http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : SHIM JAEGAL (검색결과 5 건)
- 무료
- 기관 내 무료
- 유료
-
Shim, Jaegal,Lee, Junho Korean Society for Molecular Biology 2005 Molecules and cells Vol.19 No.3
<P>The adaptor protein (AP) complexes are involved in membrane transport of many proteins. There are 3 AP complexes in C. elegans unlike mammals that have four. To study the biological functions of the AP-3 complexes of C. elegans, we sought homologues of the mouse and human genes that encode subunits of the AP-3 complexes by screening C. elegans genomic and EST sequences. We identified single copies of homologues of the m3, s3, b3 and d genes. The medium chain of AP-3 is encoded by a single gene in C. elegans but two different genes in mammals. Since there are no known mutations in these genes in C. elegans, we performed RNAi to assess their functions in development. RNAi of each of the genes caused embryonic and larval lethal phenotypes. APM-3 is expressed in most cells, particularly strongly in spermatheca and vulva. We conclude that the products of the C. elegans m3, s3, b3 and d genes are essential for embryogenesis and larval development.</P>
-
Kim, Seongseop,Park, Dae-Hun,Shim, Jaegal Korean Society for Molecular Biology 2008 Molecules and cells Vol.26 No.4
<P>5-Fluorouracil (5-FU), a pyrimidine antagonist, has a long history in cancer treatment. The targeted pyrimidine biosynthesis pathway includes dihydropyrimidine dehydrogenase (DPD), which converts 5-FU to an inactive metabolite, and thymidylate synthase (TS), which is a major target of 5-FU. Using Caenorhabditis elegans as a model system to study the functional and resistance mechanisms of anti-cancer drugs, we examined these two genes in order to determine the extent of molecular conservation between C. elegans and humans. Overexpression of the worm DPD and TS homologs (DPYD-1 and Y110A7A.4, respectively) suppressed germ cell death following 5-FU exposure. In addition, DPYD-1 depletion by RNAi resulted in 5-FU sensitivity, while treatment with Y110A7A.4 RNAi and 5-FU resulted in similar patterns of embryonic death. Thus, the pathway of 5-FU function appears to be highly conserved between C. elegans and humans at the molecular level.</P>
-
Kim, Seongseop,Park, Dae‐,Hun,Kim, Tai Hoon,Hwang, Moogak,Shim, Jaegal Blackwell Publishing Ltd 2009 The FEBS journal Vol.276 No.17
<P>Pyrimidine biosynthesis enzymes function in many cellular processes and are closely associated with pyrimidine antagonists used in cancer chemotherapy. These enzymes are well characterized from bacteria to mammals, but not in a simple metazoan. To study the pyrimidine biosynthesis pathway in <I>Caenorhabditis elegans</I>, we screened for mutants exhibiting resistance to the anticancer drug 5‐fluorouracil (5‐FU). In several strains, mutations were identified in ZK783.2, the worm homolog of human uridine phosphorylase (UP). UP is a member of the pyrimidine biosynthesis family of enzymes and is a key regulator of uridine homeostasis. <I>C.?elegans</I> UP homologous protein (UPP‐1) exhibited both uridine and thymidine phosphorylase activity <I>in vitro</I>. Knockdown of other pyrimidine biosynthesis enzyme homologs, such as uridine monophosphate kinase and uridine monophosphate synthetase, also resulted in 5‐FU resistance. Uridine monophosphate kinase and uridine monophosphate synthetase proteins are redundant, and show different, tissue‐specific expression patterns in <I>C.?elegans.</I> Whereas pyrimidine biosynthesis pathways are highly conserved between worms and humans, no human thymidine phosphorylase homolog has been identified in <I>C.?elegans.</I> UPP‐1 functions as a key regulator of the pyrimidine salvage pathway in <I>C.?elegans</I>, as mutation of <I>upp‐1</I> results in strong 5‐FU resistance.</P>
-
TopBP1 deficiency impairs V(D)J recombination during lymphocyte development.
Kim, Jieun,Lee, Sung Kyu,Jeon, Yoon,Kim, Yehyun,Lee, Changjin,Jeon, Sung Ho,Shim, Jaegal,Kim, In-Hoo,Hong, Seokmann,Kim, Nayoung,Lee, Ho,Seong, Rho Hyun Published for the European Molecular Biology Organ 2014 The EMBO journal Vol.33 No.3
<P>TopBP1 was initially identified as a topoisomerase II-β-binding protein and it plays roles in DNA replication and repair. We found that TopBP1 is expressed at high levels in lymphoid tissues and is essential for early lymphocyte development. Specific abrogation of TopBP1 expression resulted in transitional blocks during early lymphocyte development. These defects were, in major part, due to aberrant V(D)J rearrangements in pro-B cells, double-negative and double-positive thymocytes. We also show that TopBP1 was located at sites of V(D)J rearrangement. In TopBP1-deficient cells, γ-H2AX foci were found to be increased. In addition, greater amount of γ-H2AX product was precipitated from the regions where TopBP1 was localized than from controls, indicating that TopBP1 deficiency results in inefficient DNA double-strand break repair. The developmental defects were rescued by introducing functional TCR αβ transgenes. Our data demonstrate a novel role for TopBP1 as a crucial factor in V(D)J rearrangement during the development of B, T and iNKT cells.</P>
-
DE XU, HONG,CHO, SOON-CHANG,BANG, MI-AE,BAE, CHUN-SIK,CHOI, YEONSHIK,LI, YONG-CHUN,LIM, SEUNG-KIL,SHIM, JAEGAL,PARK, DAE-HUN D.A. Spandidos 2015 International journal of oncology Vol.46 No.6
<P>The World Health Organization (WHO) has reported that cancer is one of the most prevalent diseases and a leading cause of death worldwide. Many anticancer drug development studies have been pursued over the last few decades and several viable drugs have been discovered, such as paclitaxel, topotecan and irinotecan. Previously, our research group uncovered the cytocidal and cytostatic effects of the plant <I>Stephania delavayi</I> Diels. In this study, we determined the active chemical to be 6,7-di-O-acetylsinococuline (FK-3000). The FK-3000 half maximal inhibitory concentration (IC<SUB>50</SUB>) in MDA-MB-231 breast carcinoma cells at 48 h was 0.52 μg/ml and it induced apoptosis in a dose- and time-dependent manner. FK-3000 suppressed NF-κB nuclear translocation, decreased NF-κB phosphorylation, and decreased COX-2 protein expression. MDA-MB-231 xenografted mice were treated with FK-3000, Taxol, or their combination for 21 days. The tumor size was smallest in the co-treatment group, indicating that FK-3000 may have a synergistic effect with Taxol. FK-3000 treatment showed no adverse effects on blood cell counts, serum protein levels, or pathology. These studies demonstrate that FK-3000, isolated from <I>S. delavayi</I> Diels., is a promising, pathway-specific anticancer agent that exhibits low toxicity.</P>
연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
