PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
20017940-12	2009	CONCLUSIONS: The study data indicate that the therapeutic mechanism of chloroquine action may be attributable, at least in part, to reduction of ASB activity, leading to increased chondroitin-4-sulphation in human placental, bronchial epithelial, and cerebrovascular cells.	chondroitin-4	180-193	arylsulfatase B	Homo sapiens	145-148	
20152898-4	2010	In this report, we present the role of ASB in the regulation of the kininogen-bradykinin axis owing to its effect on chondroitin-4-sulfation and the interaction of C4S with kininogen.	chondroitin-4	117-130	arylsulfatase B	Homo sapiens	39-42	
20152898-7	2010	When ASB was overexpressed, the cellular kininogen that associated with C4S declined, suggesting a vital role for chondroitin-4-sulfation in regulating the kininogen-C4S interaction.	chondroitin-4	114-127	arylsulfatase B	Homo sapiens	5-8