PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
18779575-4	2008	Defects in MMACHC represent the most common cause of inborn errors of B(12) metabolism, and our results explain the observation that fibroblasts from these patients are poorly responsive to vitamin B(12) but show some metabolic correction with aquocobalamin, a cofactor form lacking the cyanide ligand, which is mirrored by patients showing poorer clinical responsiveness to cyano- versus aquocobalamin.	aquacobalamin	244-257	metabolism of cobalamin associated C	Homo sapiens	11-17