• Molecules and Cells
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• v.37 no.8
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• pp.569-574
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• 2014

As a scaffold, SLX4/FANCP interacts with multiple proteins involved in genome integrity. Although not having recognizable catalytic domains, SLX4 participates in diverse genome maintenance pathways by delivering nucleases where they are needed, and promoting their cooperative execution to prevent genomic instabilities. Physiological importance of SLX4 is emphasized by the identification of causative mutations of SLX4 genes in patients diagnosed with Fanconi anemia (FA), a rare recessive genetic disorder characterized by genomic instability and predisposition to cancers. Recent progress in understanding functional roles of SLX4 has greatly expanded our knowledge in the repair of DNA interstrand crosslinks (ICLs), Holliday junction (HJ) resolution, telomere homeostasis and regulation of DNA damage response induced by replication stress. Here, these diverse functions of SLX4 are reviewed in detail.

• The Korean Journal of Zoology
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• v.18 no.3
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• pp.131-140
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• 1975

Dose response for the nuscheduled DNA synthesis induced by various concentration of MMS was dose dependent and directly proportional to dose increased. Time dependence of unscheduled DNA synthesis was continued up to 4 hours, with the peak appearing 2$\\sim$3 hours after treatment with MMS and $^3 H$-thymidine labeling. Single treatment with BUdR or IUdR does not induce unscheduled DNA synthesis. BUdR and IUdR greatly enhanced MMS-induced unscheduled DNA synthesis, but the dose responses were different from that of single treatment with MMS. IUdR was found to be more effective sensitizer on MMS-induced unscheduled DNA synthesis.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1993.04a
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• pp.137-137
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• 1993

방사선, 자외선, 화학물질 등 여러 변이원에 의해 생긴 DNA 손상의 대부분은 생체내에 존재하는 효소들에 의해 수복(repair)되어 DNA는 안정하게 유지된다. T$_4$ phage 유래의 T$_4$ endonuclease V는 자외선에 의해 DNA에 pyrimidine dimer가 생겼을때 이것을 특이적으로 절제 수복하는 효소이다. 인간의 질환인 색소성 걸피증(Xeroderma pigmentosum)은 태양광선, 특히 자외선에 의해 고빈도로 피부암을 발생한다. 이 질환은 유전적으로 DNA 수복기구에 장애가 있기 때문에 일어난다. 색소성 건피증의 배양세포에 T$_4$ endonuclease V를 도입하면 세포의 DNA 수복능력이 회복되기 때문에 인간과 phage라는 서로 멀리 떨어진 생물종에 공통의 DNA 수복기구가 존재하고 있다는 것을 알 수 있다.

• Molecules and Cells
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• v.26 no.4
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• pp.350-355
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• 2008

Chk2 is a well characterized protein kinase with key roles in the DNA damage response. Chk2 is activated by phosphorylation following DNA damage, and relays that signal to various substrate proteins to induce cell cycle arrest, DNA repair, and apoptosis. In order to identify novel components of the Chk2 signaling pathway in Drosophila, we screened 2,240 EP misexpression lines for dominant modifiers of an adult rough eye phenotype caused by Chk2 overexpression in postmitotic cells of the eye imaginal disc. The rough eye phenotype was suppressed by mutation of the ATM kinase, a well-described activator of Chk2. Twenty-five EP modifiers were identified (three enhancers and 22 suppressors), none of which correspond to previously known components of Chk2 signaling. Three EPs caused defects in G2 arrest after irradiation with incomplete penetrance when homozygous, and are likely directly involved in the response to DNA damage. Possible roles for these modifiers in the DNA damage response and Chk2 signaling are discussed.

• Proceedings of the Zoological Society Korea Conference
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• 1998.04a
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• pp.18-18
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• 1998

No Abstract, See Full Text

• Proceedings of the Korean Nuclear Society Conference
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• 2005.05a
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• pp.998-999
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• 2005

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.133.3-134
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• 2000

• Proceedings of the Korean Society of Life Science Conference
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• 2003.10a
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• pp.127-127
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• 2003

• Proceedings of the Zoological Society Korea Conference
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• 1999.10b
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• pp.251.2-251
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• 1999

No Abstract, See Full Text

• BMB Reports
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• v.56 no.2
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• pp.102-107
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• 2023

Genome editing using CRISPR-associated technology is widely used to modify the genomes rapidly and efficiently on specific DNA double-strand breaks (DSBs) induced by Cas9 endonuclease. However, despite swift advance in Cas9 engineering, structural basis of Cas9-recognition and cleavage complex remains unclear. Proper assembly of this complex correlates to effective Cas9 activity, leading to high efficacy of genome editing events. Here, we develop a CRISPR/Cas9-RAD51 plasmid constitutively expressing RAD51, which can bind to single-stranded DNA for DSB repair. We show that the efficiency of CRISPR-mediated genome editing can be significantly improved by expressing RAD51, responsible for DSB repair via homologous recombination (HR), in both gene knock-out and knock-in processes. In cells with CRISPR/Cas9-RAD51 plasmid, expression of the target genes (cohesin SMC3 and GAPDH) was reduced by more than 1.9-fold compared to the CRISPR/Cas9 plasmid for knock-out of genes. Furthermore, CRISPR/Cas9-RAD51 enhanced the knock-in efficiency of DsRed donor DNA. Thus, the CRISPR/Cas9-RAD51 system is useful for applications requiring precise and efficient genome edits not accessible to HR-deficient cell genome editing and for developing CRISPR/Cas9-mediated knockout technology.