• BMB Reports
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• v.52 no.10
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• pp.607-612
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• 2019

During meiosis, programmed double-strand breaks (DSBs) are repaired via recombination pathways that are required for faithful chromosomal segregation and genetic diversity. In meiotic progression, the non-homologous end joining (NHEJ) pathway is suppressed and instead meiotic recombination initiated by nucleolytic resection of DSB ends is the major pathway employed. This requires diverse recombinase proteins and regulatory factors involved in the formation of crossovers (COs) and non-crossovers (NCOs). In mitosis, spontaneous DSBs occurring at the G1 phase are predominantly repaired via NHEJ, mediating the joining of DNA ends. The Ku complex binds to these DSB ends, inhibiting additional DSB resection and mediating end joining with Dnl4, Lif1, and Nej1, which join the Ku complex and DSB ends. Here, we report the role of the Ku complex in DSB repair using a physical analysis of recombination in Saccharomyces cerevisiae during meiosis. We found that the Ku complex is not essential for meiotic progression, DSB formation, joint molecule formation, or CO/NCO formation during normal meiosis. Surprisingly, in the absence of the Ku complex and functional Mre11-Rad50-Xrs2 (MRX) complex, a large portion of meiotic DSBs was repaired via the recombination pathway to form COs and NCOs. Our data suggested that Ku complex prevents meiotic recombination in the elimination of MRX activity.

• Journal of Veterinary Clinics
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• v.21 no.3
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• pp.253-258
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• 2004

DNA double-strand break (DSB) is a serious treat for the cells including mutations, chromosome rearrangements, and even cell death if not repaired or misrepaired. Ku heterodimer regulatory DNA binding subunits (Ku70/Ku80) bound to double strand DNA breaks are able to interact with 470-kDa DNA-dependent protein kinase catalytic subunit (DNA-PKcs), and the interaction is essential for DNA-dependent protein kinase (DNA-PK) activity. The Ku80 mutants were designed to bind Ku70 but not DNA end binding activity and the peptides were treated in breast cancer cells for co-therapy strategy to see whether the targeted inhibition of DNA-dependent protein kinase (DNA-PK) activity sensitized breast cancer cells to ionizing irradiation or chemotherapy drug to develop a treatment of breast tumors by targeting proteins involved in damage-signaling pathway and/or DNA repair. We designed domains of Ku80 mutants, 26 residues of amino acids (HN-26) as a control peptide or 38 (HNI-38) residues of amino acids which contain domains of the membrane-translocation hydrophobic signal sequence and the nuclear localization sequence, but HNI-38 has additional twelve residues of peptide inhibitor region. We observed that the synthesized peptide (HNI-38) prevented DNA-PKcs from binding to Ku70/Ku80, resulting in inactivation of DNA-PK complex activity in breast cancer cells (MDA-465 and MDA-468). Consequently, the peptide treated cells exhibited poor to no DNA repair, and became highly sensitive to irradiation or chemotherapy drugs. The growth of breast cancer cells was also inhibited. These results demonstrate the possibility of synthetic peptide to apply breast cancer therapy to induce apoptosis of cancer cells.

• 한국연소학회:학술대회논문집
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• 2014.11a
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• pp.349-350
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• 2014

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.1
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• pp.9-14
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• 2003

Recent studies indicated that cancer cells become resistant to ionizing radiation (IR) and chemotherapy drugs by enhanced DNA repair of the lesions. Therefore, it is expected to increase the killing of cancer cells and reduce drug resistance by inhibiting DNA repair pathways that tumor cells rely on to escape chemotherapy. There are a number of key human DNA repair pathways which depend on multimeric polypeptide activities. For example, Ku heterodimer regulatory DNA binding subunits (Ku70/Ku80) on binding to double strand DNA breaks (DSBs) are able to interact with 470-kDa DNA-dependent protein kinase catalytic subunit (DNA-PKcs), and are essential for DNA-dependent protein kinase (DNA-PK) activity. It has been known that DNA-PK is an important factor for DNA repair and also is a sensor-transmitting damage signal to downstream targets, leading to cell cycles arrest. Our ultimate goal is to develop a treatment of breast tumors by targeting proteins involved in damage-signaling pathway and/or DNA repair. This would greatly facilitate tumor cell cytotoxic activity and programmed cell death through DNA damaging drug treatment. Therefore, we designed a domain of Ku80 mutants that binds to Ku70 but not DNA end binding activity and used the peptide in co-therapy strategy to see whether the targeted inhibition of DNA-PK activity sensitized breast cancer cells to irradiation or chemotherapy drug. We observed that the synthesized peptide (HNI-38) prevented DNA-PKcs from binding to Ku70/Ku80, thus resulting in inactivation of DNA-PK activity. Consequently, the peptide treated cells exhibited poor to no DNA repair, and became highly sensitive to IR or chemotherapy drugs, and the growth of breast cancer cells was inhibited. Additionally, the results obtained in the present study also support the physiological role of resistance of cancer cells to IR or chemotherapy.

• Journal of Dairy Science and Biotechnology
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• v.33 no.4
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• pp.271-275
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• 2015

Colloidal semiconductor CdSe-ZnS core-shell nanocrystal quantum dot (Qdot) are luminescent inorganic fluorophores that show potential to overcome some of the functional limitations encountered with organic dyes in fluorescence labeling applications. Salmonella Enteritidis has emerged as a major cause of human salmonellosis worldwide since the 1980s. A rapid, specific, and sensitive method for the detection of Salmonella Enteritidis was developed using Qdot as a fluorescence marker coupled with immunomagnetic separation. Magnetic beads coated with anti-Salmonella Enteritidis antibodies were employed to selectively capture the target bacteria, and biotin-conjugated anti-Salmonella antibodies were added to form sandwich immune complexes. After magnetic separation, the immune complexes were labeled with Qdot via biotin-streptavidin conjugation, and fluorescence measurement was carried out using a fluorescence measurement system. The detection limit of the Qdot method was a Salmonella Enteritidis concentration of $10^3$ colony-forming units (CFU)/mL, whereas the conventional fluorescein isothiocyanate-based method required over $10^5CFU/mL$. The total detection time was within 2 h. In addition to the potential for general nanotechnology development, these results suggest a new rapid detection method of various pathogenic bacteria from a complex food matrix.

• Journal of Sensor Science and Technology
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• v.32 no.6
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• pp.357-369
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• 2023

Wound healing is a complex and dynamic process, making the accurate and timely assessment of skin wounds a crucial aspect of effective wound care management, especially for chronic wounds. Unlike conventional wound dressings that simply cover the wound area once some form of medicine is administered onto the wound, recent studies have introduced versatile approaches to smart wound dressings capable of interacting with wound fluids to monitor physicochemical and pathological parameters to determine the wound healing status. Such electrochemical wound dressings can be integrated with on-demand, closed-loop drug delivery or stimulation systems and ultimately expanded into an ideal technological platform for the prevention, treatment, and management of skin wounds or illnesses. This article briefly reviews the wound healing mechanism and recent strategies for effective wound care management. Specifically, this review discusses the following aspects of smart wound dressings: sensor-integrated smart bandages to detect wound biomarkers, smart bandages developed to accelerate wound healing, and wireless, closed-loop automatic (on-demand) wound healing systems. This review concludes by providing future perspectives on effective wound care management.

• Journal of Life Science
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• v.13 no.3
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• pp.241-247
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• 2003

While the DNA-protein kinase (DNA-PK) complex, comprised of DNA-PKcs and Ku80, is primary involved in the repair of DNA double-strand breaks, it is also believed to participate in additional cellular processes. Here, treatment of embryo fibroblasts (MEFs) derived from either wild-type (Wt) or DNA-PKcs-null (DNA-$PKcs^{-/-}$) mice with various stress inducing agents revealed that adriamycin was markedly more cytotoxic for $Ku80^{-/-}MEFs$ and led to their long-term accumulation in the $G_2$/M phase. This differential response was not due to differences in DNA repair, since adrimycin-triggered DNA damage was repaired with comparable efficiency in both Wt and $Ku80^{-/-}MEFs$, but was associated with differences in the expression of important cell cycle regulatory genes. Our results support the notion that Ku80-mediated cytoprotection and $G_2$/M-progression are not only dependent on the cell's DNA repair but also may reflect Ku80's influence on additional cellular processes such as gene expression.

• YAKHAK HOEJI
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• v.33 no.3
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• pp.191-202
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• 1989

Indomethacin, a non-steroidal antiinflammatory drug inducing gastric irritation, was microencapsulated using pectin-gelatin complex coacervation method. Optimum conditions for microencapsulation and dissolution characteristics of the microcapsules were studied. The optimum pH and pectin-gelatin ratio for microencapsulation were 3.8 and 1:2 respectively. As concentration of colloid solution increased, wall thickness of microcapsules were increased. The dissolution rate of Indomethacin-pectin-gelatin microcapsules prepared by 1.5% and 2% colloid solution were similar but slower than that of Indomethacin-pectin-gelatin microcapsules prepared by 1% colloid solution. The 50% release time ($T_{50%}$) of Indomethacin-pectin-gelatin microcapsules prepared by 1%, 1.5% and 2% colloid solutions were 3 min, 5 min, and 6 min respectively while that of Indomethacin powder was 50 min.

• YAKHAK HOEJI
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• v.33 no.6
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• pp.324-332
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• 1989

Drug release from sulfanilamide granules coated with a polyelectrlyte complex of sodium tripolyphosphate and chitosan was studied. The coating film thickness increased with increasing concentration of chitosan in the coating solution and the drug release rates of the coated granules were significantly reduced comparing with those of the uncoated granules. $T_{50%}$ of the uncoated granules was 6 minutes, but those of the granules coated with chitosan-sodium tripolyphosphate from 0.5, 0.7, and 0.9% (w/v) chitosan-HCl solution were 27, 135, and 180 minutes, respectively in distilled water. In dissolution medium at pH 6.8, $T_{50%}$ of the uncoated granules was 4 minutes, but those of the granules coated with chitosan-sodium tripolyphosphate from 0.5, 0.7, and 0.9(w/v)% chitosan-HCl solution, were 32, 135, and 160 minutes, respectively.

• The Journal of Korean Institute of Communications and Information Sciences
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• v.33 no.12C
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• pp.1062-1067
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• 2008

ABBA codes, a class of quasi-orthognal space-time block codes (QoSTBC) proposed by Tirkkonen and others, allow full rate and a fast maximum likelihood (ML) decoding, but do not have full diversity. In this paper, a linear complex precoder is proposed for ABBA codes to achieve full rate and full diversity. Moreover, the same diversity produce as that of orthogonal space-time block code with linear complex precoder (OSTBC-LCP) is achieved. Meanwhile, the size of the linear complex precoder can be reduced by half without affecting performance, which means the same complexity of decoding as that of the conventional ABBA code is guaranteed.