PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
15661368-1	2005	The purpose of this study was to determine whether activation of ATP-sensitive K+ (KATP) channels with diazoxide (DIZ) is able to prevent the cleavage of cytosolic mu-calpain and abrogate the elevation of nuclear c-Fos and c-Jun protein (c-Fos, c-Jun) expressions after hypoxic-ischemia (HI) in brain.	Diazoxide	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218	
15661368-1	2005	The purpose of this study was to determine whether activation of ATP-sensitive K+ (KATP) channels with diazoxide (DIZ) is able to prevent the cleavage of cytosolic mu-calpain and abrogate the elevation of nuclear c-Fos and c-Jun protein (c-Fos, c-Jun) expressions after hypoxic-ischemia (HI) in brain.	Diazoxide	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	238-243	
14725963-6	2004	Interestingly, low c-Fos and c-Jun expressions were found both in diazoxide and EA groups, 24 h after HI.	Diazoxide	66-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24	
32817784-6	2020	Confocal microscopy revealed that diazoxide also led to nuclear translocation of the transcription factors c-Fos and NFkappaB, which was also blocked by NAC or 5-HD.	Diazoxide	34-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112	
32817784-8	2020	Conclusions: Our results suggest that opening mitochondrial potassium ATP channels with diazoxide upregulates the expression of STIM1 and Orai1 by de novo synthesis by a mechanism that involves NFkB, c-Fos, and ROS via MAPK/ERK signaling.	Diazoxide	88-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	200-205