PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
22725664-8	2012	Observation of the hydroxyl trapping properties of EdAG suggests that the busulfan metabolite EdAG may contribute to or mitigate redox-related cytotoxicity associated with the therapeutic use of busulfan, and reaffirms indicators that support a role in free radical biology for dehydroalanine-containing peptides and proteins.	Busulfan	74-82	hemogen	Homo sapiens	51-55	
22725664-8	2012	Observation of the hydroxyl trapping properties of EdAG suggests that the busulfan metabolite EdAG may contribute to or mitigate redox-related cytotoxicity associated with the therapeutic use of busulfan, and reaffirms indicators that support a role in free radical biology for dehydroalanine-containing peptides and proteins.	Busulfan	74-82	hemogen	Homo sapiens	94-98	
22725664-8	2012	Observation of the hydroxyl trapping properties of EdAG suggests that the busulfan metabolite EdAG may contribute to or mitigate redox-related cytotoxicity associated with the therapeutic use of busulfan, and reaffirms indicators that support a role in free radical biology for dehydroalanine-containing peptides and proteins.	Busulfan	195-203	hemogen	Homo sapiens	51-55	
22725664-8	2012	Observation of the hydroxyl trapping properties of EdAG suggests that the busulfan metabolite EdAG may contribute to or mitigate redox-related cytotoxicity associated with the therapeutic use of busulfan, and reaffirms indicators that support a role in free radical biology for dehydroalanine-containing peptides and proteins.	Busulfan	195-203	hemogen	Homo sapiens	94-98	
32958252-12	2020	These findings continue to support the growing concept that EdAG, an underrecognized phase II metabolite of busulfan, plays a role in untoward cellular toxicities during busulfan pharmacotherapy.	Busulfan	108-116	hemogen	Homo sapiens	60-64	
32958252-0	2020	Electrophilic reactivity of the Busulfan metabolite, EdAG, towards cellular thiols and inhibition of human thioredoxin-1.	Busulfan	32-40	hemogen	Homo sapiens	53-57	
32958252-3	2020	A phase II generated metabolite of busulfan, EdAG (gamma-glutamyldehydroalanylglycine), is a dehydroalanine analog of glutathione (GSH) with an electrophilic moiety, suggesting it may bind to proteins and disrupt biological function.	Busulfan	35-43	hemogen	Homo sapiens	45-49	
32958252-12	2020	These findings continue to support the growing concept that EdAG, an underrecognized phase II metabolite of busulfan, plays a role in untoward cellular toxicities during busulfan pharmacotherapy.	Busulfan	170-178	hemogen	Homo sapiens	60-64	
26278353-0	2015	The busulfan metabolite EdAG irreversibly glutathionylates glutaredoxins.	Busulfan	4-12	hemogen	Homo sapiens	24-28	
26278353-2	2015	Busulfan is metabolized via conjugation with glutathione (GSH) followed by intramolecular rearrangement to the GSH analog gamma-glutamyl-dehydroalanyl -glycine (EdAG).	Busulfan	0-8	hemogen	Homo sapiens	161-165	
26501085-0	2015	Supporting data for characterization of the busulfan metabolite EdAG and the Glutaredoxins that it adducts.	Busulfan	44-52	hemogen	Homo sapiens	64-68	
26501085-1	2015	This article describes data related to a research article titled "The Busulfan Metabolite EdAG Irreversibly Glutathionylates Glutaredoxins" [1].	Busulfan	70-78	hemogen	Homo sapiens	90-94	
26501085-2	2015	EdAG is an electrophilic GSH analog formed in vivo from busulfan, which is used in hematopoietic stem cell transplants.	Busulfan	56-64	hemogen	Homo sapiens	0-4