PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
9244169-3	1996	Further studies were performed to determine whether human chorionic gonadotropin (hCG) can interact with the insulin-like growth factor-I (IGF-I) signaling pathway to increase tyrosine phosphorylation of IRS-I.	Tyrosine	176-184	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85	
9244169-7	1996	The increased tyrosine phosphorylation of IRS-I seen in response to IGF-I stimulation following treatment with either hCG or forskolin was not due to an increase in IRS-I content.	Tyrosine	14-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	118-121	
9244169-9	1996	Thus, we conclude that hCG/LH and IGF-I signaling pathways "cross-talk" to increase the levels of IRS-I tyrosine phosphorylation.	Tyrosine	104-112	hypertrichosis 2 (generalised, congenital)	Homo sapiens	23-26	
7846554-6	1994	However, the suppressive effect of tyrosine on hCG- induced progesterone production was more pronounced in small luteal cells.	Tyrosine	35-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	47-50	
7973829-5	1994	Tyr had suppressive effect on hCG-induced progesterone production.	Tyrosine	0-3	hypertrichosis 2 (generalised, congenital)	Homo sapiens	30-33	
2548285-5	1989	hCG, cAMP and progesterone all could significantly increase the content of tyrosine in the suspensions, suggesting the release of "endogenous tyrosine".	Tyrosine	75-83	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3	
2548285-5	1989	hCG, cAMP and progesterone all could significantly increase the content of tyrosine in the suspensions, suggesting the release of "endogenous tyrosine".	Tyrosine	142-150	hypertrichosis 2 (generalised, congenital)	Homo sapiens	0-3	
3130224-0	1987	Effects of tyrosine and its analogues on hCG-induced progesterone production by rat corpus luteum in vitro.	Tyrosine	11-19	hypertrichosis 2 (generalised, congenital)	Homo sapiens	41-44	
16620962-3	2007	Western blot analyses indicated that treatment of trophoblastic SGHPL-5 cells and purified term trophoblasts with potentially EGF-contaminated hCG (hCG-A) resulted in auto-phosphorylation of the EGF receptor at tyrosine 1173 whereas supplementation of another urine-purified hCG preparation (hCG-B), recombinant holo-hCG or recombinant alphahCG had no effects.	Tyrosine	211-219	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146	
16620962-3	2007	Western blot analyses indicated that treatment of trophoblastic SGHPL-5 cells and purified term trophoblasts with potentially EGF-contaminated hCG (hCG-A) resulted in auto-phosphorylation of the EGF receptor at tyrosine 1173 whereas supplementation of another urine-purified hCG preparation (hCG-B), recombinant holo-hCG or recombinant alphahCG had no effects.	Tyrosine	211-219	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151	
16620962-3	2007	Western blot analyses indicated that treatment of trophoblastic SGHPL-5 cells and purified term trophoblasts with potentially EGF-contaminated hCG (hCG-A) resulted in auto-phosphorylation of the EGF receptor at tyrosine 1173 whereas supplementation of another urine-purified hCG preparation (hCG-B), recombinant holo-hCG or recombinant alphahCG had no effects.	Tyrosine	211-219	hypertrichosis 2 (generalised, congenital)	Homo sapiens	148-151