PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
23671120-7	2013	Because depletion of PRMT5 lowers hepatic glucose production and gluconeogenic gene expression, these results demonstrate how a chromatin-modifying enzyme regulates a metabolic program through epigenetic changes that impact the phosphorylation of a transcription factor in response to hormonal stimuli.	Glucose	42-49	protein arginine methyltransferase 5	Homo sapiens	21-26	
27708221-0	2016	PRMT5 competitively binds to CDK4 to promote G1-S transition upon glucose induction in hepatocellular carcinoma.	Glucose	66-73	protein arginine methyltransferase 5	Homo sapiens	0-5	
27708221-2	2016	Here, we report that upon glucose induction, protein arginine methyltransferase 5 (PRMT5) exerts a profound effect on the G1-S cell cycle progression via directly interacting with cyclin dependent kinase 4 (CDK4) in hepatocellular carcinoma (HCC).	Glucose	26-33	protein arginine methyltransferase 5	Homo sapiens	45-81	
27708221-2	2016	Here, we report that upon glucose induction, protein arginine methyltransferase 5 (PRMT5) exerts a profound effect on the G1-S cell cycle progression via directly interacting with cyclin dependent kinase 4 (CDK4) in hepatocellular carcinoma (HCC).	Glucose	26-33	protein arginine methyltransferase 5	Homo sapiens	83-88	
27708221-4	2016	Mechanistically, glucose promotes the interaction between PRMT5 and CDK4, which leads to activation of CDK4-RB-E2F-mediated transcription via releasing CDKN2A from CDK4.	Glucose	17-24	protein arginine methyltransferase 5	Homo sapiens	58-63	
27708221-5	2016	Moreover, the PRMT5 competitive inhibition of the interaction between CDK4 and CDKN2A is important for glucose-induced growth of HCC cells.	Glucose	103-110	protein arginine methyltransferase 5	Homo sapiens	14-19