PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
23511120-8	2013	Diphenyleneiodonium (a nonspecific NOX inhibitor) or small interfering RNA for p22phox prevented glyLDL-induced increases in the levels of NOX4, HSF1, or PAI-1 in MEFs.	diphenyleneiodonium	0-19	NADPH oxidase 4	Mus musculus	139-143	
20185797-10	2010	Nox4 is primarily localized in mitochondria and upregulation of Nox4 enhanced both rotenone- and diphenyleneiodonium-sensitive O(2)(-) production in mitochondria.	diphenyleneiodonium	97-116	NADPH oxidase 4	Mus musculus	0-4	
22784094-7	2013	Furthermore, NADPH oxidase 4 (Nox4) expression was induced in ASCs by UVB irradiation, and Nox4 silencing by small interfering RNA, like DPI, significantly reduced UVB-induced ROS generation.	diphenyleneiodonium	137-140	NADPH oxidase 4	Mus musculus	91-95	
22749956-4	2012	Nox4 contributed more than 80% of diphenylene iodonium-sensitive H(2)O(2) formation of freshly isolated tubules determined by Amplex Red assay.	diphenyleneiodonium	34-54	NADPH oxidase 4	Mus musculus	0-4	
21029048-12	2011	Dominant-negative Nox4 also mimicked this effect of NAC and DPI.	diphenyleneiodonium	60-63	NADPH oxidase 4	Mus musculus	18-22	
20185797-10	2010	Nox4 is primarily localized in mitochondria and upregulation of Nox4 enhanced both rotenone- and diphenyleneiodonium-sensitive O(2)(-) production in mitochondria.	diphenyleneiodonium	97-116	NADPH oxidase 4	Mus musculus	64-68	
19925862-8	2010	The induction of chronic oxidative stress in HSCs by TBI is probably attributable to the up-regulation of NADPH oxidase 4 (NOX4), because irradiated HSCs expressed an increased level of NOX4, and inhibition of NOX activity with diphenylene iodonium but not apocynin significantly reduced TBI-induced increases in ROS production, oxidative DNA damage, and DNA DSBs in HSCs and dramatically improved HSC clonogenic function.	diphenyleneiodonium	228-248	NADPH oxidase 4	Mus musculus	106-121	
19925862-8	2010	The induction of chronic oxidative stress in HSCs by TBI is probably attributable to the up-regulation of NADPH oxidase 4 (NOX4), because irradiated HSCs expressed an increased level of NOX4, and inhibition of NOX activity with diphenylene iodonium but not apocynin significantly reduced TBI-induced increases in ROS production, oxidative DNA damage, and DNA DSBs in HSCs and dramatically improved HSC clonogenic function.	diphenyleneiodonium	228-248	NADPH oxidase 4	Mus musculus	123-127	
19925862-8	2010	The induction of chronic oxidative stress in HSCs by TBI is probably attributable to the up-regulation of NADPH oxidase 4 (NOX4), because irradiated HSCs expressed an increased level of NOX4, and inhibition of NOX activity with diphenylene iodonium but not apocynin significantly reduced TBI-induced increases in ROS production, oxidative DNA damage, and DNA DSBs in HSCs and dramatically improved HSC clonogenic function.	diphenyleneiodonium	228-248	NADPH oxidase 4	Mus musculus	186-190	
35413508-5	2022	Similarly, NOX4 inhibitor diphenyleneiodonium chloride (DPI) induces concomitant downregulation of the mitochondrial and glycolytic metabolism.	diphenyleneiodonium	26-54	NADPH oxidase 4	Mus musculus	11-15	
35413508-5	2022	Similarly, NOX4 inhibitor diphenyleneiodonium chloride (DPI) induces concomitant downregulation of the mitochondrial and glycolytic metabolism.	diphenyleneiodonium	56-59	NADPH oxidase 4	Mus musculus	11-15	
35413508-11	2022	Collectively, our work shows that the combinatorial therapy of autophagy activator THP and NOX4 inhibitor DPI may be considered as a therapeutic avenue against HCC.	diphenyleneiodonium	106-109	NADPH oxidase 4	Mus musculus	91-95