PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30033048-2	2018	Our previous studies have demonstrated that high blood ammonia levels may lead to hepatocyte apoptosis, as NH4Cl loading caused metabolic acidosis and an increase in sodium-hydrogen exchanger isoform 1 (NHE1).	Ammonium Chloride	107-112	solute carrier family 9 member A1	Homo sapiens	203-207	
7511337-1	1994	It has recently been demonstrated that uremic metabolic acidosis and experimental metabolic acidosis caused by ingestion of ammonium chloride coincide with increased Na(+)-H+ exchanger (NHE-1) activity in human blood cells.	Ammonium Chloride	124-141	solute carrier family 9 member A1	Homo sapiens	186-191	
30033048-3	2018	In this study, we established a hyperammonia hepatocyte model to determine the role of NHE1 in the regulation of hepatocyte apoptosis induced by NH4Cl.	Ammonium Chloride	145-150	solute carrier family 9 member A1	Homo sapiens	87-91	
30033048-5	2018	The results showed that intracellular pH dropped and NHE1 activity increased in hepatocytes under NH4Cl treatment.	Ammonium Chloride	98-103	solute carrier family 9 member A1	Homo sapiens	53-57	
30033048-6	2018	As expected, decreased pHi induced by NH4Cl was associated with increased apoptosis, low cell proliferation and ATP depletion, which was exacerbated by exposure to the NHE1 inhibitor cariporide.	Ammonium Chloride	38-43	solute carrier family 9 member A1	Homo sapiens	168-172	
30033048-7	2018	We also found that NH4Cl treatment stimulated PI3K and Akt phosphorylation and this effect was considerably reduced by NHE1 inhibition.	Ammonium Chloride	19-24	solute carrier family 9 member A1	Homo sapiens	119-123	
28055960-8	2017	NHE1-ko abolished recovery from NH4Cl pre-pulse cellular acid loading while both NHE1 and CA9 knockout reduced resting pHi.	Ammonium Chloride	32-37	solute carrier family 9 member A1	Homo sapiens	0-4