PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17342739-2	2007	The mechanisms involved are unclear but progesterone receptor (PGR) antagonists have been shown to inhibit cholesterol synthesis and induce apoptosis.	Cholesterol	107-118	progesterone receptor	Rattus norvegicus	40-61	
17342739-2	2007	The mechanisms involved are unclear but progesterone receptor (PGR) antagonists have been shown to inhibit cholesterol synthesis and induce apoptosis.	Cholesterol	107-118	progesterone receptor	Rattus norvegicus	63-66	
17342739-5	2007	It has been suggested that PGR antagonists in a similar manner induce apoptosis by decreasing cholesterol synthesis and thereby protein isoprenylation.	Cholesterol	94-105	progesterone receptor	Rattus norvegicus	27-30	
17342739-6	2007	In this study we hypothesized that the mechanism by which the nuclear PGR antagonist Org 31,710 induces apoptosis in rat periovulatory granulosa cells, is by decreasing cholesterol synthesis and thereby general cell protein isoprenylation.	Cholesterol	169-180	progesterone receptor	Rattus norvegicus	70-73	
17342739-12	2007	In conclusion, we demonstrate that the PGR antagonist inhibits cholesterol synthesis in granulosa cells but reduced protein isoprenylation is not the mediating mechanism of increased apoptosis as previously hypothesized.	Cholesterol	63-74	progesterone receptor	Rattus norvegicus	39-42	
15385411-0	2005	Progesterone-receptor antagonists and statins decrease de novo cholesterol synthesis and increase apoptosis in rat and human periovulatory granulosa cells in vitro.	Cholesterol	63-74	progesterone receptor	Rattus norvegicus	0-21	
15385411-8	2005	These results show that PR antagonists reduce cholesterol synthesis in periovulatory granulosa cells and that cholesterol synthesis is important for granulosa cell survival.	Cholesterol	46-57	progesterone receptor	Rattus norvegicus	24-26