Center for Genomic Integrity

유전체 항상성 연구단

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유전체 항상성 연구단

DNA is the building block for the genome and provides the blueprint for almost every aspect of life. DNA can be damaged by endogenous assaults such as replication errors, oxidative stress or by exogenous challenges such as radiation or toxic chemicals. Failure to repair such damage results in cell death or the accumulation of changes in DNA that can cause genetic diseases including cancers or can lead to premature aging.
Research at the IBS Center for Genomic Integrity is concerned with the many DNA damage response and repair pathways that can sense and repair damaged DNA and signal to cells that there is an urgent problem to be addressed. We also study the link of these pathways to other parts of cellular metabolism, including DNA replication, cell cycle regulation or transcription.
Our research spans many disciplines and techniques, including molecular, cell, chemical and structural biology, genetics, biochemistry and the use of animal models. Finally, we are interested in leveraging our research to develop small molecule modulators of DNA repair pathways as probes and to exploit vulnerabilities of tumors in therapeutic settings.


Synthetic lethality, DNA Repair, DNA Reconbination, DNA Damage Response, Cancer, Aging


DNA Repair, Synthetic lethality, Cancer, DNA Damage Response, ATAD5, PCNA, CRISPR, CRISPR-Cas9

Research Keywords and Topics

• Composition For Inducing Apoptosis of Cancer Cell And Method For Inducing Apoptosis of Cancer Cell Using the Same
암세포 사멸 유도용 조성물 및 상기 조성물을 이용한 암세포 사멸유도 방법 연구
• Molecular Analysis of DNA replication, repair, recombination genes and proteins
DNA 복제, 손상복구, 재조합에 관련된 유전자와 단백질의 분자적 연구
• Cellular Response to DNA damaging agents
DNA에 손상을 주는 내외부적 요인에 의한 세포의 반응 과정 연구
• Animal models to understand defects in DNA replication, repair, recombination
DNA 복제, 손상복구, 재조합에 관련된 유전자의 이상이 mouse, zebrafish에 미치는 영향의 연구
• Identification of potential precision therapeutic molecules for cancers and aging
암이나 노화를 저해할 수있는 물질을 DNA 손상복구에 표적화하여 개발

Research Publications

• CELL REPORTS, PCNA Unloading Is Negatively Regulated by BET Proteins, Kang M, Kim J, Ryu E, Ha N, Hwang S, Kim B, Ra J, Kim Y, Hwang J, Myung K, Kang S. (2019.12)
• NATURE COMMUNICATIONS, ATAD5 promotes replication restart by regulating RAD51 and PCNA in response to replication stress, Park S, Kang N, Song E, Wie M, Lee E, Hwang S, Lee D, Ra J, Park I, Park J, Kang S, Park J, Hohng S, Lee K, Myung K. (2019.12)
• NUCLEIC ACIDS RESEARCH, CTCF cooperates with CtIP to drive homologous recombination repair of double-strand breaks, Hwang S, Kang M, Baik C, Lee Y, Hang N, Kim B, Han J, Jeong J, Park D, Myung K, Lee J. (2019.09)
• NUCLEIC ACIDS RESEARCH, The structure of human EXD2 reveals a chimeric 3′ to 5′ exonuclease domain that discriminates substrates via metal coordination, Park J, Lee S, Jeong H, Kang M, Haute L, Minczuk M, Seo J, Jun Y, Myung K, Rhee H, Lee C. (2019.07)
• NATURE COMMUNICATIONS, Regulation of PCNA cycling on replicating DNA by RFC and RFC-like complexes (2019.06)


•US patent 61/930,291 (E-039-2014/0-US-01) Compounds and Method for treating PARP1-deficient cancers
•KOREA patentComposition For Inducing Apoptosis of Cancer Cell And Method For Inducing Apoptosis of Cancer Cell Using the Same


  • LA. 생명과학
  • LA01. 분자세포생물학
  • LA0199. 달리 분류되지 않는 분자세포 생물학


  • 건강한 생명사회 지향
  • 021600. 유전자조작/전달기술


  • 녹색기술관련 과제 아님
  • 녹색기술관련 과제 아님
  • 999. 녹색기술 관련과제 아님


  • BT 분야
  • 기초/기반기술
  • 020114. 생명현상 및 기능연구