• 한국미생물학회:학술대회논문집
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• 한국미생물학회 1998년도 제38회 춘계학술발표대회
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• pp.49.1-49.1
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• 1998

• Asian Pacific Journal of Cancer Prevention
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• 제14권6호
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• pp.3669-3676
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• 2013

Faithful transmission of genetic information depends on accurate chromosome segregation as cells exit from mitosis, and errors in chromosomal segregation are catastrophic and may lead to aneuploidy which is the hallmark of cancer. In eukaryotes, an elaborate molecular control system ensures proper orchestration of events at mitotic exit. Phosphorylation of specific tyrosyl residues is a major control mechanism for cellular proliferation and the activities of protein tyrosine kinases and phosphatases must be integrated. Although mitotic kinases are well characterized, phosphatases involved in mitosis remain largely elusive. Here we identify a novel variant of mouse protein tyrosine phosphatase containing domain 1 (Ptpcd1), that we named Ptpcd2. Ptpcd1 is a Cdc14 related centrosomal phosphatase. Our newly identified Ptpcd2 shared a significant homology to yeast Cdc14p (34.1%) and other Cdc14 family of phosphatases. By subcellular fractionation Ptpcd2 was found to be enriched in the cytoplasm and nuclear pellets with catalytic phosphatase activity. By means of immunofluorescence, Ptpcd2 was spatiotemporally regulated in a cell cycle dependent manner with cytoplasmic abundance during mitosis, followed by nuclear localization during interphase. Overexpression of Ptpcd2 induced mitotic exit with decreased levels of some mitotic markers. Moreover, Ptpcd2 failed to colocalize with the centrosomal marker ${\gamma}$-tubulin, suggesting it as a non-centrosomal protein. Taken together, Ptpcd2 phosphatase appears a non-centrosomal variant of Ptpcd1 with probable mitotic functions. The identification of this new phosphatase suggests the existence of an interacting phosphatase network that controls mammalian mitosis and provides new drug targets for anticancer modalities.

• 생명과학회지
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• 제23권6호
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• pp.832-837
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• 2013

본 연구에서는 생체 내 구성요소 및 에너지원으로서 중요한 역할을 하는 글루타민 결핍에 의한 인체 전립선 PC3 암세포의 증식에 관한 기전 연구를 실시하였다. 글루타민 결핍에 의한 PC3 세포의 증식억제는 세포주기 G2/M arrest와 연관성이 있었으나, apoptosis 유발 현상은 관찰되지 않았다. 글루타민 결핍에 의한 G2/M arrest는 전사 및 번역 수준에서 Cdc2, cyclin A 및 cyclin B1의 발현 억제 및 p53 비의존적인 p21(WAF1/CIP1)의 발현 증가와 연관성이 있었다. 아울러 글루타민 결핍은 Chk1 및 Chk2의 인산화를 증가시켰으나, Cdc25C의 인산화는 감소시켰다. 본 연구의 결과는 글루타민 결핍에 의한 PC3 세포의 증식억제가 apoptosis 유발과는 상관없이 G2/M arrest를 유발시킨다는 첫 번째 증거이다.

• 대한한방내과학회지
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• 제30권2호
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• pp.375-387
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• 2009

Objective : Gyehyuldeung (GHD) has been widely used in oriental medicine for the treatments of cardiovascular and neurological disorders. Thus, its potential facilitatory activity on axonal regeneration was investigated in the rats. Methods: Sprague-Dawley rats were given crush injury at the sciatic nerve and the changes of axon growth after nerve injury on each nerve injury model were investigated with anti-NF-200 antibody, DiI, GAP-43 protein and Cdc2 protein Results : GHD-mediated enhancement of axonal regeneration after crush injury was measured in both qualitative and quantitative ways by immunofluorescence staining with anti-NF-200 antibody and retrograde tracing of fluorescence dye DiI. GAP-43 protein levels were elevated by GHD treatments in the distal injured sciatic nerve and DRG sensory neurons. The neurite outgrowth of DRG sensory neurons was facilitated by GHD treatment when co-cultured with Schwann cells and astrocytes prepared from injured sciatic nerves and injured spinal cord tissues, respectively. It was observed that Cdc2 protein was up-regulated in co-cultured Schwann cells or astrocytes and Cdc2 protein signals were co-localized to a certain extent with those of phospho-vimentin protein. Conclusions : These results suggest that GHD may play a facilitatory role in axonal regeneration by acting on the injured axons and adjacent non-neuronal cells. The current findings may be useful for the development of therapeutic targets through more specific explorations on molecular interactions between herbal components and endogenous factors.

• 한국정보과학회논문지:시스템및이론
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• 제37권1호
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• pp.8-18
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• 2010

기존의 전통적인 저장 서버는 중복 데이터 블록에 의해서 저장 공간과 네트워크 대역폭의 낭비가 발생되고 있다. 이와 같은 문제를 해결하기 위하여, 다양한 중복 제거 메커니즘이 제시되었으나, 대부분 Contents-Defined Chunking (CDC) 기법을 사용하는 백업 서버에 한정되었다. 왜냐하면 CDC 기법은 앵커를 사용하여 중복 블록을 쉽게 추적할 수 있기 때문에 파일의 업데이트를 관찰하기 유리한 백업 시스템에서 널리 사용되고 있는 것이다. 본 논문에서는 저장 시스템 성능을 개선하기 위하여, 새로운 중복 제거 메커니즘을 제시하고 있다. 범용적인 중복제거 서버를 구축하기 위한 효율적인 알고리즘에 초점을 맞추고 있으며, 이를 통하여 백업 서버, P2P 서버, FTP 서버와 같은 다양한 시스템에 활용이 가능하게 하는 것을 목표로 한다. 실험 결과 제안한 알고리즘이 중복 영역의 블록을 찾아내는 시간을 최소화하고 효율적으로 저장 시스템을 관리하는 것을 보였다.

• 보건교육건강증진학회지
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• 제22권4호
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• pp.57-72
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• 2005

Objectives: To investigate the status of health education in elementary schools. Methods: 620 school nurses were surveyed by questionnaires from September to December in 2003. Results: 1) Among the school nurses under inquiry of planning of health education, 3.3% and 9.3% of them did not prepare for teaching plan. 2) The average time for health education by a school nurse was 96.8 hours a year, and handouts for health education were distributed 10.6 times. Among the contents of health education, sex education took the largest portion of health education with 24.6 hours a year. 3) With regard to the contents of health education covered by school nurses, sex education ranked first with 90.2%, next came drug abuse with 78.4%, dental health, CDC, disease control, healthy life and smoking, body structure and function and growth and development safety, alcohol, nutrition and environmental health followed them. 4) The main contents of education were CDC, dental health sex, healthy life and disease control for 1st, 2nd and 3rd grade students, sex, CDC, disease control and safety for 4th grade students, and sex, CDC, drug abuse and smoking for 5th and 6th grade students. 5) 72.6% of school nurses used class room for health education, 20.0% and 7.4% of them used grade and others such as broadcast, respectively. 6) 42.1% of school nurses used blackboard, 37.0% and 18.6% of them used visual media and handout as a teaching aids for health education. 7) 31.6% of school nurses replied that education time was insufficient 9.5% and 15.9% of them replied the contents of health education were inadequate and methods of health education were inappropriate, respectively. Conclusions: For the successful school health education, it would be in need of sufficient time for health education by opening health education course and of modify the various working conditions of school nurses, and those of effective educational materials and media for health education.

• Molecules and Cells
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• 제21권2호
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• pp.251-260
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• 2006

During mitosis, genomic integrity is maintained by the proper coordination of anaphase entry and mitotic exit via mitotic checkpoints. In budding yeast, mitotic exit is controlled by a regulatory cascade called the mitotic exit network (MEN). The MEN is regulated by a small GTPase, Tem1p, which in turn is controlled by a two-component GAP, Bfa1p-Bub2p. Recent results suggested that phosphorylation of Bfa1p by the polorelated kinase Cdc5p is also required for triggering mitotic exit, since it decreases the GAP activity of Bfa1p-Bub2p. However, the dispensability of GEF Lte1p for mitotic exit has raised questions about regulation of the MEN by the GTPase activity of Tem1p. We isolated a Bfa1p mutant, $Bfa1p^{E438K}$, whose overexpression only partially induced anaphase arrest. The molecular and biochemical functions of $Bfa1p^{E438K}$ are similar to those of wild type Bfa1p, except for decreased GAP activity. Interestingly, in $BFA1^{E438K}$ cells, the MEN could be regulated with nearly wild type kinetics at physiological temperature, as well as in response to various checkpoint-activating signals, but the cells were more sensitive to spindle damage than wild type. These results suggest that the GAP activity of Bfa1p-Bub2p is responsible for the mitotic arrest caused by spindle damage and Bfa1p overproduction. In addition, the viability of cdc5-2 ${\Delta}bfa1 $ cells was not reduced by $BFA1^{E438K}$, suggesting that Cdc5p also regulates Bfa1p to activate mitotic exit by other mechanism(s), besides phosphorylation.

• Journal of Microbiology
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• 제45권3호
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• pp.227-233
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• 2007

In budding yeast, septin plays as a scaffold to recruits protein components and regulates crucial cellular events including bud site selection, bud morphogenesis, Cdc28 activation pathway, and cytokinesis. Phosphorylation of Bni5 isolated as a suppressor for septin defect is essential to Swe1-dependent regulation of bud morphogenesis and mitotic entry. The mechanism by which Bni5 regulates normal septin function is not completely understood. Here, we provide evidence that Bni5 phosphorylation is important for interaction with septin component Cdc11 and for timely delocalization from septin filament at late mitosis. Phosphorylation-deficient bni5-4A was synthetically lethal with $hof1{\Delta}$. bni5-4A cells had defective structure of septin ring and connected cell morphology, indicative of defects in cytokinesis. Two-hybrid analysis revealed that bni5-4A has a defect in direct interaction with Cdc11 and Cdc12. GFP-tagged bni5-4A was normally localized at mother-bud neck of budded cells before middle of mitosis. In contrast, at large-budded telophase cells, bni5-4A-GFP was defective in localization and disappeared from the neck approximately 2 min earlier than that of wild type, as evidenced by time-lapse analysis. Therefore, earlier delocalization of bni5-4A from septin filament is consistent with phosphorylation-dependent interaction with the septin component. These results suggest that timely de localization of Bni5 by phosphorylation is important for septin function and regulation of cytokinesis.

• 동의생리병리학회지
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• 제19권6호
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• pp.1640-1646
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• 2005

An oriental medicinal drugs Jahageo (JHG, Hominis placenta) were examined to determine its effects on the responsiveness of central nervous system neurons after injury. We found that JHG was involved in neurite outgrowth of DRG sensory axons. JHG treatment also increased expression of axonal growth-associated protein GAP-43 in DRG sensory neurons after sciatic nerve injury and in the injured spinal cord. JHG treatment during the spinal cord injury increased induction levels of cell division cycle 2 (Cdc2) protein in DRG as well as in the spinal cord. Histochemical investigation showed that induced Cdc2 in the injured spinal cord was found in non-neuronal cells. These results suggest that JHG regulates activities of non-neuronal cells such as oligodendrocyte and astrocyte in responses to spinal cord injury and protects neuronal responsiveness after axonal damage.

• 동의생리병리학회지
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• 제20권5호
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• pp.1303-1310
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• 2006

In oriental medicine, Samul-tang (SMT) has been used for the treatment of cardiovascular diseases and neuronal disorders. Here, possible effects of SMT on axonal regeneration after the spinal cord injury were examined. SMT treatment induced increases in regeneration-related proteins GAP-43, cell division cycle 2 (Cdc2) and phospho-Erk1/2 in the peripheral sciatic nerves after crush injury. Increased levels of Cdc2 and phospho-Erk1/2 were observe mostly in the gray matter area and some in the dorsomedial white matter. These increases correlated with increased cell numbers in affected areas. Moreover, axons of corticospinal tract (CST) showed increased sprouting in the injured spinal cord when administrated with SMT compared with saline-treated control. Thus, the present data indicate that SMT may be useful for identifying active components and for therapeutic application toward the treatment of spinal cord disorders after injury.