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여지은 용인대학교 2011 용인대학교 논문집 Vol.29 No.-
The purpose of this qualitative research was to understand deeply the essence lived a process of learning experience through the phenomenological approach. The participants for this study were five female judo players who is going to University. Each participants were interviewed from three times to four times. The collected data from the in-depth interview was made description of anecdotes, lived experiences and a phenomenon. The essence of learning experience for female judo players was described a way not wanted but had to go, perception change for living own life and anxiety to another way for the future. This study was performed to explore lived life of female judo players related to learning experience. It was found that through the way not special just of necessity.
( Eun Ji Yeo ),( Won Sik Eum ),( Hyeon Ji Yeo ),( Yeon Joo Choi ),( Eun Jeong Sohn ),( Hyun Jung Kwon ),( Dae Won Kim ),( Duk-soo Kim ),( Sung-woo Cho ),( Jinseu Park ),( Kyu Hyung Han ),( Keun Wook L 한국응용약물학회 2021 Biomolecules & Therapeutics(구 응용약물학회지) Vol.29 No.3
Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H<sub>2</sub>O<sub>2</sub>-treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NF-κB, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.
SOHN, EUN JEONG,SHIN, MIN JEA,EUM, WON SIK,KIM, DAE WON,YONG, JI IN,RYU, EUN JI,PARK, JUNG HWAN,CHO, SU BIN,CHA, HYUN JU,KIM, SANG JIN,YEO, HYEON JI,YEO, EUN JI,CHOI, YEON JOO,IM, SEUNG KWON,KWEON, HA Spandidos Publications 2016 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.38 No.1
<P>Oxidative stress-induced apoptosis is associated with neuronal cell death and ischemia. The NOL3 [nucleolar protein 3 (apoptosis repressor with CARD domain)] protein protects against oxidative stress-induced cell death. However, the protective mechanism responsible for this effect as well as the effects of NOL3 against oxidative stress in ischemia remain unclear. Thus, we examined the protective effects of NOL3 protein on hydrogen peroxide (H2O2)-induced oxidative stress and the mechanism responsible for these effects in hippocampal neuronal HT22 cells and in an animal model of forebrain ischemia using Tat-fused NOL3 protein (Tat-NOL3). Purified Tat-NOL3 protein transduced into the H2O2-exposed HT22 cells and inhibited the production of reactive oxygen species (ROS), DNA fragmentation and reduced mitochondrial membrane potential (Delta(Psi m)). In addition, Tat-NOL3 prevented neuronal cell death through the regulation of apoptotic signaling pathways including Bax, Bcl-2, caspase-2, -3 and -8, PARP and p53. In addition, Tat-NOL3 protein transduced into the animal brains and significantly protected against neuronal cell death in the CA1 region of the hippocampus by regulating the activation of microglia and astrocytes. Taken together, these findings demonstrate that Tat-NOL3 protein protects against oxidative stress-induced neuronal cell death by regulating oxidative stress and by acting as an anti-apoptotic protein. Thus, we suggest that Tat-NOL3 represents a potential therapeutic agent for protection against ischemic brain injury.</P>
Yeo, Hyeon Ji,Shin, Min Jea,Yeo, Eun Ji,Choi, Yeon Joo,Kim, Dae Won,Kim, Duk-Soo,Eum, Won Sik,Choi, Soo Young Elsevier 2019 FREE RADICAL BIOLOGY AND MEDICINE Vol.135 No.-
<P><B>Abstract</B></P> <P>Cytokine-induced apoptosis inhibitor 1 (CIAPIN1) protein is widely expressed in the brain and it is known that this protein is involved in cell survival including dopaminergic neuronal cells. Oxidative stress is known as one of the major causes of degenerative diseases including ischemia. In this study, we investigated the effect of CIAPIN1 protein on hippocampal neuronal (HT-22) cell damage induced by hydrogen peroxide (H<SUB>2</SUB>O<SUB>2</SUB>) and in an animal model of ischemia using Tat-CIAPIN1 fusion protein which can transduce into cells. Tat-CIAPIN1 protein transduced into HT-22 cells and significantly inhibited cell death, DNA fragmentation, and reactive oxygen species (ROS) generation. Also, Tat-CIAPIN1 protein enhances cell survival via the regulation of Akt, MAPK, NF-κB and apoptotic signaling pathways in the H<SUB>2</SUB>O<SUB>2</SUB> treated cells. In an ischemic animal model, Tat-CIAPIN1 protein transduced into the brain and protected neuronal cell death of hippocampal CA1 region induced by ischemic insult. In conclusion, we demonstrated that Tat-CIAPIN1 protein has protective effects against hippocampal neuronal cell damage induced by ischemic injury, suggesting that Tat-CIAPIN1 protein may provide a potential therapeutic agent for ischemia.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Tat-CIAPIN1 transduces into HT-22 cells and animal brain. </LI> <LI> Transduced Tat-CIAPIN1 protects against H<SUB>2</SUB>O<SUB>2</SUB>-induced cellular toxicity. </LI> <LI> Tat-CIAPIN1 regulates MAPK and apoptosis signaling pathways. </LI> <LI> Tat-CIAPIN1 protects against neuronal cell death in an ischemic animal model. </LI> <LI> Tat-CIAPIN1 can be a therapeutic agent for neuronal diseases including ischemia. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Heterologous Production of 4-O-Demethylbarbamide, a Marine Cyanobacterial Natural Product
( Eun Ji Kim ),( Jong Hyun Lee ),( Hyukjae Choi ),( Alban R Pereira ),( Yeon Hee Ban ),( Young Ji Yoo ),( Eunji Kim ),( Je Won Park ),( David H Sherman ),( William H Gerwick ),( Yeo Joon Yoon ) 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0
Heterologous expression of the barbamide biosynthetic gene cluster, obtained from the marine cyanobacterium Moorea producens, in the terrestrial actinobacterium Streptomyces venezuelae, resulted in the production of a new barbamidecongener 4-O-demethylbarbamide, demonstrating the potential of this approach for investigating the assembly and tailoring of complex marine natural products.