Hepatitis B virus X protein induces angiogenesis by stabilizing hypoxia-inducible factor-1α 1 EUN-JOUNG MOON * ,† , CHUL-HO JEONG * , JOO-WON JEONG * , KWANG ROK KIM * , DAE-YEUL YU ‡ , SEISHI MURAKAMI § , CHUL WOO KIM || and KYU-WON KIM * ,2 * Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 151-742, Korea, † Department of Molecular Biology, Pusan National University, Busan 609-735, Korea, ‡ Korea Research Institute of Bioscience and Biotechnology, Daejon 305-333, Korea, § Department of Molecular Biology, Division of Molecular Oncology, Cancer Research Institute, Kanazawa University, Kanazawa 920, Japan, || Cancer Research Center, Department of Pathology, Seoul National University College of Medicine, Seoul 110-799, Korea 2 Correspondence: College of Pharmacy, Seoul National University, Seoul 151-742, Korea. E-mail: qwonkim@plaza.snu.ac.kr <h3>SPECIFIC AIMS</h3> Hepatocellular carcinoma (HCC) is a highly vascularized solid tumor. One of the major risk factors for HCC is the infection of hepatitis B virus (HBV). Although HBx, the protein encoded by the X gene of the HBV genome, has been implicated in HBV-mediated hepatocarcinogenesis, the relationship between HBx and the hypervascularity of HCC remains unclear. Therefore, the aim of this study is to determine the role
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Hepatitis B virus X protein induces angiogenesis by stabilizing hypoxia-inducible factor-1α
MOON, EUN-JOUNG; JEONG, CHUL-HO; JEONG, JOO-WON; KIM, KWANG ROK; YU, DAE-YEUL; MURAKAMI, SEISHI; KIM, CHUL WOO; KIM, KYU-WON
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, Volume 18 (2): 382
Fed of American Socs for Experimental Biology – Feb 1, 2004
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