PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
3093007-5	1986	Prior to coupling, the subunits of hCG were crosslinked with 1-ethyl-3-(dimethylamino propyl) carbodiimide and the sialic acid residues were subjected to periodate oxidation to yield aldehyde groups which could react with the hydrazides of the gel.	N-Acetylneuraminic Acid	115-126	hypertrichosis 2 (generalised, congenital)	Homo sapiens	35-38	
29645229-16	1998	Sialic acid content in choriocarcinoma hCG was extremely lower compared to that in normal hCG.	N-Acetylneuraminic Acid	0-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42	
7745007-9	1995	Further studies with hCG, asialo-hCG, asialoagalacto-hCG, and deglycosylated hCG revealed that removal of sialic acid caused a marked increase in both its affinity for hTSHr and its cAMP-releasing potency, whereas removal of further carbohydrate, although it slightly enhanced receptor binding, was detrimental to adenylate cyclase activation.	N-Acetylneuraminic Acid	106-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	21-24	
7745007-9	1995	Further studies with hCG, asialo-hCG, asialoagalacto-hCG, and deglycosylated hCG revealed that removal of sialic acid caused a marked increase in both its affinity for hTSHr and its cAMP-releasing potency, whereas removal of further carbohydrate, although it slightly enhanced receptor binding, was detrimental to adenylate cyclase activation.	N-Acetylneuraminic Acid	106-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36	
7745007-9	1995	Further studies with hCG, asialo-hCG, asialoagalacto-hCG, and deglycosylated hCG revealed that removal of sialic acid caused a marked increase in both its affinity for hTSHr and its cAMP-releasing potency, whereas removal of further carbohydrate, although it slightly enhanced receptor binding, was detrimental to adenylate cyclase activation.	N-Acetylneuraminic Acid	106-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36	
7745007-9	1995	Further studies with hCG, asialo-hCG, asialoagalacto-hCG, and deglycosylated hCG revealed that removal of sialic acid caused a marked increase in both its affinity for hTSHr and its cAMP-releasing potency, whereas removal of further carbohydrate, although it slightly enhanced receptor binding, was detrimental to adenylate cyclase activation.	N-Acetylneuraminic Acid	106-117	hypertrichosis 2 (generalised, congenital)	Homo sapiens	33-36	
14562685-2	2003	The purified hCG-preparations from various blood group donors were shown to differ in their sialic acid content.	N-Acetylneuraminic Acid	92-103	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16	
9833611-16	1998	Sialic acid content in choriocarcinoma hCG was extremely lower compared to that in normal hCG.	N-Acetylneuraminic Acid	0-11	hypertrichosis 2 (generalised, congenital)	Homo sapiens	39-42	
6245583-5	1980	Removal of sialic acid from hCG increased this rate; removal of other carbohydrate residues decreased it.	N-Acetylneuraminic Acid	11-22	hypertrichosis 2 (generalised, congenital)	Homo sapiens	28-31	
7460824-6	1981	Thus, sialic acid alone and/or differences in subunit assembly seem to be responsible for the electrophoretic heterogeneity of highly purified hCG.	N-Acetylneuraminic Acid	6-17	hypertrichosis 2 (generalised, congenital)	Homo sapiens	143-146	
217642-1	1978	Removal of the sugar residues internal to sialic acid from the hCG molecule markedly diminished the ability of hCG to stimulate cAMP accumulation by porcine granulosa cells during a 30-min incubation period.	N-Acetylneuraminic Acid	42-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	63-66	
217642-1	1978	Removal of the sugar residues internal to sialic acid from the hCG molecule markedly diminished the ability of hCG to stimulate cAMP accumulation by porcine granulosa cells during a 30-min incubation period.	N-Acetylneuraminic Acid	42-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	111-114	
217642-2	1978	At the same time, removal of sugars internal to sialic acid enabled the resulting hCG derivatives to become competitive inhibitors of hCG stimulation of cAMP accumulation.	N-Acetylneuraminic Acid	48-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	82-85	
217642-2	1978	At the same time, removal of sugars internal to sialic acid enabled the resulting hCG derivatives to become competitive inhibitors of hCG stimulation of cAMP accumulation.	N-Acetylneuraminic Acid	48-59	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137	
217642-4	1978	It would, therefore, seem that hCG with sugars internal to sialic acid removed is able to bind to the receptor, but that, once bound, it is unable to activate adenylate cyclase.	N-Acetylneuraminic Acid	59-70	hypertrichosis 2 (generalised, congenital)	Homo sapiens	31-34	
5063546-0	1972	Biological properties of hCG after removal of terminal sialic acid and galactose residues.	N-Acetylneuraminic Acid	55-66	hypertrichosis 2 (generalised, congenital)	Homo sapiens	25-28