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( Ji-su Baek ),( Jong-min Kim ),( Hye-ryung Kim ),( Ji-hoon Park ),( Yeun-kyung Shin ),( Hae-eun Kang ),( Jung-hoon Kwon ),( Won-jae Lee ),( Min Jang ),( Sang-kwon Lee ),( Ho-seong Cho ),( Yeonsu Oh ) 한국동물위생학회 2023 韓國家畜衛生學會誌 Vol.46 No.4
In this study, a new triplex real-time quantitative reverse transcription polymerase chain reaction (tqRT-PCR) assay was developed for the rapid and differential detection of three feline viral pathogens including feline calicivirus (FCV), feline herpesvirus 1 (FHV-1), and influenza A virus (IAV) in a single reaction. The assay specifically amplified three targeted viral genes with a detection limit of below 10 copies/reaction. The assay showed high repeatability and reproducibility, with intra- and inter-assay coefficients of variation of less than 1%. Based on the diagnostic results of the assay using 120 clinical samples obtained from cats with feline respiratory disease complex (FRDC)-suspected signs, the prevalence of FCV, FHV-1, or IAV was 43.3%, 22.5%, or 0%, respectively, indicating that the diagnostic sensitivity was comparable or superior to those of previously reported monoplex qRT-PCR/qPCR assays. The dual infection rate for FCV and FHV-1 was 8.3%. These results indicate that FCV and FHV-1 are widespread and that co-infection with FCV and FHV-1 frequently occur in the Korean cat population. The developed tqRT-PCR assay will serve as a promising tool for etiological and epidemiological studies of these three bacterial pathogens, and the prevalence data for three feline viruses obtained in this study will contribute to expanding knowledge about the epidemiology of FRDC in the current Korean cat population.
ZBTB7A suppresses glioblastoma tumorigenesis through the transcriptional repression of EPB41L5
Jeong Ji-Hoon,Park Seung-Ho,Kim Hyunhee,Nam Hae Yun,Kim Sung-Hak,Jeong Minseok,Kong Min-Jeong,Son Jihyun,Jeong Ji-Eun,Song Ji-Hye,Kim Seong Who,Choi Kyung-Chul 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Glioblastoma multiforme (GBM), the most aggressive and malignant glioma, has a poor prognosis. Although patients with GBM are treated with surgery, chemotherapy, and radiation therapy, GBM is highly resistant to treatment, making it difficult and expensive to treat. In this study, we analyzed the Gene Expression Profiling Interactive Analysis dataset, the Cancer Genome Atlas dataset, and Gene Expression Omnibus array data. ZBTB7A (also called FBI1/POKEMON/LRF) was found to be highly expressed in low-grade glioma but significantly downregulated in patients with GBM. ZBTB7A is a transcription factor that plays an important role in many developmental stages, including cell proliferation. The activation of epithelial-mesenchymal transition (EMT) is a key process in cancer progression and metastasis. Erythrocyte membrane protein band 4.1 like 5 (EPB41L5) is an essential protein for EMT progression and metastasis in various types of cancer. We found that ZBTB7A depletion in U87 cells induced GBM progression and metastasis. Based on RNA sequencing data, ZBTB7A directly binds to the promoter of the EPB41L5 gene, reducing its expression and inhibiting GBM progression. We demonstrated that ZBTB7A dramatically inhibits GBM tumor growth through transcriptional repression of EPB41L5. Thus, both ZBTB7A and EPB41L5 may be potential biomarkers and novel therapeutic targets for GBM treatment. Overall, we discovered the role of a novel tumor suppressor that directly inhibits GBM progression (ZBTB7A) and identified EPB41L5 as a therapeutic target protein for patients with GBM.
Seo, Ji Hae,Cha, Jong-Ho,Park, Ji-Hyeon,Jeong, Chul-Ho,Park, Zee-Yong,Lee, Hye-Suk,Oh, Seung Hyun,Kang, Ju-Hee,Suh, Se Won,Kim, Kyoung Hoon,Ha, Jun Yong,Han, Sang Hee,Kim, Se-Hee,Lee, Ji-Won,Park, Jeo American Association for Cancer Research 2010 Cancer Research Vol.70 No.11
<P>The N-acetyltransferase arrest defective 1 (ARD1) is an important regulator of cell growth and differentiation that has emerged recently as a critical molecule in cancer progression. However, the regulation of the enzymatic and biological activities of human ARD1 (hARD1) in cancer is presently poorly understood. Here, we report that hARD1 undergoes autoacetylation and that this modification is essential for its functional activation. Using liquid chromatography-tandem mass spectrometry and site-directed mutational analyses, we identified K136 residue as an autoacetylation target site. K136R mutation abolished the ability of hARD1 to promote cancer cell growth in vitro and tumor xenograft growth in vivo. Mechanistic investigations revealed that hARD1 autoacetylation stimulated cyclin D1 expression through activation of the transcription factors beta-catenin and activator protein-1. Our results show that hARD1 autoacetylation is critical for its activation and its ability to stimulate cancer cell proliferation and tumorigenesis.</P>
PACAP inhibits tumor growth and interferes with clusterin in cervical carcinomas
Lee, Ji-Hae,Lee, Ji-Yeon,Rho, Seung Bae,Choi, Jong-Soon,Lee, Dong-Gi,An, Sungwhan,Oh, Taejeong,Choi, Don-Chan,Lee, Seung-Hoon Elsevier 2014 FEBS letters Vol.588 No.24
<P><B>Abstract</B></P> <P>Secretory clusterin (sCLU), an anti-apoptotic protein, is overexpressed in many tumors and enhances tumorigenesis and chemo-resistance. However, the regulation mechanism controlling the sCLU maturation process or activity remains undetermined. In this study, we found PACAP as a negative regulator of CLU. Overexpression of the PACAP gene in cervical cancer cell lines lacking PACAP expression significantly inhibited cell growth and induced apoptosis. We further demonstrated that interaction of PACAP with CLU significantly downregulated CLU expression and secretion, inhibited the Akt–Raf–ERK pathway, and suppressed the growth of human tumor xenografts in nude mice. This novel inhibitory function of PACAP may be applicable for developing novel molecular therapies for tumors with increased sCLU expression.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Over-expression of PACAP inhibits cervical cancer cell growth and induced apoptosis. </LI> <LI> PACAP directly interacts with CLU and the specific binding sites were identified. </LI> <LI> The interaction inhibited expression and secretion of sCLU. </LI> <LI> The interaction results in inhibition of the pro-survival activity of clusterin and of the clusterin downstream Akt/Raf/ERK signaling pathway, resulting in apoptotic cell death. </LI> </UL> </P>
Autoacetylation regulates differentially the roles of ARD1 variants in tumorigenesis
SEO, JI HAE,PARK, JI-HYEON,LEE, EUN JI,VO, TAM THUY LU,CHOI, HOON,JANG, JAE KYUNG,WEE, HEE-JUN,AHN, BUM JU,CHA, JONG-HO,SHIN, MIN WOOK,KIM, KYU-WON Spandidos Publications 2015 International journal of oncology Vol.46 No.1
김종훈(Jong-Hoon Kim),장정훈(Choung-Hoon Chang),김지연(Ji-Yeon Kim),문은혜(Eun-Hae Mun),원경미(Kyoung-Mi Won),천경미(Kyoung-Mi Cheon),한지연(Ji-Yeon Han) 한국정보과학회 1999 한국정보과학회 학술발표논문집 Vol.26 No.2Ⅱ
웹 기반 교육은 학습자 중심의 교육 환경을 마련해주고 있으며 학습자는 웹을 통해 스스로 학습하는 완전한 개별학습뿐 아니라 학습자의 수준에 따른 심화 학습을 유도할 수 있고 교과서로 학습하는 것보다 다양한 학습 자료를 활용할 수 있으며 자기 주도적 학습을 할 수 있는 이짐이 있다. 이에 본 연구에서는 학습자가 자기 주도적으로 학습할 수 있는 음악과 웹 기반 코스웨어를 개발하였다. 특히 본 코스웨어는 초등 1, 3, 5학년의 음악과를 MIDI를 활용하여 개발하였다. 이의 개발로 학습자의 흥미와 호기심을 유발시켜 학습 의욕을 가져오는 환경을 구축하였다.