2篇
您的检索式：作者名="Jae Hun Cheong"
|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Bile acid increases expression of the histamine-producing enzyme,histidine decarboxylase,in gastric cells显示文摘AIM:To investigate the effect of bile acid on the expression of histidine decarboxylase(HDC),which is a major enzyme involved in histamine production,and gene expression of gastric transcription factors upon cooperative activation.METHODS:HDC expression was examined by immunohistochemistry,reverse transcriptase polymerase chain reaction,and promoter assay in human gastric precancerous tissues,normal stomach tissue,and gastric cancer cell lines.The relationship between gastric precancerous state and HDC expression induced by bile acid was determined.The association between the expression of HDC and various specific transcription factors in gastric cells was also evaluated.MKN45 and AGS human gastric carcinoma cell lines were transfected with farnesoid X receptor(FXR),small heterodimer partner(SHP),and caudal-type homeodomain transcription factor(CDX)1 expression plasmids.The effects of various transcription factors on HDC expression were monitored by luciferase-reporter promoter assay.RESULTS:Histamine production and secretion in the stomach play critical roles in gastric acid secretion and in the pathogenesis of gastric diseases.Here,we show that bile acid increased the expression of HDC,which is a rate-limiting enzyme of the histamine production pathway.FXR was found to be a primary regulatory transcription factor for bile acid-induced HDC expression.In addition,the transcription factors CDX1 and SHP synergistically enhanced bile acid-induced elevation of HDC gene expression.We confirmed similar expression patterns for HDC,CDX1,and SHP in patient tissues.CONCLUSION:HDC production in the stomach is associated with bile acid exposure and its related transcriptional regulation network of FXR,SHP,and CDX1. | Hye Jin Ku Hye Young Kim Hyeong Hoe Kim Hee Ju Park Jae Hun Cheong | 2014 | World Journal of Gastroenterology2014，20，1： | 3 |
| 2 | Sorafenib suppresses hepatitis B virus gene expression viainhibiting JNK pathway显示文摘Aim:Hepatitis B virus(HBV)infection is a major cause of chronic liver diseases.Sorafenib is a multikinase inhibitor and an approved anti-liver cancer drug.Here we demonstrated the antiviral effect of sorafenib on HBV gene expression.Methods:To investigate the effect of sorafenib on HBV gene expression,a luciferase assay was performed with×1.3 Cp-luciferase HBV construct and reverse transcriptase polymerase chain reaction(PCR),real-time PCR,and Western blotting analyses were performed using HepG2 cells derived from hepatocellular carcinoma and Chang liver cells derived from a normal liver tissue.Results:Sorafenib suppressed HBV gene expression via inhibiting the JNK pathway.In this process,the farnesoid X receptor(FXR),a transcription factor that has been reported to increase HBV replication and gene expression,was under control of the JNK pathway.Notably,JNK activation increased FXR protein levels,not mRNA levels.Conclusion:Sorafenib suppressed HBV gene expression via inhibiting the JNK pathway,which regulates FXR activity. | Hyun Kook Cho Ju Ran Kim So Young Kim Yi Yi Kyaw Aye Aye Win Jae Hun Cheong | 2015 | Hepatoma Research2015，1，1： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员