PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
1251575-3	1976	By carbodiimide treatment of human erythrocyte glycoproteins, which causes intramolecular coupling of N-acetylneuraminic acid carboxyl groups and nucleophilic centers of the glycoprotein backbone, Pr3 antigen activity is strongly increased, while Pr1 and Pr2 determinants are inactivated.	Carbodiimides	3-15	proteinase 3	Homo sapiens	197-200	
6183733-2	1982	Haemagglutination inhibition studies disclosed the subspecificity anti-Pr3, since the cold agglutinin was strongly inhibited by carbodiimide-treated erythrocyte glycoproteins.	Carbodiimides	128-140	proteinase 3	Homo sapiens	71-74	
6729936-6	1984	On the basis of an increased inhibition by sialoglycoproteins after periodate oxidation and carbodiimide treatment, respectively, three anti- Pr2 and five anti-Pr3 were found.	Carbodiimides	92-104	proteinase 3	Homo sapiens	160-163