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아데노바이러스를 이용한 B형 간염바이러스 X 유전자 발현에 따른 유전자 발현의 변화
주희은,한광협,류왕식 대한간학회 2002 Clinical and Molecular Hepatology(대한간학회지) Vol.8 No.4
Background/Aims: Hepatitis B virus (HBV) is the etiological factor for hepatocellular carcinoma (HCC). Numerous evidence has indicated a link between chronic infection with HBV and the development of HCC. Among the four proteins encoded by HBV, Hepatitis B virus X gene(HBx), best characterized as a transcriptional transactivator, gained attention owing to its presumptive role in oncogenesis. Further, HBx has been shown to stimulate signal transduction pathways such as Ras-MAPK pathway, NF-κB, and Src kinase. The pleiotropic events caused by HBx may be the key to understanding the HBV-mediated oncogenicity. However, the specific roles of HBx in oncogenesis remain largely elusive. To explore the role of HBx in hepatocarcinogenesis, we examined the deregulation of host genes induced by HBx expression. Methods: HBx was ectopically expressed in HepG2 cells using a recombinant adenovirus to transiently express HBx. Gene expression profiling of HBx was conducted on cDNA microarrays that contained 1,028 cDNAs. Results: A number of oncogenes and genes that are involved in cell growth, DNA repair, cell cycle regulation, and cell motility were deregulated by HBx. Conclusions: Theses results suggest that HBx regulates transcription in a way that contributes to the proliferation of hepatocytes, a probable early event of HCC.(Korean J Hepatol 2002;8:371-380) 목적: B형 간염바이러스(Hepatitis B virus, HBV)는 간세포암을 일으키는 주요인이다. HBV가 encoding하는 X 단백질(HBx)은 잠재적으로 종양유발의 성질을 가지고 있으며 transcriptional transactivator로 알려져 있다. 또한 HBx는 pleio- tropic signaling activitor로, Ras-Raf-MAPK 체계, NF-κB, Src kinase, Ca++ signaling 등의 신호전달체계를 활성화시킴으로써 세포사멸을 유도하고 세포증식을 촉진한다. HBx의 이러한 특성으로 HBV와 관련한 종양유발에 HBx가 중요한 역할을 할 것이라고 추정된다. 하지만 어떠한 기작으로 HBx가 종양유발에 기여하는지에 대해서는 아직 명확하지 않다. 본 연구에서는 HBx가 간세포암 발생에 어떤 역할을 하는지 알아보기 위해서, HBx를 발현시킬 때 전사가 어떻게 deregulation되는지 알아보고자 하였다. 대상과 방법: 1,028개의 cDNA 클론을 가지고 있는 cDNA microarray를 이용하여 HepG2 세포에 HBx를 유전자재조합 아데노바이러스를 통해 발현시킨 후, 유전자 발현 양상을 조사하였다. 결과: HBx로 인해 oncogenes 뿐만 아니라 세포성장조절인자 및 사이토카인, DNA 재생, 세포주기, 세포 운동성에 관여하는 유전자들의 발현이 증가한 것으로 나타났다. 결론: 이러한 결과는 HBx가 세포의 성장을 촉진하는 유전자의 발현을 유도함으로써 간세포암의 형성에 기여할 것임을 시사한다.색인단어: B형 간염바이러스/B형 간염바이러스 X 유전자, 유전자재조합 아데노바이러스, cDNA microarray
아데노바이러스를 이용한 B형 간염바이러스 X 유전자 발현에 따른 유전자 발현의 변화
주회은,한광협,류왕식 대한간학회 2002 Clinical and Molecular Hepatology(대한간학회지) Vol.8 No.4
목적: B형 간염바이러스(Hepatitis B virus, HBV)는 간세포암을 일으키는 주요인이다. HBV 가 encoding하는 X 단백질(HBx)은 잠재적으로 종양유발의 성질을 가지고 있으며 transcriptional transactivator로 알려져 있다. 또한 HBx는 pleio- tropic signaling activitor로, Ras-Raf-MAPK 체계, NF-κB, Src kinase, Ca++ signaling 등의 신호전달 체계를 활성화시킴으로써 세포사멸을 유도하고 세포증식을 촉진한다. HBx의 이러한 특성으로 HBV 와 관련한 종양유발에 HBx가 중요한 역할을 할 것 이라고 추정된다. 하지만 어떠한 기작으로 HBx가 종양유발에 기여하는지에 대해서는 아직 명확하지 않다. 본 연구에서는 HBx가 간세포암 발생에 어떤 역할을 하는지 알아보기 위해서, HBx를 발현시킬 때 전사가 어떻게 deregulation되는지 알아보고자 하였다. 대상과 방법: 1,028개의 cDNA 클론을 가 지고 있는 cDNA microarray를 이용하여 HepG2 세포에 HBx를 유전자재조합 아데노바이러스를 통해 발현시킨 후, 유전자 발현 양상을 조사하였다. 결과: HBx로 인해 oncogenes 뿐만 아니라 세포성장조절 인자 및 사이토카인, DNA 재생, 세포주기, 세포 운동성에 관여하는 유전자들의 발현이 증가한 것으로 나타났다. 결론: 이러한 결과는 HBx가 세포의 성장을 촉진하는 유전자의 발현을 유도함으로써 간세포 암의 형성에 기여할 것임을 시사한다. Background/Aims: Hepatitis B virus (HBV) is the etiological factor for hepatocellular carcinoma (HCC). Numerous evidence has indicated a link between chronic infection with HBV and the development of HCC. Among the four proteins encoded by HBV, Hepatitis B virus X gene(HBx), best characterized as a transcriptional transactivator, gained attention owing to its presumptive role in oncogenesis. Further, HBx has been shown to stimulate signal transduction pathways such as Ras-MAPK pathway, NF-κB, and Src kinase. The pleiotropic events caused by HBx may be the key to understanding the HBV-mediated oncogenicity. However, the specific roles of HBx in oncogenesis remain largely elusive. To explore the role of HBx in hepatocarcinogenesis, we examined the deregulation of host genes induced by HBx expression. Methods: HBx was ectopically expressed in HepG2 cells using a recombinant adenovirus to transiently express HBx. Gene expression profiling of HBx was conducted on cDNA microarrays that contained 1,028 cDNAs. Results: A number of oncogenes and genes that are involved in cell growth, DNA repair, cell cycle regulation, and cell motility were deregulated by HBx. Conclusions: Theses results suggest that HBx regulates transcription in a way that contributes to the proliferation of hepatocytes, a probable early event of HCC.(Korean J Hepatol 2002;8:371-380)
각종 간질환에서 RT - PCR을 이용한 G형 간염바이러스 RNA의 검출률
한광협,최원,박영년,황영웅,류왕식,박은신,이관식,전재윤,문영명,박찬일 대한간학회 1997 Clinical and Molecular Hepatology(대한간학회지) Vol.3 No.2
Background / Aim : Recently, nucleotide sequences from a novel virus, termed hepatitis G virus(HGV), were identified in serum from a patient with cryptogenic hepatitis and suggested as agent of non A-E hapatitis HGV has been isolated from patients with various liver disease but clinical implications of this new agent remain largely unresolved . In Korea, the etiology of substantial fraction of hepatitis has remined undefined rate of HGV. Methods : To determine the implication of HGV, medical records of 115 patients with various liver diseases were reviewed. Of 115 patients, 63 were male and 52 were female. Their mean age was 44 years(19-74) and their mean AST and ALT were 121.3±278.7 IU/L and 172.2±253.3 IU/L, infected with hepatitis B and/or C virus and 20(17.4%) had non-viral identifiable liver diseases. Results : 1.HGV RNA was detected in 15 (13.0%) patients of 115 patients. 2. Among the 15 HGV RNA positive cases, 7 were male and 8 were female. Their mean age was 48 years(19-72) and their mean AST and ALT were 71.9±45.2 IU/L and 97.4±66.8 IU/L, respectively. 3 . HGV RNA was detected in 8 (13.85) of 58 patients without obvious causes if their liver diseases and in 7(18.9%) of 37 patients infected with HBV and/or HCV. However, HGV RNA was not detected from 20 patients with non-viral liver diseases such as alcoholic liver diseases, autoimmune hepatitis, PBC, or fatty liver. 4. HGV RNA was detected in 5 (19.2%) of 26 patients with acute hepatitis in 6 (9.4%) of 64 patients with chronic hepatitis, in 1 (14.3%) of 7 patients with liver cirrhosis, and in 3 (27.3%) of 11 patients with hepatocellular carcinoma. 5. There was no statistically significant difference in sex, age, history of transfusion, serum ALT level, etiologies and status of HGV infection is quite high among the patients who have no specific cause of acute or chronic liver diseases and HGV can be confected with HBV and/or HCV infection in Korea.
Hye-Jin Lee,Jehan Lee,Myeong-Kyun Shin,류왕식 한국분자세포생물학회 2008 Molecules and cells Vol.25 No.4
A hepadnaviruses replicates its DNA genome via reverse transcription of an RNA template (pregenomic RNA or pgRNA), which has a cap structure at the 5′ end and a poly(A) tail at the 3′ end. We have previously shown that the 5′ cap is indispensable for encapsidation of the pgRNA. A speculative extension of the above finding is that the cap contributes to encapsidation via its interaction with the poly(A) tail, possibly involving eIF4E-eIF4G-PABP interaction. To test this hypothesis, poly(A)-less pgRNAs were generated via cleavage by a cis-acting hepatitis delta virus ribozyme sequence. We found that accumulation of the poly(A)- less pgRNA was markedly diminished, mostly likely due to its reduced stability. Importantly, however, the remaining poly(A)-less pgRNAs were nonetheless encapsidated and reverse transcribed normally when the reduced stability was taken account. Our finding clearly contradicts the notion that the poly(A) tail has any function in encapsidation and viral reverse transcription.
대한간학회지 제2차 춘계학술대회 초록집 : 한국인 간질환 환자에서 G 형 간염 바이러스 감염
한광협 ( Han Gwang Hyeob ),박영년 ( Park Yeong Nyeon ),최원 ( Choe Won ),황영웅 ( Hwang Yeong Ung ),류왕식 ( Lyu Wang Sig ),오승희 ( O Seung Hui ),이관식 ( Lee Gwan Sig ),전재윤 ( Jeon Jae Yun ),문영명 ( Mun Yeong Myeong ),강진경 대한간학회 1996 Clinical and Molecular Hepatology(대한간학회지) Vol.2 No.2(S)