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 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 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