Prof. Liaw, Hungjiun

Associate Professor
Prof. Liaw, Hungjiun
TEL:+886-6-275-7575 ext.58127    研究室:58104 or 58114轉22

Research interests:Chromosome damage repair mechanism、Cancer Genomics、Yeast Genetics.
Introduction of Laboratory:

The major interest of my laboratory is DNA damage response (DDR) in eukaryotic cells. We specifically focus on the DNA damage tolerance pathways and chromatin modification and remodeling in the maintenance of genome integrity. We have used the genetic, biochemical, and molecular approaches to elucidate the mechanism underlying genomic instability.


Ph.D. Degree Biochemistry, Tulane University, USA


2016  Associate Professor Department of Life Sciences, National Cheng Kung University
2010  Assistant Professor Department of Life Sciences, National Cheng Kung University
2006  Postdoc fellow National Human Genome Research Institute, NIH, USA

Awards and Honors




Periodical articles (Link)

Conference paper

  1. Su WP, Ho YC, Wu CK, Hsu SH, Shiu JL, Huang JC, Chang SB, Chiu WT, Hung JJ, Liu TL, Wu WS, Wu PY, Su WC, Chang JY, Liaw HJ*. (2017) Chronic treatment with cisplatin induces chemoresistance through the TIP60-mediated Fanconi anemia and homologous recombination repair pathways. Scientific Reports 7: 3879.
  2. Su WP, Hsu SH, Chia LC, Lin JY, Chang SB, Jiang ZD, Lin YJ, Shih MY, Chen YC, Chang MS, Yang WB, Hung JJ, Hung PC, Wu WS, Myung KJ, Liaw HJ*. (2016) Combined interactions of plant homeodomain and chromodomain regulate NuA4 activity at DNA double-strand breaks. Genetics. 202, 77-92.
  3. Su WP, Hsu SH, Wu CK, Chang SB, Lin YJ, Yang WB, Hung JJ, Chiu WT, Tzeng SF, Chang JY, Su WC, Liaw HJ*. (2014) Chronic low-dose cisplatin treatment induces replication dependent sister chromatid recombination to confer cisplatin resistant phenotype in nasopharyngeal carcinoma. Oncotarget. 5: 6323-37.
  4. Motegi A#, Liaw HJ#, Lee KY, Roest HP, Maas A, Wu X, Moinova H, Markowitz SD, Hao Ding, Hoeijmakers JHJ, and Myung KJ. (2008) Polyubiquitination of proliferating cell nuclear antigen by HLTF and SHPRH prevents genomic instability from stalled replication forks. Proc. Natl. Acad. Sci. USA. 105(34): 12411-6. (# equal contribution)