Labortory of Genomic Instability and Cancer8
Maintenance of genomic integrity is of fundamental importance to all life. Safeguarding genomic integrity from genotoxic stresses is critical for biology of a cell. DNA repair or DNA damage responses are under sophisticated controls that must be accurately and rapidly executed, when the genome integrity is challenged. Understanding the molecular regulation of DNA damage response factors that promote genome stability is a significant subject for basic biological perspective as well as clinical aspects. Our laboratory studies molecular mechanisms of maintaining genome integrity, by studying the functions of proteins involved in DNA damage response and DNA repair. Below are the main areas we are currently focusing on:
1. Molecular mechanisms that suppress DNA replication defects and chromosomal instabilities
a. Replication fork stress caused by transcription-induced conflicts
b. Cellular response to DNA double strand breaks
c. Deciphering the roles of Fanconi Anemia-associated proteins in replication fork stability.
2. Identification of ubiquitin-proteasome machineries in tumor suppression and genomic stability.
Advisor Professor : Kee, Younghoon
Labortory of Genomic Instability and Cancer Homepage
1. Molecular mechanisms that suppress DNA replication defects and chromosomal instabilities
a. Replication fork stress caused by transcription-induced conflicts
b. Cellular response to DNA double strand breaks
c. Deciphering the roles of Fanconi Anemia-associated proteins in replication fork stability.
2. Identification of ubiquitin-proteasome machineries in tumor suppression and genomic stability.
Advisor Professor : Kee, Younghoon
Labortory of Genomic Instability and Cancer Homepage
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Recent Submissions
- Nucleoporins cooperate with Polycomb silencers to promote transcriptional repression and repair at DNA double-strand breaks
- Multifaceted roles of CCAR family proteins in the DNA damage response and cancer
- OTUD5 limits replication fork instability by organizing chromatin remodelers
- Splicing factor SRSF3 represses translation of p21(cip1/waf1) mRNA
- SIAH2 regulates DNA end resection and replication fork recovery by promoting CtIP ubiquitination
