PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34425254-2	2021	AMP-activated protein kinase (AMPK) is an alphabetagamma heterotrimer which inhibits macrophage inflammation and the synthesis of fatty acids and cholesterol in the liver through phosphorylation of acetyl-CoA carboxylase (ACC) and HMG-CoA reductase (HMGCR), respectively.	Fatty Acids	130-141	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	250-255	
7959015-1	1994	AMP-activated protein kinase (AMPK) phosphorylates and inactivates acetyl-CoA carboxylase and beta-hydroxy beta-methylglutaryl-coenzyme A (HMG-CoA) reductase which are the major enzymes involved in fatty acid and lipid biosyntheses.	Fatty Acids	198-208	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	94-157	
26784936-4	2016	The fatty acid niacin conjugate 5 has been shown to be an inhibitor of the sterol regulatory element binding protein (SREBP), a key regulator of cholesterol metabolism proteins such as PCSK9, HMG-CoA reductase, ATP citrate lyase, and NPC1L1.	Fatty Acids	4-14	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	192-209	
12419552-4	2002	For example, statins modulate activation of the class-I transcription factor sterol responsive element-binding protein (SREBP), whose target genes including hydroxyl-methyl-glutaryl acetyl Coenzyme-A (HMG-CoA) reductase, HMG-CoA synthase, and the low-density lipoprotein receptor, all of which are involved in cholesterol and fatty acid metabolism.	Fatty Acids	326-336	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	157-219	
34834649-3	2021	Herein, AG fractions were tested against HMG-CoA reductase (HMGR) and fatty acid synthase (FAS), two important enzymes involved in cholesterol and fatty acid synthesis, respectively.	Fatty Acids	147-157	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	41-58	
29518109-9	2018	Decreased lipid levels at higher BMI were accompanied by downregulated expression of PPARdelta and other genes related to lipid metabolism, including those encoding acetyl-CoA carboxylase and HMG-CoA reductase, the rate-limiting enzymes for fatty acid and cholesterol synthesis, respectively.	Fatty Acids	241-251	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	192-209	
29480487-2	2018	Some of the well-known substrates of AMPK are acetyl-CoA carboxylase (ACC) and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, regulatory enzymes of fatty acid and cholesterol synthesis, respectively.	Fatty Acids	160-170	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	79-136	
26632252-7	2015	For the first time we herein identified ACACA, FASN (the key enzymes of de novo fatty acid synthesis), HMGCR (the key enzyme of de novo cholesterol synthesis) and CYP27B1 as direct targets of hsa-miR-195.	Fatty Acids	80-90	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	103-108	
25733328-6	2015	MPD also decreases the gene expressions of HMGCR, FAS and ACC for cholesterol and fatty acid synthesis.	Fatty Acids	82-92	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	43-48	
22355267-6	2012	In addition, mRNA levels of several SREBP regulated genes involved in cholesterol and fatty-acid synthesis including ACSS2, FDPS, IDI1, MVD, HMGCR, and CYP51A1 were decreased significantly with antibody treatment of primary human hepatocytes.	Fatty Acids	86-96	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	141-146