44-50
14993246-6	2004	Secretion of triacylglycerol and apoB was decreased following apoA-I incubation with ABCA1-expressing but not abca1(-/-) hepatocytes.	Triglycerides	13-28	apolipoprotein A-I	Mus musculus	62-68
15026428-1	2004	The liver X receptor/retinoid X receptor (LXR/RXR)-regulated gene ABCA1 effluxes cellular cholesterol and phospholipid to apolipoprotein A1 (apoA1), which is the rate-limiting step in high-density lipoprotein synthesis.	Cholesterol	90-101	apolipoprotein A-I	Mus musculus	122-139
15026428-1	2004	The liver X receptor/retinoid X receptor (LXR/RXR)-regulated gene ABCA1 effluxes cellular cholesterol and phospholipid to apolipoprotein A1 (apoA1), which is the rate-limiting step in high-density lipoprotein synthesis.	Cholesterol	90-101	apolipoprotein A-I	Mus musculus	141-146
15026428-1	2004	The liver X receptor/retinoid X receptor (LXR/RXR)-regulated gene ABCA1 effluxes cellular cholesterol and phospholipid to apolipoprotein A1 (apoA1), which is the rate-limiting step in high-density lipoprotein synthesis.	Phospholipids	106-118	apolipoprotein A-I	Mus musculus	122-139
15026428-1	2004	The liver X receptor/retinoid X receptor (LXR/RXR)-regulated gene ABCA1 effluxes cellular cholesterol and phospholipid to apolipoprotein A1 (apoA1), which is the rate-limiting step in high-density lipoprotein synthesis.	Phospholipids	106-118	apolipoprotein A-I	Mus musculus	141-146
15026428-6	2004	Expression of exogenous ABCA1 restores apoA1-dependent cholesterol efflux in Sertoli TM4 cells.	Cholesterol	55-66	apolipoprotein A-I	Mus musculus	39-44
15017358-9	2004	The findings support a model of cholesterol efflux that requires direct physical interactions between apoA-I and ATP-binding cassette transporter A1, and can explain Tangier disease and other HDL deficiencies.	Cholesterol	32-43	apolipoprotein A-I	Mus musculus	102-108
14703508-0	2004	ABCA1 mediates concurrent cholesterol and phospholipid efflux to apolipoprotein A-I.	Cholesterol	26-37	apolipoprotein A-I	Mus musculus	65-83
14703508-0	2004	ABCA1 mediates concurrent cholesterol and phospholipid efflux to apolipoprotein A-I.	Phospholipids	42-54	apolipoprotein A-I	Mus musculus	65-83
14703508-2	2004	In the current study using RAW264.7 cells, ABCA1-mediated free cholesterol and phospholipid efflux to apolipoprotein A-I (apoA-I) were tightly coupled to each other both temporally and after treatment with ABCA1 inhibitors.	Cholesterol	63-74	apolipoprotein A-I	Mus musculus	102-120
14703508-2	2004	In the current study using RAW264.7 cells, ABCA1-mediated free cholesterol and phospholipid efflux to apolipoprotein A-I (apoA-I) were tightly coupled to each other both temporally and after treatment with ABCA1 inhibitors.	Cholesterol	63-74	apolipoprotein A-I	Mus musculus	122-128
14703508-2	2004	In the current study using RAW264.7 cells, ABCA1-mediated free cholesterol and phospholipid efflux to apolipoprotein A-I (apoA-I) were tightly coupled to each other both temporally and after treatment with ABCA1 inhibitors.	Phospholipids	79-91	apolipoprotein A-I	Mus musculus	102-120
14703508-2	2004	In the current study using RAW264.7 cells, ABCA1-mediated free cholesterol and phospholipid efflux to apolipoprotein A-I (apoA-I) were tightly coupled to each other both temporally and after treatment with ABCA1 inhibitors.	Phospholipids	79-91	apolipoprotein A-I	Mus musculus	122-128
14729855-2	2004	In murine macrophage cell line RAW264 cells, cAMP induced expression of ABCA1, release of cellular phospholipid and cholesterol by apolipoprotein A-I (apoA-I), and reversible binding of apoA-I to the cell.	Cyclic AMP	45-49	apolipoprotein A-I	Mus musculus	131-149
14729855-2	2004	In murine macrophage cell line RAW264 cells, cAMP induced expression of ABCA1, release of cellular phospholipid and cholesterol by apolipoprotein A-I (apoA-I), and reversible binding of apoA-I to the cell.	Cyclic AMP	45-49	apolipoprotein A-I	Mus musculus	151-157
14729855-2	2004	In murine macrophage cell line RAW264 cells, cAMP induced expression of ABCA1, release of cellular phospholipid and cholesterol by apolipoprotein A-I (apoA-I), and reversible binding of apoA-I to the cell.	Cyclic AMP	45-49	apolipoprotein A-I	Mus musculus	186-192
14729855-2	2004	In murine macrophage cell line RAW264 cells, cAMP induced expression of ABCA1, release of cellular phospholipid and cholesterol by apolipoprotein A-I (apoA-I), and reversible binding of apoA-I to the cell.	Phospholipids	99-111	apolipoprotein A-I	Mus musculus	131-149
14729855-2	2004	In murine macrophage cell line RAW264 cells, cAMP induced expression of ABCA1, release of cellular phospholipid and cholesterol by apolipoprotein A-I (apoA-I), and reversible binding of apoA-I to the cell.	Phospholipids	99-111	apolipoprotein A-I	Mus musculus	151-157
14729855-2	2004	In murine macrophage cell line RAW264 cells, cAMP induced expression of ABCA1, release of cellular phospholipid and cholesterol by apolipoprotein A-I (apoA-I), and reversible binding of apoA-I to the cell.	Cholesterol	116-127	apolipoprotein A-I	Mus musculus	131-149
14729855-2	2004	In murine macrophage cell line RAW264 cells, cAMP induced expression of ABCA1, release of cellular phospholipid and cholesterol by apolipoprotein A-I (apoA-I), and reversible binding of apoA-I to the cell.	Cholesterol	116-127	apolipoprotein A-I	Mus musculus	151-157
14729855-3	2004	The apoA-I-dependent lipid release was directly proportional to the cAMP-induced binding of apoA-I, and was inhibited 70% by a monoclonal antibody selective to lipid-free apoA-I, 725-1E2.	Cyclic AMP	68-72	apolipoprotein A-I	Mus musculus	4-10
14729855-3	2004	The apoA-I-dependent lipid release was directly proportional to the cAMP-induced binding of apoA-I, and was inhibited 70% by a monoclonal antibody selective to lipid-free apoA-I, 725-1E2.	Cyclic AMP	68-72	apolipoprotein A-I	Mus musculus	92-98
14729855-3	2004	The apoA-I-dependent lipid release was directly proportional to the cAMP-induced binding of apoA-I, and was inhibited 70% by a monoclonal antibody selective to lipid-free apoA-I, 725-1E2.	Cyclic AMP	68-72	apolipoprotein A-I	Mus musculus	92-98
14729855-6	2004	Lipid-free apoA-II liberated apoA-I from HDL by displacement and thereby markedly expanded the cAMP-induced part of the cholesterol release to the HDL-containing medium, and the antibody inhibited this part also by 70%.	Cyclic AMP	95-99	apolipoprotein A-I	Mus musculus	11-17
14729855-6	2004	Lipid-free apoA-II liberated apoA-I from HDL by displacement and thereby markedly expanded the cAMP-induced part of the cholesterol release to the HDL-containing medium, and the antibody inhibited this part also by 70%.	Cholesterol	120-131	apolipoprotein A-I	Mus musculus	11-17
14729855-7	2004	Binding experiments of the double-labeled reconstituted HDL showed that cAMP induced reversible binding of apoA-I but not the association of cholesteryl ester with the cells.	Cyclic AMP	72-76	apolipoprotein A-I	Mus musculus	107-113
14729855-9	2004	The data implicated that the ABCA1-dependent cholesterol release to HDL is mediated by apoA-I dissociated from HDL.	Cholesterol	45-56	apolipoprotein A-I	Mus musculus	87-93
14729861-6	2004	Prebeta LpA-I contained one to four molecules of phosphatidylcholine per molecule of apoA-I, whereas LFA-I contained less than one.	Phosphatidylcholines	49-68	apolipoprotein A-I	Mus musculus	85-91
14726413-3	2004	METHODS AND RESULTS: Expression of ABCA1, apoA-I-mediated cellular lipid release, and HDL production were enhanced in cAMP analogue-treated RAW264 cells by verapamil, and similar effects were also observed with other calcium channel blockers.	Cyclic AMP	118-122	apolipoprotein A-I	Mus musculus	42-48
14726413-3	2004	METHODS AND RESULTS: Expression of ABCA1, apoA-I-mediated cellular lipid release, and HDL production were enhanced in cAMP analogue-treated RAW264 cells by verapamil, and similar effects were also observed with other calcium channel blockers.	Verapamil	156-165	apolipoprotein A-I	Mus musculus	42-48
14726413-7	2004	CONCLUSIONS: The data demonstrated that verapamil increases ABCA1 expression through LXR-independent mechanism and thereby increases apoA-I-mediated cellular lipid release and production of HDL.	Verapamil	40-49	apolipoprotein A-I	Mus musculus	133-139
14984740-0	2004	An inhibitor of acylCoA: cholesterol acyltransferase increases expression of ATP-binding cassette transporter A1 and thereby enhances the ApoA-I-mediated release of cholesterol from macrophages.	Cholesterol	25-36	apolipoprotein A-I	Mus musculus	138-144
14984740-4	2004	In this condition, the ACAT inhibitor increased reversible binding of apoA-I to the cells and enhanced apoA-I-mediated release of cellular cholesterol and phospholipid, but did not influence nonspecific cellular cholesterol efflux to lipid microemulsion.	Cholesterol	139-150	apolipoprotein A-I	Mus musculus	103-109
14984740-4	2004	In this condition, the ACAT inhibitor increased reversible binding of apoA-I to the cells and enhanced apoA-I-mediated release of cellular cholesterol and phospholipid, but did not influence nonspecific cellular cholesterol efflux to lipid microemulsion.	Phospholipids	155-167	apolipoprotein A-I	Mus musculus	103-109
14748729-3	2004	The mechanism of action of ABCA1 is still unclear, but requires the transfer of phospholipid and cholesterol to apolipoprotein A1 bound by or close to the transporter.	Phospholipids	80-92	apolipoprotein A-I	Mus musculus	112-129
14644392-0	2003	Cytotoxic cellular cholesterol is selectively removed by apoA-I via ABCA1.	Cholesterol	19-30	apolipoprotein A-I	Mus musculus	57-63
14644392-5	2003	Incubation of cells with ACAT inhibitor plus apoA-I resulted in FC efflux (0.39 +/- 0.02%/h) along with a reduction in cytotoxicity (26.30 +/- 5.80%), measured by adenine release.	Adenine	163-170	apolipoprotein A-I	Mus musculus	45-51
14644392-7	2003	Co-incubation of ACAT inhibitor plus the cholesterol transport inhibitor U18666A or the antioxidant Probucol reduced efflux to apoA-I, but not to SUV.	Cholesterol	41-52	apolipoprotein A-I	Mus musculus	127-133
14644392-7	2003	Co-incubation of ACAT inhibitor plus the cholesterol transport inhibitor U18666A or the antioxidant Probucol reduced efflux to apoA-I, but not to SUV.	3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-one	73-80	apolipoprotein A-I	Mus musculus	127-133
14644392-7	2003	Co-incubation of ACAT inhibitor plus the cholesterol transport inhibitor U18666A or the antioxidant Probucol reduced efflux to apoA-I, but not to SUV.	Probucol	100-108	apolipoprotein A-I	Mus musculus	127-133
12951361-3	2003	Even without apoA-I and HDL, apoA-I-/-/apoE-/- mice had the same amount of aorta cholesteryl ester as apoE-/- mice.	Cholesterol Esters	81-98	apolipoprotein A-I	Mus musculus	29-35
14643795-3	2003	HSL Tg macrophages exhibit twofold greater efflux of cholesterol to apoA-I in vitro, suggesting the potential rate-limiting role of cholesteryl ester hydrolysis in efflux.	Cholesterol	53-64	apolipoprotein A-I	Mus musculus	68-74
14560020-1	2003	ABCA1, the mutant molecule in Tangier Disease, mediates efflux of cellular cholesterol to apoA-I and is induced by liver X receptor (LXR)/retinoid X receptor (RXR) transcription factors.	Cholesterol	75-86	apolipoprotein A-I	Mus musculus	90-96
12928428-0	2003	Effects of apolipoprotein A-I on ATP-binding cassette transporter A1-mediated efflux of macrophage phospholipid and cholesterol: formation of nascent high density lipoprotein particles.	Phospholipids	99-111	apolipoprotein A-I	Mus musculus	11-29
12928428-0	2003	Effects of apolipoprotein A-I on ATP-binding cassette transporter A1-mediated efflux of macrophage phospholipid and cholesterol: formation of nascent high density lipoprotein particles.	Cholesterol	116-127	apolipoprotein A-I	Mus musculus	11-29
14504179-5	2003	Eight weeks later, HDL cholesterol levels and apoA-I levels were markedly increased in the mice that received DMPC.	Dimyristoylphosphatidylcholine	110-114	apolipoprotein A-I	Mus musculus	46-52
14504179-9	2003	Jejunal apoA-I synthesis and plasma apoA-I levels were increased 2- to 3-fold in mice receiving DMPC but not soy or egg lecithin.	Dimyristoylphosphatidylcholine	96-100	apolipoprotein A-I	Mus musculus	8-14
14504179-9	2003	Jejunal apoA-I synthesis and plasma apoA-I levels were increased 2- to 3-fold in mice receiving DMPC but not soy or egg lecithin.	Dimyristoylphosphatidylcholine	96-100	apolipoprotein A-I	Mus musculus	36-42
14504179-10	2003	CONCLUSIONS: DMPC (but not lecithin) raises HDL cholesterol and apoA-I, improves HDL function, and prevents lesions or causes their regression in apoE-null mice.	Dimyristoylphosphatidylcholine	13-17	apolipoprotein A-I	Mus musculus	64-70
12920050-2	2003	SR-BI mediates selective HDL cholesterol uptake by formation of a productive lipoprotein/receptor complex, which requires specific structural domains and conformation states of apolipoprotein A-I present in HDL particles.	Cholesterol	29-40	apolipoprotein A-I	Mus musculus	177-195
14529830-1	2003	The antiatherogenic effect of high-density lipoprotein (HDL) and its major protein component apolipoprotein A-I (apoA-I) has been largely attributed to their key roles in reverse cholesterol transport (RCT) and cellular cholesterol efflux.	Cholesterol	179-190	apolipoprotein A-I	Mus musculus	93-111
14529830-1	2003	The antiatherogenic effect of high-density lipoprotein (HDL) and its major protein component apolipoprotein A-I (apoA-I) has been largely attributed to their key roles in reverse cholesterol transport (RCT) and cellular cholesterol efflux.	Cholesterol	179-190	apolipoprotein A-I	Mus musculus	113-119
14529830-1	2003	The antiatherogenic effect of high-density lipoprotein (HDL) and its major protein component apolipoprotein A-I (apoA-I) has been largely attributed to their key roles in reverse cholesterol transport (RCT) and cellular cholesterol efflux.	Cholesterol	220-231	apolipoprotein A-I	Mus musculus	93-111
14529830-1	2003	The antiatherogenic effect of high-density lipoprotein (HDL) and its major protein component apolipoprotein A-I (apoA-I) has been largely attributed to their key roles in reverse cholesterol transport (RCT) and cellular cholesterol efflux.	Cholesterol	220-231	apolipoprotein A-I	Mus musculus	113-119
12937162-0	2003	Induction of fatal inflammation in LDL receptor and ApoA-I double-knockout mice fed dietary fat and cholesterol.	Cholesterol	100-111	apolipoprotein A-I	Mus musculus	52-58
12937162-11	2003	In conclusion, LDLr(-/-) and LDLr(-/-)/apoA-I(-/-) mice showed dramatic TPC differences in response to dietary fat and cholesterol challenge, while despite these differences both genotypes accumulated similar levels of aortic cholesterol.	Cholesterol	119-130	apolipoprotein A-I	Mus musculus	39-45
12937162-11	2003	In conclusion, LDLr(-/-) and LDLr(-/-)/apoA-I(-/-) mice showed dramatic TPC differences in response to dietary fat and cholesterol challenge, while despite these differences both genotypes accumulated similar levels of aortic cholesterol.	Cholesterol	226-237	apolipoprotein A-I	Mus musculus	39-45
12948871-6	2003	Elevated levels of intracellular cholesterol stimulate the liver X receptor pathway, enhancing the expression of ABCA1, which increases intracellular trafficking of excess cholesterol to the cell surface for interaction with lipid-poor apolipoprotein A-I to form nascent HDL.	Cholesterol	33-44	apolipoprotein A-I	Mus musculus	236-254
12948871-6	2003	Elevated levels of intracellular cholesterol stimulate the liver X receptor pathway, enhancing the expression of ABCA1, which increases intracellular trafficking of excess cholesterol to the cell surface for interaction with lipid-poor apolipoprotein A-I to form nascent HDL.	Cholesterol	172-183	apolipoprotein A-I	Mus musculus	236-254
12900335-0	2003	Overexpression of apolipoprotein A-I promotes reverse transport of cholesterol from macrophages to feces in vivo.	Cholesterol	67-78	apolipoprotein A-I	Mus musculus	18-36
12900335-3	2003	We developed a novel approach to trace reverse transport of labeled cholesterol specifically from macrophages to the liver and feces in vivo and have applied this approach to investigate the ability of apoA-I overexpression to promote macrophage-specific reverse cholesterol transport.	Cholesterol	263-274	apolipoprotein A-I	Mus musculus	202-208
12900335-8	2003	ApoA-I overexpression led to significantly higher 3H-cholesterol in plasma, liver, and feces.	Tritium	50-52	apolipoprotein A-I	Mus musculus	0-6
12900335-8	2003	ApoA-I overexpression led to significantly higher 3H-cholesterol in plasma, liver, and feces.	Cholesterol	53-64	apolipoprotein A-I	Mus musculus	0-6
12900335-10	2003	CONCLUSIONS: Injection of 3H-cholesterol-labeled macrophage foam cells is a method of measuring reverse cholesterol transport specifically from macrophages to feces in vivo, and apoA-I overexpression promotes macrophage-specific reverse cholesterol transport.	Tritium	26-28	apolipoprotein A-I	Mus musculus	178-184
12900335-10	2003	CONCLUSIONS: Injection of 3H-cholesterol-labeled macrophage foam cells is a method of measuring reverse cholesterol transport specifically from macrophages to feces in vivo, and apoA-I overexpression promotes macrophage-specific reverse cholesterol transport.	Cholesterol	29-40	apolipoprotein A-I	Mus musculus	178-184
12754274-4	2003	Lipid efflux onto apolipoprotein A-I (apoA-I), which depends on ABCA1, was comparable in adipocytes and preadipocytes, demonstrating a differential regulation of ABCA1 mRNA and cholesterol efflux.	Cholesterol	177-188	apolipoprotein A-I	Mus musculus	18-36
12754274-4	2003	Lipid efflux onto apolipoprotein A-I (apoA-I), which depends on ABCA1, was comparable in adipocytes and preadipocytes, demonstrating a differential regulation of ABCA1 mRNA and cholesterol efflux.	Cholesterol	177-188	apolipoprotein A-I	Mus musculus	38-44
12671027-2	2003	Exchangeable apolipoproteins apolipoprotein A-I (apoA-I), apoA-II, apoE-2, apoE-3, and apoE-4 as phospholipid complexes bind like HDL3 to SR-BI via their multiple amphipathic alpha-helices; the concentrations required to reduce the binding of HDL3 to SR-BI by 50% (IC50) were similar and in the range of 35-50 microgram protein/ml.	Phospholipids	97-109	apolipoprotein A-I	Mus musculus	49-55
12732610-5	2003	Here we hypothesize that L-4F, an apoA-1 mimetic, preserves vasodilation in hypercholesterolemia and SCD by decreasing mechanisms that increase O2*- generation.	Superoxides	144-146	apolipoprotein A-I	Mus musculus	34-40
12547832-6	2003	With primary hepatocytes from ABCA1-deficient mice, the expression and net secretion of adenoviral-generated endogenous apoA-I was unchanged compared with control mice, but (3)H-phospholipids associated with endo apoA-I and exo apoA-I decreased by 63 and 25%, respectively.	Phospholipids	178-191	apolipoprotein A-I	Mus musculus	213-219
12547832-6	2003	With primary hepatocytes from ABCA1-deficient mice, the expression and net secretion of adenoviral-generated endogenous apoA-I was unchanged compared with control mice, but (3)H-phospholipids associated with endo apoA-I and exo apoA-I decreased by 63 and 25%, respectively.	Phospholipids	178-191	apolipoprotein A-I	Mus musculus	213-219
12488454-2	2003	We have mapped the domains of lipid-free apoA-I that promote cAMP-dependent and cAMP-independent cholesterol and phospholipid efflux.	Cyclic AMP	61-65	apolipoprotein A-I	Mus musculus	41-47
12488454-2	2003	We have mapped the domains of lipid-free apoA-I that promote cAMP-dependent and cAMP-independent cholesterol and phospholipid efflux.	Cyclic AMP	80-84	apolipoprotein A-I	Mus musculus	41-47
12488454-2	2003	We have mapped the domains of lipid-free apoA-I that promote cAMP-dependent and cAMP-independent cholesterol and phospholipid efflux.	Cholesterol	97-108	apolipoprotein A-I	Mus musculus	41-47
12488454-2	2003	We have mapped the domains of lipid-free apoA-I that promote cAMP-dependent and cAMP-independent cholesterol and phospholipid efflux.	Phospholipids	113-125	apolipoprotein A-I	Mus musculus	41-47
12473673-0	2003	Enhancement of scavenger receptor class B type I-mediated selective cholesteryl ester uptake from apoA-I(-/-) high density lipoprotein (HDL) by apolipoprotein A-I requires HDL reorganization by lecithin cholesterol acyltransferase.	Cholesterol Esters	68-85	apolipoprotein A-I	Mus musculus	98-104
12473673-0	2003	Enhancement of scavenger receptor class B type I-mediated selective cholesteryl ester uptake from apoA-I(-/-) high density lipoprotein (HDL) by apolipoprotein A-I requires HDL reorganization by lecithin cholesterol acyltransferase.	Cholesterol Esters	68-85	apolipoprotein A-I	Mus musculus	144-162
12473673-1	2003	The severe depletion of cholesteryl ester (CE) in adrenocortical cells of apoA-I(-/-) mice suggests that apolipoprotein (apo) A-I plays an important role in the high density lipoprotein (HDL) CE selective uptake process mediated by scavenger receptor BI (SR-BI) in vivo.	Cholesterol Esters	24-41	apolipoprotein A-I	Mus musculus	74-80
12473673-1	2003	The severe depletion of cholesteryl ester (CE) in adrenocortical cells of apoA-I(-/-) mice suggests that apolipoprotein (apo) A-I plays an important role in the high density lipoprotein (HDL) CE selective uptake process mediated by scavenger receptor BI (SR-BI) in vivo.	Cholesterol Esters	24-41	apolipoprotein A-I	Mus musculus	105-129
12576511-5	2003	ApoA-I-dependent cholesterol efflux was increased 2.6-fold in primary hepatocytes isolated 1 day after rABCA1-GFP-AdV infusion.	Cholesterol	17-28	apolipoprotein A-I	Mus musculus	0-6
12228236-3	2002	Similarly, when apolipoprotein A-I removed cellular cholesterol, phosphatidylcholine, and sphingomyelin to generate high density lipoprotein, cholesterol synthesis from acetate subsequently increased, and sphingomyelin synthesis from acetate and serine also increased.	Cholesterol	52-63	apolipoprotein A-I	Mus musculus	16-34
12228236-3	2002	Similarly, when apolipoprotein A-I removed cellular cholesterol, phosphatidylcholine, and sphingomyelin to generate high density lipoprotein, cholesterol synthesis from acetate subsequently increased, and sphingomyelin synthesis from acetate and serine also increased.	Phosphatidylcholines	65-84	apolipoprotein A-I	Mus musculus	16-34
12228236-3	2002	Similarly, when apolipoprotein A-I removed cellular cholesterol, phosphatidylcholine, and sphingomyelin to generate high density lipoprotein, cholesterol synthesis from acetate subsequently increased, and sphingomyelin synthesis from acetate and serine also increased.	Sphingomyelins	90-103	apolipoprotein A-I	Mus musculus	16-34
12228236-3	2002	Similarly, when apolipoprotein A-I removed cellular cholesterol, phosphatidylcholine, and sphingomyelin to generate high density lipoprotein, cholesterol synthesis from acetate subsequently increased, and sphingomyelin synthesis from acetate and serine also increased.	Cholesterol	142-153	apolipoprotein A-I	Mus musculus	16-34
12228236-3	2002	Similarly, when apolipoprotein A-I removed cellular cholesterol, phosphatidylcholine, and sphingomyelin to generate high density lipoprotein, cholesterol synthesis from acetate subsequently increased, and sphingomyelin synthesis from acetate and serine also increased.	Acetates	169-176	apolipoprotein A-I	Mus musculus	16-34
12228236-3	2002	Similarly, when apolipoprotein A-I removed cellular cholesterol, phosphatidylcholine, and sphingomyelin to generate high density lipoprotein, cholesterol synthesis from acetate subsequently increased, and sphingomyelin synthesis from acetate and serine also increased.	Sphingomyelins	205-218	apolipoprotein A-I	Mus musculus	16-34
12228236-3	2002	Similarly, when apolipoprotein A-I removed cellular cholesterol, phosphatidylcholine, and sphingomyelin to generate high density lipoprotein, cholesterol synthesis from acetate subsequently increased, and sphingomyelin synthesis from acetate and serine also increased.	Acetates	234-241	apolipoprotein A-I	Mus musculus	16-34
12228236-3	2002	Similarly, when apolipoprotein A-I removed cellular cholesterol, phosphatidylcholine, and sphingomyelin to generate high density lipoprotein, cholesterol synthesis from acetate subsequently increased, and sphingomyelin synthesis from acetate and serine also increased.	Serine	246-252	apolipoprotein A-I	Mus musculus	16-34
12228236-5	2002	D609 also inhibited the cholesterol removal by apoA-I not only from the astrocytes but also from BALB/3T3 and RAW264 cells.	tricyclodecane-9-yl-xanthogenate	0-4	apolipoprotein A-I	Mus musculus	47-53
12228236-5	2002	D609 also inhibited the cholesterol removal by apoA-I not only from the astrocytes but also from BALB/3T3 and RAW264 cells.	Cholesterol	24-35	apolipoprotein A-I	Mus musculus	47-53
12228236-7	2002	ApoA-I-stimulated translocation of newly synthesized cholesterol to cytosol was also decreased by D609.	Cholesterol	53-64	apolipoprotein A-I	Mus musculus	0-6
12228236-8	2002	A diacylglycerol analog increased the apoA-I-mediated cholesterol release, whereas ceramide did not influence it.	Diglycerides	2-16	apolipoprotein A-I	Mus musculus	38-44
12228236-8	2002	A diacylglycerol analog increased the apoA-I-mediated cholesterol release, whereas ceramide did not influence it.	Cholesterol	54-65	apolipoprotein A-I	Mus musculus	38-44
12228236-9	2002	We concluded that removal of cellular sphingomyelin by apolipoproteins is replenished by transfer of phosphorylcholine from phosphatidylcholine to ceramide, and this reaction may limit the removal of cholesterol by apoA-I.	Sphingomyelins	38-51	apolipoprotein A-I	Mus musculus	215-221
12208466-11	2002	In summary, in this relatively short-term murine model, simultaneous reduction of cholesterol and expression of apoA-I was associated with higher levels of apoA-I than expression of apoA-I alone but did not result in greater reduction in atherosclerosis compared with either one alone.	Cholesterol	82-93	apolipoprotein A-I	Mus musculus	156-162
12208466-11	2002	In summary, in this relatively short-term murine model, simultaneous reduction of cholesterol and expression of apoA-I was associated with higher levels of apoA-I than expression of apoA-I alone but did not result in greater reduction in atherosclerosis compared with either one alone.	Cholesterol	82-93	apolipoprotein A-I	Mus musculus	156-162
12181325-0	2002	The role of apolipoprotein A-I helix 10 in apolipoprotein-mediated cholesterol efflux via the ATP-binding cassette transporter ABCA1.	Cholesterol	67-78	apolipoprotein A-I	Mus musculus	12-30
12181325-1	2002	Recent studies of Tangier disease have shown that the ATP-binding cassette transporter A1 (ABCA1)/apolipoprotein A-I (apoA-I) interaction is critical for high density lipoprotein particle formation, apoA-I integrity, and proper reverse cholesterol transport.	Cholesterol	236-247	apolipoprotein A-I	Mus musculus	98-116
12181325-1	2002	Recent studies of Tangier disease have shown that the ATP-binding cassette transporter A1 (ABCA1)/apolipoprotein A-I (apoA-I) interaction is critical for high density lipoprotein particle formation, apoA-I integrity, and proper reverse cholesterol transport.	Cholesterol	236-247	apolipoprotein A-I	Mus musculus	118-124
12181325-1	2002	Recent studies of Tangier disease have shown that the ATP-binding cassette transporter A1 (ABCA1)/apolipoprotein A-I (apoA-I) interaction is critical for high density lipoprotein particle formation, apoA-I integrity, and proper reverse cholesterol transport.	Cholesterol	236-247	apolipoprotein A-I	Mus musculus	199-205
12181325-5	2002	To better understand this interaction, we created several truncation mutants of apoA-I and then followed up with more specific point mutants and helix translocation mutants to identify and characterize the locations of apoA-I required for ABCA1-mediated cholesterol efflux.	Cholesterol	254-265	apolipoprotein A-I	Mus musculus	219-225
12181325-8	2002	We noted a strong positive correlation between cholesterol efflux and the lipid binding characteristics of apoA-I when mutations were made in helix 10.	Cholesterol	47-58	apolipoprotein A-I	Mus musculus	107-113
12000760-0	2002	Apolipoprotein A-I is necessary for the in vivo formation of high density lipoprotein competent for scavenger receptor BI-mediated cholesteryl ester-selective uptake.	Cholesterol Esters	131-148	apolipoprotein A-I	Mus musculus	0-18
12000760-1	2002	The severe depletion of cholesteryl ester (CE) in steroidogenic cells of apoA-I(-/-) mice suggests that apolipoprotein (apo) A-I plays a specific role in the high density lipoprotein (HDL) CE-selective uptake process mediated by scavenger receptor BI (SR-BI) in vivo.	Cholesterol Esters	24-41	apolipoprotein A-I	Mus musculus	73-79
12000760-1	2002	The severe depletion of cholesteryl ester (CE) in steroidogenic cells of apoA-I(-/-) mice suggests that apolipoprotein (apo) A-I plays a specific role in the high density lipoprotein (HDL) CE-selective uptake process mediated by scavenger receptor BI (SR-BI) in vivo.	Cholesterol Esters	24-41	apolipoprotein A-I	Mus musculus	104-128
12117740-4	2002	Compared with apoA-I mice, apoA-I/sPLA2 mice had significantly lower plasma levels of phospholipids, HDL cholesterol, and apoA-I (each P&lt;0.01).	Phospholipids	86-99	apolipoprotein A-I	Mus musculus	27-33
12117740-4	2002	Compared with apoA-I mice, apoA-I/sPLA2 mice had significantly lower plasma levels of phospholipids, HDL cholesterol, and apoA-I (each P&lt;0.01).	Phospholipids	86-99	apolipoprotein A-I	Mus musculus	27-33
12117740-4	2002	Compared with apoA-I mice, apoA-I/sPLA2 mice had significantly lower plasma levels of phospholipids, HDL cholesterol, and apoA-I (each P&lt;0.01).	Cholesterol	105-116	apolipoprotein A-I	Mus musculus	27-33
12117740-4	2002	Compared with apoA-I mice, apoA-I/sPLA2 mice had significantly lower plasma levels of phospholipids, HDL cholesterol, and apoA-I (each P&lt;0.01).	Cholesterol	105-116	apolipoprotein A-I	Mus musculus	27-33
12117740-5	2002	HDL from apoA-I/sPLA2 mice was significantly depleted in phospholipids and cholesteryl esters (each P&lt;0.001) but was enriched in protein and triglycerides (each P&lt;0.001).	Phospholipids	57-70	apolipoprotein A-I	Mus musculus	9-15
12117740-5	2002	HDL from apoA-I/sPLA2 mice was significantly depleted in phospholipids and cholesteryl esters (each P&lt;0.001) but was enriched in protein and triglycerides (each P&lt;0.001).	Cholesterol Esters	75-93	apolipoprotein A-I	Mus musculus	9-15
12117740-5	2002	HDL from apoA-I/sPLA2 mice was significantly depleted in phospholipids and cholesteryl esters (each P&lt;0.001) but was enriched in protein and triglycerides (each P&lt;0.001).	Triglycerides	144-157	apolipoprotein A-I	Mus musculus	9-15
12133304-8	2002	CONCLUSION: Expression of the h-apoA1 gene in C57BL/6 mice enables them to reduce the accumulation of cholesterol in v-SMC.	Cholesterol	102-113	apolipoprotein A-I	Mus musculus	32-37
11907146-7	2002	7 alphaRAW cells also displayed small but significant increases in the rate of efflux of [(3)H]cholesterol to both delipidated apolipoprotein A1 and to HDL.Thus, CYP7A1 expression in RAW cultured macrophages prevented the accumulation of cholesterol from acetyl-LDL via both increased metabolism and efflux of cholesterol.	[(3)h]cholesterol	89-106	apolipoprotein A-I	Mus musculus	127-144
11907146-7	2002	7 alphaRAW cells also displayed small but significant increases in the rate of efflux of [(3)H]cholesterol to both delipidated apolipoprotein A1 and to HDL.Thus, CYP7A1 expression in RAW cultured macrophages prevented the accumulation of cholesterol from acetyl-LDL via both increased metabolism and efflux of cholesterol.	Cholesterol	95-106	apolipoprotein A-I	Mus musculus	127-144
11820773-3	2002	After incubation for 6 or 24 h, 3H-cholesterol efflux to free apoA-I (10 microg/ml) was significantly higher with macrophages derived from C3H mice compared to C57BL/6 mice.	Tritium	32-34	apolipoprotein A-I	Mus musculus	62-68
11820773-3	2002	After incubation for 6 or 24 h, 3H-cholesterol efflux to free apoA-I (10 microg/ml) was significantly higher with macrophages derived from C3H mice compared to C57BL/6 mice.	Cholesterol	35-46	apolipoprotein A-I	Mus musculus	62-68
11804981-1	2002	When apolipoprotein A-I mimetic peptides synthesized from either D- or L-amino acids were given orally to LDL receptor-null mice, only the peptide synthesized from D-amino acids was stable in the circulation and enhanced the ability of HDL to protect LDL against oxidation.	d- or l-amino acids	65-84	apolipoprotein A-I	Mus musculus	5-23
11804981-1	2002	When apolipoprotein A-I mimetic peptides synthesized from either D- or L-amino acids were given orally to LDL receptor-null mice, only the peptide synthesized from D-amino acids was stable in the circulation and enhanced the ability of HDL to protect LDL against oxidation.	Deuterium	65-66	apolipoprotein A-I	Mus musculus	5-23
11786298-0	2001	Stably transfected ABCA1 antisense cell line has decreased ABCA1 mRNA and cAMP-induced cholesterol efflux to apolipoprotein AI and HDL.	Cyclic AMP	74-78	apolipoprotein A-I	Mus musculus	109-126
11786298-0	2001	Stably transfected ABCA1 antisense cell line has decreased ABCA1 mRNA and cAMP-induced cholesterol efflux to apolipoprotein AI and HDL.	Cholesterol	87-98	apolipoprotein A-I	Mus musculus	109-126
11742873-7	2001	The cellular cholesterol efflux capacity of HDL from apoA-I/apoA-II mice was very similar to that of apoA-I mice.	Cholesterol	13-24	apolipoprotein A-I	Mus musculus	53-59
11742873-7	2001	The cellular cholesterol efflux capacity of HDL from apoA-I/apoA-II mice was very similar to that of apoA-I mice.	Cholesterol	13-24	apolipoprotein A-I	Mus musculus	60-66
11742873-8	2001	Thus, the Arg123-Tyr166 central domain of apoA-I is critical for reducing oxidative stress, macrophage homing, and early atherosclerosis in apoE knockout mice independent of its role in HDL production and cholesterol efflux.	Cholesterol	205-216	apolipoprotein A-I	Mus musculus	42-48
11742879-7	2001	Induction of ABCA1 with cAMP, however, did increase sterol efflux to exogenously added apoA1 from both cell types.	Cyclic AMP	24-28	apolipoprotein A-I	Mus musculus	87-92
11742879-7	2001	Induction of ABCA1 with cAMP, however, did increase sterol efflux to exogenously added apoA1 from both cell types.	Sterols	52-58	apolipoprotein A-I	Mus musculus	87-92
11742879-8	2001	Inhibitors of ABCA1 activity significantly reduced (by 40% to 50%) sterol efflux from both J774E(+) and J774E(-) cells treated with cAMP and apoA1.	Sterols	67-73	apolipoprotein A-I	Mus musculus	141-146
11716766-2	2001	An important step in this reverse cholesterol-transport pathway is the uptake of cellular cholesterol by a specific subclass of small, lipid-poor apolipoprotein A-I particles designated pre beta-HDL.	Cholesterol	34-45	apolipoprotein A-I	Mus musculus	146-164
11716766-2	2001	An important step in this reverse cholesterol-transport pathway is the uptake of cellular cholesterol by a specific subclass of small, lipid-poor apolipoprotein A-I particles designated pre beta-HDL.	Cholesterol	90-101	apolipoprotein A-I	Mus musculus	146-164
11606258-1	2001	To induce atherogenesis in mice, a high fat (HF) diet is supplemented with cholic acid (CA), which increases apoB-containing particles and lower apoA-I-containing particles.	Cholic Acid	75-86	apolipoprotein A-I	Mus musculus	145-151
11559713-1	2001	Recently, ATP-binding cassette transporter A1 (ABCA1), the defective molecule in Tangier disease, has been shown to stimulate phospholipid and cholesterol efflux to apolipoprotein A-I (apoA-I); however, little is known concerning the cellular cholesterol pools that act as the source of cholesterol for ABCA1-mediated efflux.	Phospholipids	126-138	apolipoprotein A-I	Mus musculus	165-183
11559713-1	2001	Recently, ATP-binding cassette transporter A1 (ABCA1), the defective molecule in Tangier disease, has been shown to stimulate phospholipid and cholesterol efflux to apolipoprotein A-I (apoA-I); however, little is known concerning the cellular cholesterol pools that act as the source of cholesterol for ABCA1-mediated efflux.	Phospholipids	126-138	apolipoprotein A-I	Mus musculus	185-191
11559713-1	2001	Recently, ATP-binding cassette transporter A1 (ABCA1), the defective molecule in Tangier disease, has been shown to stimulate phospholipid and cholesterol efflux to apolipoprotein A-I (apoA-I); however, little is known concerning the cellular cholesterol pools that act as the source of cholesterol for ABCA1-mediated efflux.	Cholesterol	143-154	apolipoprotein A-I	Mus musculus	165-183
11559713-1	2001	Recently, ATP-binding cassette transporter A1 (ABCA1), the defective molecule in Tangier disease, has been shown to stimulate phospholipid and cholesterol efflux to apolipoprotein A-I (apoA-I); however, little is known concerning the cellular cholesterol pools that act as the source of cholesterol for ABCA1-mediated efflux.	Cholesterol	143-154	apolipoprotein A-I	Mus musculus	185-191
11559713-1	2001	Recently, ATP-binding cassette transporter A1 (ABCA1), the defective molecule in Tangier disease, has been shown to stimulate phospholipid and cholesterol efflux to apolipoprotein A-I (apoA-I); however, little is known concerning the cellular cholesterol pools that act as the source of cholesterol for ABCA1-mediated efflux.	Cholesterol	243-254	apolipoprotein A-I	Mus musculus	165-183
11559713-1	2001	Recently, ATP-binding cassette transporter A1 (ABCA1), the defective molecule in Tangier disease, has been shown to stimulate phospholipid and cholesterol efflux to apolipoprotein A-I (apoA-I); however, little is known concerning the cellular cholesterol pools that act as the source of cholesterol for ABCA1-mediated efflux.	Cholesterol	243-254	apolipoprotein A-I	Mus musculus	185-191
11559713-1	2001	Recently, ATP-binding cassette transporter A1 (ABCA1), the defective molecule in Tangier disease, has been shown to stimulate phospholipid and cholesterol efflux to apolipoprotein A-I (apoA-I); however, little is known concerning the cellular cholesterol pools that act as the source of cholesterol for ABCA1-mediated efflux.	Cholesterol	243-254	apolipoprotein A-I	Mus musculus	165-183
11559713-1	2001	Recently, ATP-binding cassette transporter A1 (ABCA1), the defective molecule in Tangier disease, has been shown to stimulate phospholipid and cholesterol efflux to apolipoprotein A-I (apoA-I); however, little is known concerning the cellular cholesterol pools that act as the source of cholesterol for ABCA1-mediated efflux.	Cholesterol	243-254	apolipoprotein A-I	Mus musculus	185-191
11559713-3	2001	Consistent with this idea, macrophages from Niemann-Pick C1 mice that have an inability to exit cholesterol from late endosomes/lysosomes showed a profound defect in cholesterol efflux to apoA-I.	Cholesterol	96-107	apolipoprotein A-I	Mus musculus	188-194
11559713-3	2001	Consistent with this idea, macrophages from Niemann-Pick C1 mice that have an inability to exit cholesterol from late endosomes/lysosomes showed a profound defect in cholesterol efflux to apoA-I.	Cholesterol	166-177	apolipoprotein A-I	Mus musculus	188-194
11559713-4	2001	In contrast, phospholipid efflux to apoA-I was normal in Niemann-Pick C1 macrophages, as was cholesterol efflux following plasma membrane cholesterol labeling.	Phospholipids	13-25	apolipoprotein A-I	Mus musculus	36-42
11701467-0	2001	Increased cholesterol efflux in apolipoprotein AI (ApoAI)-producing macrophages as a mechanism for reduced atherosclerosis in ApoAI((-/-)) mice.	Cholesterol	10-21	apolipoprotein A-I	Mus musculus	32-49
11701467-0	2001	Increased cholesterol efflux in apolipoprotein AI (ApoAI)-producing macrophages as a mechanism for reduced atherosclerosis in ApoAI((-/-)) mice.	Cholesterol	10-21	apolipoprotein A-I	Mus musculus	51-56
11701467-0	2001	Increased cholesterol efflux in apolipoprotein AI (ApoAI)-producing macrophages as a mechanism for reduced atherosclerosis in ApoAI((-/-)) mice.	Cholesterol	10-21	apolipoprotein A-I	Mus musculus	126-131
11701467-1	2001	The concentration of apolipoprotein (apo) AI in the artery wall is thought to enhance cellular cholesterol efflux and protect against atherosclerosis.	Cholesterol	95-106	apolipoprotein A-I	Mus musculus	21-44
11701467-3	2001	We hypothesized that macrophage production of apoAI would increase cholesterol efflux and reduce atherogenesis.	Cholesterol	67-78	apolipoprotein A-I	Mus musculus	46-51
11546785-3	2001	Treatment of human fibroblasts and murine RAW264 macrophages with cholesterol and/or 8-bromo-cyclic AMP, which induces ABCA1 expression, enhanced apoA-I-mediated alpha-TOH efflux.	Cholesterol	66-77	apolipoprotein A-I	Mus musculus	146-152
11546785-3	2001	Treatment of human fibroblasts and murine RAW264 macrophages with cholesterol and/or 8-bromo-cyclic AMP, which induces ABCA1 expression, enhanced apoA-I-mediated alpha-TOH efflux.	8-Bromo Cyclic Adenosine Monophosphate	85-103	apolipoprotein A-I	Mus musculus	146-152
11546785-3	2001	Treatment of human fibroblasts and murine RAW264 macrophages with cholesterol and/or 8-bromo-cyclic AMP, which induces ABCA1 expression, enhanced apoA-I-mediated alpha-TOH efflux.	-toh	167-171	apolipoprotein A-I	Mus musculus	146-152
11433352-9	2001	The resulting increase in nitric-oxide production might be critical to the atheroprotective properties of HDL and ApoA-I.	Nitric Oxide	26-38	apolipoprotein A-I	Mus musculus	114-120
11425766-0	2001	High-dose recombinant apolipoprotein A-I(milano) mobilizes tissue cholesterol and rapidly reduces plaque lipid and macrophage content in apolipoprotein e-deficient mice.	Cholesterol	66-77	apolipoprotein A-I	Mus musculus	22-40
11425766-2	2001	BACKGROUND: Repeated doses of recombinant apolipoprotein A-I(Milano) phospholipid complex (apoA-I(m)) reduce atherosclerosis and favorably change plaque composition in rabbits and mice.	Phospholipids	69-81	apolipoprotein A-I	Mus musculus	42-60
11425766-2	2001	BACKGROUND: Repeated doses of recombinant apolipoprotein A-I(Milano) phospholipid complex (apoA-I(m)) reduce atherosclerosis and favorably change plaque composition in rabbits and mice.	Phospholipids	69-81	apolipoprotein A-I	Mus musculus	91-97
11425766-3	2001	In this study, we tested whether a single high dose of recombinant apoA-I(m) could rapidly mobilize tissue cholesterol and reduce plaque lipid and macrophage content in apoE-deficient mice.	Cholesterol	107-118	apolipoprotein A-I	Mus musculus	67-73
11425766-6	2001	One hour after injection, the plasma cholesterol efflux-promoting capacity was nearly 2-fold higher in recombinant apoA-I(m)-treated mice compared with saline and DPPC-treated mice (P&lt;0.01).	Cholesterol	37-48	apolipoprotein A-I	Mus musculus	115-121
11425766-7	2001	Compared with baseline values, serum free cholesterol, an index of tissue cholesterol mobilization, increased 1.6-fold by 1 hour after recombinant apoA-I(m) injection, and it remained significantly elevated at 48 hours (P&lt;0.01).	Cholesterol	42-53	apolipoprotein A-I	Mus musculus	147-153
11425766-8	2001	Mice receiving recombinant apoA-I(m) had 40% to 50% lower lipid content (P&lt;0.01) and 29% to 36% lower macrophage content (P&lt;0.05) in their plaques compared with the saline- and DPPC-treated mice, respectively.	Sodium Chloride	171-177	apolipoprotein A-I	Mus musculus	27-33
11425766-8	2001	Mice receiving recombinant apoA-I(m) had 40% to 50% lower lipid content (P&lt;0.01) and 29% to 36% lower macrophage content (P&lt;0.05) in their plaques compared with the saline- and DPPC-treated mice, respectively.	1,2-Dipalmitoylphosphatidylcholine	183-187	apolipoprotein A-I	Mus musculus	27-33
11425766-9	2001	CONCLUSIONS: A single high dose of recombinant apoA-I(m) rapidly mobilizes tissue cholesterol and reduces plaque lipid and macrophage content in apoE-deficient mice.	Cholesterol	82-93	apolipoprotein A-I	Mus musculus	47-53
11279093-4	2001	Compared with macrophages from control mice, macrophages from these transgenics had increases in apoA-I cholesterol efflux heightened in response to increases in cell cholesterol content.	Cholesterol	104-115	apolipoprotein A-I	Mus musculus	97-103
11279093-4	2001	Compared with macrophages from control mice, macrophages from these transgenics had increases in apoA-I cholesterol efflux heightened in response to increases in cell cholesterol content.	Cholesterol	167-178	apolipoprotein A-I	Mus musculus	97-103
11278646-4	2001	In contrast, infusion of apoA-I.phospholipid complexes (rHDL) that resemble nascent HDL markedly stimulated cholesterol efflux from tissues into plasma.	Phospholipids	32-44	apolipoprotein A-I	Mus musculus	25-31
11278646-4	2001	In contrast, infusion of apoA-I.phospholipid complexes (rHDL) that resemble nascent HDL markedly stimulated cholesterol efflux from tissues into plasma.	Cholesterol	108-119	apolipoprotein A-I	Mus musculus	25-31
11279034-5	2001	In this study we investigated the abilities of apoA-I and apoA-II to mediate SR-BI-specific binding and selective uptake of cholesterol ester using reconstituted HDLs (rHDLs) that were homogeneous in size and apolipoprotein content.	Cholesterol Esters	124-141	apolipoprotein A-I	Mus musculus	47-53
11093738-2	2000	In mice, the deletion of apolipoprotein AI (apo AI), the major apolipoprotein in HDL, results in very low plasma HDL-cholesterol levels.	Cholesterol	117-128	apolipoprotein A-I	Mus musculus	25-42
11093738-2	2000	In mice, the deletion of apolipoprotein AI (apo AI), the major apolipoprotein in HDL, results in very low plasma HDL-cholesterol levels.	Cholesterol	117-128	apolipoprotein A-I	Mus musculus	44-50
11073852-2	2000	Expression of human apoA-II in transgenic mice fed a chow diet leads to (1) a bimodal distribution of high density lipoprotein (HDL) size as in humans, (2) a reduction in total cholesterol concentration that is mainly due to a reduction in non-HDL cholesterol level, and (3) a dramatic reduction in mouse endogenous apoA-I and apoA-II.	Cholesterol	177-188	apolipoprotein A-I	Mus musculus	20-26
11073852-2	2000	Expression of human apoA-II in transgenic mice fed a chow diet leads to (1) a bimodal distribution of high density lipoprotein (HDL) size as in humans, (2) a reduction in total cholesterol concentration that is mainly due to a reduction in non-HDL cholesterol level, and (3) a dramatic reduction in mouse endogenous apoA-I and apoA-II.	Cholesterol	248-259	apolipoprotein A-I	Mus musculus	20-26
11196441-0	2000	Roles of scavenger receptor BI and APO A-I in selective uptake of HDL cholesterol by adrenal cells.	Cholesterol	70-81	apolipoprotein A-I	Mus musculus	35-42
10998462-4	2000	Moreover, probucol was reported to inhibit apoA-I mediated cholesterol efflux from mouse macrophages.	Cholesterol	59-70	apolipoprotein A-I	Mus musculus	43-49
11031214-2	2000	Overexpression of apoC-III in mice causes hypertriglyceridemia and induces atherogenesis, whereas overexpression of apoA-I or apoA-IV increases cholesterol in plasma high density lipoprotein (HDL) and protects against atherosclerosis.	Cholesterol	144-155	apolipoprotein A-I	Mus musculus	116-122
10893411-1	2000	Studies show that lipid-free apoA-I stimulates release of cholesterol and phospholipid from fibroblasts and macrophages.	Cholesterol	58-69	apolipoprotein A-I	Mus musculus	29-35
10893411-1	2000	Studies show that lipid-free apoA-I stimulates release of cholesterol and phospholipid from fibroblasts and macrophages.	Phospholipids	74-86	apolipoprotein A-I	Mus musculus	29-35
10893411-7	2000	The stimulation of efflux exhibits specificity for apoA-I, high density lipoprotein, and other apolipoproteins as cholesterol acceptors, but not for small unilamellar vesicles, bile acid micelles, or cyclodextrin.	Cholesterol	114-125	apolipoprotein A-I	Mus musculus	51-57
10998247-2	2000	Preincubation of the cells with 300 microM dibutyryl cyclic (dBc) AMP for 16 h induced specific binding of apolipoprotein (apo) A-I to the cells and apoA-I-mediated HDL formation with cellular lipids, neither of which was detected in the absence of dBcAMP.	Bucladesine	43-69	apolipoprotein A-I	Mus musculus	149-155
10998247-2	2000	Preincubation of the cells with 300 microM dibutyryl cyclic (dBc) AMP for 16 h induced specific binding of apolipoprotein (apo) A-I to the cells and apoA-I-mediated HDL formation with cellular lipids, neither of which was detected in the absence of dBcAMP.	Bucladesine	249-255	apolipoprotein A-I	Mus musculus	149-155
10998247-3	2000	Dose-dependent changes of the apoA-I specific binding and the apoA-I-mediated cholesterol release were largely superimposable.	Cholesterol	78-89	apolipoprotein A-I	Mus musculus	62-68
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Bucladesine	67-73	apolipoprotein A-I	Mus musculus	39-45
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Bucladesine	67-73	apolipoprotein A-I	Mus musculus	187-193
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Bucladesine	67-73	apolipoprotein A-I	Mus musculus	187-193
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Dactinomycin	97-110	apolipoprotein A-I	Mus musculus	39-45
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Dactinomycin	97-110	apolipoprotein A-I	Mus musculus	187-193
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Dactinomycin	97-110	apolipoprotein A-I	Mus musculus	187-193
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Cycloheximide	112-125	apolipoprotein A-I	Mus musculus	39-45
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Cycloheximide	112-125	apolipoprotein A-I	Mus musculus	187-193
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Cycloheximide	112-125	apolipoprotein A-I	Mus musculus	187-193
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Puromycin	127-136	apolipoprotein A-I	Mus musculus	39-45
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Puromycin	127-136	apolipoprotein A-I	Mus musculus	187-193
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Puromycin	127-136	apolipoprotein A-I	Mus musculus	187-193
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Brefeldin A	142-153	apolipoprotein A-I	Mus musculus	39-45
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Brefeldin A	142-153	apolipoprotein A-I	Mus musculus	187-193
10998247-6	2000	To induce the cellular reactivity with apoA-I, the incubation with dBcAMP required at least 6 h. Actinomycin D, cycloheximide, puromycin, and brefeldin A suppressed both the induction of apoA-I-mediated lipid release and the apoA-I specific binding to the cells.	Brefeldin A	142-153	apolipoprotein A-I	Mus musculus	187-193
10938016-3	2000	As the native apoA-I protein disappeared from the circulation, higher molecular weight forms of apoA-I appeared, some of which contained epitopes recognized by an antibody (EO6) that recognizes oxidized phospholipids.	eo6	173-176	apolipoprotein A-I	Mus musculus	14-20
10938016-3	2000	As the native apoA-I protein disappeared from the circulation, higher molecular weight forms of apoA-I appeared, some of which contained epitopes recognized by an antibody (EO6) that recognizes oxidized phospholipids.	eo6	173-176	apolipoprotein A-I	Mus musculus	96-102
10938016-3	2000	As the native apoA-I protein disappeared from the circulation, higher molecular weight forms of apoA-I appeared, some of which contained epitopes recognized by an antibody (EO6) that recognizes oxidized phospholipids.	Phospholipids	203-216	apolipoprotein A-I	Mus musculus	96-102
11004510-9	2000	ABC1 was upregulated in RAW cells by cAMP, concurrent with the cAMP induction of lipid efflux to apolipoprotein A1.	Cyclic AMP	63-67	apolipoprotein A-I	Mus musculus	97-114
10866832-8	2000	Hepatic apoA-I mRNA decreased 30% in NTg and 180% in apoAI-Tg mice.	Nitroglycerin	37-40	apolipoprotein A-I	Mus musculus	8-14
10866832-17	2000	These studies suggest that dietary cholate regulates plasma levels of apoA-I primarily by a transcriptional mechanism via a putative bile acid response element involving a negative regulator of apoA-I, and partly by an unidentified post-transcriptional mechanism.	Cholates	35-42	apolipoprotein A-I	Mus musculus	70-76
10866832-17	2000	These studies suggest that dietary cholate regulates plasma levels of apoA-I primarily by a transcriptional mechanism via a putative bile acid response element involving a negative regulator of apoA-I, and partly by an unidentified post-transcriptional mechanism.	Cholates	35-42	apolipoprotein A-I	Mus musculus	194-200
10866832-17	2000	These studies suggest that dietary cholate regulates plasma levels of apoA-I primarily by a transcriptional mechanism via a putative bile acid response element involving a negative regulator of apoA-I, and partly by an unidentified post-transcriptional mechanism.	Bile Acids and Salts	133-142	apolipoprotein A-I	Mus musculus	70-76
10858447-5	2000	The results show that apoA-I in apoA-I/palmitoyl-oleoylphosphatidylcholine discs, HDL(3), or in a lipid-free state binds to mSR-BI with high affinity (K(d) congruent with 5-8 microgram/ml).	1-palmitoyl-2-oleoylphosphatidylcholine	39-74	apolipoprotein A-I	Mus musculus	22-28
10858447-5	2000	The results show that apoA-I in apoA-I/palmitoyl-oleoylphosphatidylcholine discs, HDL(3), or in a lipid-free state binds to mSR-BI with high affinity (K(d) congruent with 5-8 microgram/ml).	1-palmitoyl-2-oleoylphosphatidylcholine	39-74	apolipoprotein A-I	Mus musculus	32-38
10858447-7	2000	When complexed with dimyristoylphosphatidylcholine, the N-terminal and C-terminal CNBr fragments of apoA-I each bound to SR-BI in a saturable, high affinity manner, and each cross-linked efficiently to mSR-BI.	Dimyristoylphosphatidylcholine	20-50	apolipoprotein A-I	Mus musculus	100-106
10832100-4	2000	The peritoneal macrophages were assayed for apoA-I binding, apoA-I-mediated release of cellular cholesterol and phospholipid and the reduction by apoA-I of the ACAT-available intracellular cholesterol pool.	Phospholipids	112-124	apolipoprotein A-I	Mus musculus	60-66
10832100-4	2000	The peritoneal macrophages were assayed for apoA-I binding, apoA-I-mediated release of cellular cholesterol and phospholipid and the reduction by apoA-I of the ACAT-available intracellular cholesterol pool.	Phospholipids	112-124	apolipoprotein A-I	Mus musculus	60-66
10766851-0	2000	Single repeat deletion in ApoA-I blocks cholesterol esterification and results in rapid catabolism of delta6 and wild-type ApoA-I in transgenic mice.	Cholesterol	40-51	apolipoprotein A-I	Mus musculus	26-32
10766851-6	2000	However, in the absence of endogenous mouse apoA-I, Delta6 apoA-I was found exclusively in cholesterol ester-poor HDL, and lipid-free HDL fractions.	Cholesterol Esters	91-108	apolipoprotein A-I	Mus musculus	59-65
10766851-9	2000	In summary, these data show a domain corresponding to apoA-I repeat 6 is responsible for providing an essential conformation for LCAT catalyzed generation of cholesterol esters.	Cholesterol Esters	158-176	apolipoprotein A-I	Mus musculus	54-60
10766851-10	2000	Deletion of apoA-I repeat 6 not only blocks normal levels of cholesterol esterification but also exerts a dominant inhibition on the ability of wild-type apoA-I to activate LCAT in vivo.	Cholesterol	61-72	apolipoprotein A-I	Mus musculus	12-18
10671546-5	2000	In contrast, wt apoA-I and Delta4-5A-I produced significant increases in HDL cholesteryl ester.	Cholesterol Esters	77-94	apolipoprotein A-I	Mus musculus	16-22
10720173-10	2000	Ten-month-old mice fed perilla oil had a significantly greater ratio of apolipoprotein A-I (ApoA-I) to ApoA-II than those fed safflower oil.	perilla seed oil	23-34	apolipoprotein A-I	Mus musculus	72-90
10720173-10	2000	Ten-month-old mice fed perilla oil had a significantly greater ratio of apolipoprotein A-I (ApoA-I) to ApoA-II than those fed safflower oil.	perilla seed oil	23-34	apolipoprotein A-I	Mus musculus	92-98
10933584-5	2000	Addition of HDL3, apoA-I, or apoE3 to the medium led to significant cholesterol efflux, which was less efficient in apoE(-/-) macrophages than in apoE(+/+) macrophages.	Cholesterol	68-79	apolipoprotein A-I	Mus musculus	18-24
10933584-8	2000	Furthermore, in [(14)C]arachidonate labeling experiments cholesterol arachidonate hydrolysis was higher in apoE(+/+) macrophages than in apoE(-/-) macrophages in the presence of cholesterol efflux mediated by HDL3 or apoA-I.	cholesteryl arachidonate	57-81	apolipoprotein A-I	Mus musculus	217-223
10933584-8	2000	Furthermore, in [(14)C]arachidonate labeling experiments cholesterol arachidonate hydrolysis was higher in apoE(+/+) macrophages than in apoE(-/-) macrophages in the presence of cholesterol efflux mediated by HDL3 or apoA-I.	Cholesterol	57-68	apolipoprotein A-I	Mus musculus	217-223
10587455-1	1999	The apolipoprotein A-IMilano (apoA-IM) is a molecular variant of apoA-I characterized by the Arg(173)--&gt;Cys substitution, resulting in the formation of homodimers A-IM/A-IM.	Arginine	93-96	apolipoprotein A-I	Mus musculus	30-36
10587455-1	1999	The apolipoprotein A-IMilano (apoA-IM) is a molecular variant of apoA-I characterized by the Arg(173)--&gt;Cys substitution, resulting in the formation of homodimers A-IM/A-IM.	Cysteine	107-110	apolipoprotein A-I	Mus musculus	30-36
10587455-3	1999	To investigate whether the structural changes in A-IM/A-IM affect apoA-I capacity for cell cholesterol uptake, we tested the ability of four reconstituted HDL (rHDL), that contained either apoA-I or A-IM/A-IM, to remove cholesterol from Fu5AH hepatoma cells and cholesterol-loaded murine primary macrophages (MPM).	Cholesterol	91-102	apolipoprotein A-I	Mus musculus	66-72
10587455-5	1999	The small A-IM/A-IM rHDL were more efficient than the corresponding apoA-I particles as acceptors of membrane cholesterol from Fu5AH cells and MPM, and as inhibitors of cholesterol esterification in MPM.	Cholesterol	110-121	apolipoprotein A-I	Mus musculus	68-74
10581205-8	1999	Further, using Western blot analysis and protein sequencing techniques, we have identified a specific serum component, apolipoprotein-A1 (apo-A1), as a protein in serum that binds selectively to silica, thus leading to the altered chemokine response.	Silicon Dioxide	195-201	apolipoprotein A-I	Mus musculus	119-136
10581205-8	1999	Further, using Western blot analysis and protein sequencing techniques, we have identified a specific serum component, apolipoprotein-A1 (apo-A1), as a protein in serum that binds selectively to silica, thus leading to the altered chemokine response.	Silicon Dioxide	195-201	apolipoprotein A-I	Mus musculus	138-144
10581205-9	1999	We also found that apo-A1 not only binds to silica but also binds to other nonfibrous and fibrous particles such as titanium dioxide and asbestos.	Silicon Dioxide	44-50	apolipoprotein A-I	Mus musculus	19-25
10581205-9	1999	We also found that apo-A1 not only binds to silica but also binds to other nonfibrous and fibrous particles such as titanium dioxide and asbestos.	titanium dioxide	116-132	apolipoprotein A-I	Mus musculus	19-25
10500181-0	1999	Cholesterol efflux to apolipoprotein AI involves endocytosis and resecretion in a calcium-dependent pathway.	Cholesterol	0-11	apolipoprotein A-I	Mus musculus	22-39
10500181-0	1999	Cholesterol efflux to apolipoprotein AI involves endocytosis and resecretion in a calcium-dependent pathway.	Calcium	82-89	apolipoprotein A-I	Mus musculus	22-39
10500181-3	1999	In the present study, using primarily apolipoprotein AI (apoAI) as the acceptor, cAMP-dependent cholesterol efflux to apolipoprotein acceptors was associated with apoAI binding to coated pits, cellular uptake, and resecretion.	Cyclic AMP	81-85	apolipoprotein A-I	Mus musculus	38-55
10500181-3	1999	In the present study, using primarily apolipoprotein AI (apoAI) as the acceptor, cAMP-dependent cholesterol efflux to apolipoprotein acceptors was associated with apoAI binding to coated pits, cellular uptake, and resecretion.	Cholesterol	96-107	apolipoprotein A-I	Mus musculus	38-55
10479665-0	1999	Human serum Paraoxonase/Arylesterase"s retained hydrophobic N-terminal leader sequence associates with HDLs by binding phospholipids : apolipoprotein A-I stabilizes activity.	Phospholipids	119-132	apolipoprotein A-I	Mus musculus	135-153
10446067-11	1999	This may be due to "dilution" of apoE secreted by the MPMs and is consistent with our observation that the addition of exogenous apoE or apoA-I inhibits FC crystal formation in J774 macrophage foam cells cotreated with CP-113,818 plus CPT-cAMP.	CP 113	219-225	apolipoprotein A-I	Mus musculus	137-143
10446067-11	1999	This may be due to "dilution" of apoE secreted by the MPMs and is consistent with our observation that the addition of exogenous apoE or apoA-I inhibits FC crystal formation in J774 macrophage foam cells cotreated with CP-113,818 plus CPT-cAMP.	cpt-camp	235-243	apolipoprotein A-I	Mus musculus	137-143
10543393-0	1999	Apolipoprotein A-I (R151C)Paris is defective in activation of lecithin: cholesterol acyltransferase but not in initial lipid binding, formation of reconstituted lipoproteins, or promotion of cholesterol efflux.	Cholesterol	72-83	apolipoprotein A-I	Mus musculus	0-18
10543393-1	1999	ApoA-I(R151)Paris is a natural apolipoprotein (apo) A-I variant that is associated with low levels of high-density lipoprotein cholesterol (HDL-cholesterol) and the partial deficiency of lecithin:cholesterol acyl-transferase (LCAT) in the plasma of heterozygous carriers.	density lipoprotein cholesterol	107-138	apolipoprotein A-I	Mus musculus	0-6
10543393-1	1999	ApoA-I(R151)Paris is a natural apolipoprotein (apo) A-I variant that is associated with low levels of high-density lipoprotein cholesterol (HDL-cholesterol) and the partial deficiency of lecithin:cholesterol acyl-transferase (LCAT) in the plasma of heterozygous carriers.	Cholesterol	127-138	apolipoprotein A-I	Mus musculus	0-6
10543393-4	1999	Normal apoA-I and apoA-I(R151C)Paris cleared DMPC emulsions at equal rates.	Dimyristoylphosphatidylcholine	45-49	apolipoprotein A-I	Mus musculus	7-13
10543393-4	1999	Normal apoA-I and apoA-I(R151C)Paris cleared DMPC emulsions at equal rates.	Dimyristoylphosphatidylcholine	45-49	apolipoprotein A-I	Mus musculus	18-24
10543393-8	1999	During incubations for 10 min and 360 min, normal apoA-I/DPPC complexes and apoA-I(R151C)Paris/DPPC complexes were equally efficient in releasing biosynthetic cholesterol from SMCs.	1,2-Dipalmitoylphosphatidylcholine	95-99	apolipoprotein A-I	Mus musculus	76-82
10543393-8	1999	During incubations for 10 min and 360 min, normal apoA-I/DPPC complexes and apoA-I(R151C)Paris/DPPC complexes were equally efficient in releasing biosynthetic cholesterol from SMCs.	Cholesterol	159-170	apolipoprotein A-I	Mus musculus	76-82
10543393-9	1999	In the lipid-free form, apoA-I(R151C)Paris induced normal hydrolysis of cholesteryl esters and normal cholesterol efflux from lipid-loaded mouse-peritoneal macrophages.	Cholesterol Esters	72-90	apolipoprotein A-I	Mus musculus	24-30
10543393-9	1999	In the lipid-free form, apoA-I(R151C)Paris induced normal hydrolysis of cholesteryl esters and normal cholesterol efflux from lipid-loaded mouse-peritoneal macrophages.	Cholesterol	102-113	apolipoprotein A-I	Mus musculus	24-30
10543393-10	1999	In conclusion, in addition to its ability to form homo- and heterodimers, apoA-I(R151C)Paris is characterized by defective LCAT-cofactor activity but by normal lipid binding and cholesterol-efflux-promoting abilities.	Cholesterol	178-189	apolipoprotein A-I	Mus musculus	74-80
10386609-2	1999	Our findings indicate that HOCl (added as reagent or generated enzymatically by the myeloperoxidase/H2O2/Cl- system) damages apolipoprotein A-I, the major protein component of HDL3.	Hypochlorous Acid	27-31	apolipoprotein A-I	Mus musculus	125-143
10386609-2	1999	Our findings indicate that HOCl (added as reagent or generated enzymatically by the myeloperoxidase/H2O2/Cl- system) damages apolipoprotein A-I, the major protein component of HDL3.	Hydrogen Peroxide	100-104	apolipoprotein A-I	Mus musculus	125-143
10364075-0	1999	A novel mutant, ApoA-I nichinan (Glu235-->0), is associated with low HDL cholesterol levels and decreased cholesterol efflux from cells.	nichinan	23-31	apolipoprotein A-I	Mus musculus	16-22
10364075-0	1999	A novel mutant, ApoA-I nichinan (Glu235-->0), is associated with low HDL cholesterol levels and decreased cholesterol efflux from cells.	Cholesterol	73-84	apolipoprotein A-I	Mus musculus	16-22
10364075-0	1999	A novel mutant, ApoA-I nichinan (Glu235-->0), is associated with low HDL cholesterol levels and decreased cholesterol efflux from cells.	Cholesterol	106-117	apolipoprotein A-I	Mus musculus	16-22
10364075-2	1999	ApoA-I (Glu235-->0) Nichinan was caused by a 3-bp deletion of nucleotides 1998 through 2000 in exon 4 of the apoA-I gene.	nichinan	20-28	apolipoprotein A-I	Mus musculus	0-6
10364075-2	1999	ApoA-I (Glu235-->0) Nichinan was caused by a 3-bp deletion of nucleotides 1998 through 2000 in exon 4 of the apoA-I gene.	nichinan	20-28	apolipoprotein A-I	Mus musculus	109-115
10407497-2	1999	The role of high density lipoprotein (HDL) and apolipoprotein A-I (apo A-I)in promoting cholesterol efflux from cultured cells and attenuation of development of atherosclerosis in transgenic (tg) animals has been well documented.	Cholesterol	88-99	apolipoprotein A-I	Mus musculus	47-65
10407497-2	1999	The role of high density lipoprotein (HDL) and apolipoprotein A-I (apo A-I)in promoting cholesterol efflux from cultured cells and attenuation of development of atherosclerosis in transgenic (tg) animals has been well documented.	Cholesterol	88-99	apolipoprotein A-I	Mus musculus	67-74