PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21176161-6	2010	RESULTS: Loss of functional XPB or XPD but not XPA led to enhanced sensitivity towards H2O2-induced cell death.	Hydrogen Peroxide	87-91	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	35-38	
21176161-7	2010	XP-deficient lymphoblastoid cells exhibited increased susceptibility to H2O2-induced DNA damage with XPD showing the highest susceptibility and lowest repair capacity.	Hydrogen Peroxide	72-76	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	101-104	
21176161-9	2010	XPA- and XPB-deficient lymphoblastoid cells also showed differential regulation of XPD following H2O2 treatment.	Hydrogen Peroxide	97-101	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	83-86	
14688028-10	2004	The nature of these species was investigated and revealed that cancer prone XPD fibroblasts produced higher amounts of O2*- and H2O2 and lower amounts of NO* and ONOO than normal fibroblasts.	Hydrogen Peroxide	128-132	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	76-79	
35483790-4	2022	Therefore, we sought to investigate the role of XPD in oxidative DNA damage-repair by treating primary fibroblasts derived from a patient suffering from Xeroderma Pigmentosum D, with hydrogen peroxide.	Hydrogen Peroxide	183-200	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	48-51	
35483790-4	2022	Therefore, we sought to investigate the role of XPD in oxidative DNA damage-repair by treating primary fibroblasts derived from a patient suffering from Xeroderma Pigmentosum D, with hydrogen peroxide.	Hydrogen Peroxide	183-200	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	153-176