• Title/Summary/Keyword: K-Ras

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VLSI Design of a Bus Interface Controller for 32-bit RISC microprocessor (32비트 RISC 마이크로프로세서를 위한 버스 인터페이스 제어기의 설계)

  • Heo, Sang-Kyong;An, Sang-Jun;Jeong, Wook-Yeong;Kim, Young-Jun;Lee, Yong-Surk
    • Proceedings of the IEEK Conference
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    • 1999.06a
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    • pp.341-344
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    • 1999
  • 본 논문에서는 DSP 기능을 내장한 32비트 RISC 마이크로프로세서를 위한 버스 제어기를 설계하였다. 연구의 초점은 버스 타이밍, 주소 멀티플렉싱, 리프레쉬, 버스 중재 등을 제어하는 버스제어기를 온칩화 하여 CPU로 하여금 외부 램과 추가적인 장치없이 직접 연결될 수 있도록 한 것이다. 버스 제어기가 관리하는 메모리의 종류는 SRAM, ROM, DRAM, EDO DRAM이며 고속 모드(Fast page mode, EDO page mode 및 RAS-down mode)기능을 지원하며 다양한 Wait를 넣을 수 있다. 주소 영역은 4가지(EMAO-EMA3)이며 내부적으로 7개 의 레지스터가 있고 이들을 이용하여 서로 연결된 세 개의 상태 머신으로 모든 램과의 타이밍을 제어함으로써 공유블록을 활용할 수 있었다. Verilog HDL의 기술하고 Synopsys로 합성한 후 타이밍 검증을 수행한 결과 최악조건에서 53.1㎒로 동작할 수 있었다. 그 후 0.6㎛ single poly triple metal process 공정으로 레이아웃 되었고 면적은 44㎜ × 1.21㎜ 이다.

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On-line Fussy Performance Management of Profibus Networks

  • Lee, Kyung-Chang;Song Kang;Kim, Dong-Wook;Lee, Suk
    • International Journal of Precision Engineering and Manufacturing
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    • v.1 no.2
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    • pp.5-13
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    • 2000
  • Most networks for automation are tuned to an expected traffic condition ar their design stage. During their actual operations, however, the networks experience considerable changes in traffic from time to time. These traffic changes caused by common events like machine failure and production schedule change may adversely affect th network performance and, in turn , the performance of the connected devices. This paper presents experimental results for performance management of a Profibus-FMS network. The performance management aims to maintain a uniform level of network performance at all stations under changing network traffic. The performance management algorithm monitors the performance of individual network stations and commands the stations to change their timer values in order to have comparable performance at all stations. In order to determine the amount of timer change, the algorithm employs a set of fuzzy rules. The algorithm has been evaluated on a Profibus network.

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Apoptotic effect of physcion isolated from marine fungus Microsporum sp. in PC3 human prostate cancer cells

  • Ding, Yi-Shan;Kim, Won-Suk;Park, Sun Joo;Kim, Se-Kwon
    • Fisheries and Aquatic Sciences
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    • v.21 no.8
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    • pp.22.1-22.7
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    • 2018
  • Background: Apoptosis is a process of programmed cell death, and apoptosis defect results in serious diseases such as cancer. Apoptosis induction is one of the key mechanisms of anti-cancer agents. This study was aimed to find anti-prostate cancer compounds from marine-derived fungus Microsporum sp. Results: We found that physcion isolated from the fermentation broth extract of the marine fungus Microsporum sp. strain MFS-YL decreases the cell proliferation of PC3 human prostate cancer cells. Physcion induced cell apoptosis as determined by Annexin V/propidium iodide double staining. Physcion downregulated the anti-apopotoic proteins such as Ras, Bcl-xL, and Bcl-2, whereas upregulated the pro-apoptotic Bax. Physcion also activated caspase-3, caspase-8, and caspase-9. Conclusion: These results suggest that physcion from Microsporum sp. inhibits the proliferation of PC3 human prostate cancer cells via the pathway leading to apoptotic cell death. Physcion may be a potential candidate in the field of anticancer drug discovery against human prostate cancer.

Autophagy: Noble target mechanisms in natural medicines as anticancer agents (자가식세포작용: 천연물항암제로서의 신규작용기전)

  • Kang, Se-Chan
    • Journal of Plant Biotechnology
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    • v.37 no.1
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    • pp.57-66
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    • 2010
  • Programmed cell death systems are important for an active type of cell deaths. Among them, a type of programmed cell death, autophagy is activated in cancer cells in response to multiple stresses and has been demonstrated to promote tumor cell survival and drug resistance. Thus, in the area of cancer, over the time frame form around the 1940s to date, of the 155 small molecules, 73% are other than "synthetic", with 47% actually being either "natural products" or "directly derived therefrom". Autophagy has multiple physiological functions in multicellular organisms, including protein degradation and organelle turnover. Genes and proteins that constitute the basic machinery of the autophagic process were first identified in the yeast system and some of their mammalian orthologues have been characterized as well. Numerous oncogenes, including Akt1, Bcl-2, NF1, PDPK1, class I PI3K, PTEN, and Ras and oncosuppressors, inculuding Bec-1, Bif-1, DAPK-1, p53 and UVRAG suppress or promote the autophagy pathway. Regulation of autophagy in tumors is governed by similar principles of the normal cells, only in a much more complicated manner, given the frequently observed abnormal PI3K activation in cancer and the multitude of interactions between the PI3K/AKT/mTOR pathway and other cell signaling cascades, often also deregulated in tumor cells. Autophagy induction by some anticancer agents underlines the potential utility of its induction as a new cancer treatment modality of development for natural medicines.

The Role of RUNX1 in NF1-Related Tumors and Blood Disorders

  • Na, Youjin;Huang, Gang;Wu, Jianqiang
    • Molecules and Cells
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    • v.43 no.2
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    • pp.153-159
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    • 2020
  • Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder. NF1 patients are predisposed to formation of several type solid tumors as well as to juvenile myelomonocytic leukemia. Loss of NF1 results in dysregulation of MAPK, PI3K and other signaling cascades, to promote cell proliferation and to inhibit cell apoptosis. The RUNX1 gene is associated with stem cell function in many tissues, and plays a key role in the fate of stem cells. Aberrant RUNX1 expression leads to context-dependent tumor development, in which RUNX1 may serve as a tumor suppressor or an oncogene in specific tissue contexts. The co-occurrence of mutation of NF1 and RUNX1 is detected rarely in several cancers and signaling downstream of RAS-MAPK can alter RUNX1 function. Whether aberrant RUNX1 expression contributes to NF1-related tumorigenesis is not fully understood. This review focuses on the role of RUNX1 in NF1-related tumors and blood disorders, and in sporadic cancers.

A systematic mRNA control mechanism for germline stem cell homeostasis and cell fate specification

  • Lee, Myon-Hee;Mamillapalli, Srivalli Swathi;Keiper, Brett D.;Cha, Dong Seok
    • BMB Reports
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    • v.49 no.2
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    • pp.93-98
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    • 2016
  • Germline stem cells (GSCs) are the best understood adult stem cell types in the nematode Caenorhabditis elegans, and have provided an important model system for studying stem cells and their cell fate in vivo, in mammals. In this review, we propose a mechanism that controls GSCs and their cell fate through selective activation, repression and mobilization of the specific mRNAs. This mechanism is acutely controlled by known signal transduction pathways (e.g., Notch signaling and Ras-ERK MAPK signaling pathways) and P granule (analogous to mammalian germ granule)-associated mRNA regulators (FBF-1, FBF-2, GLD-1, GLD-2, GLD-3, RNP-8 and IFE-1). Importantly, all regulators are highly conserved in many multi-cellular animals. Therefore, GSCs from a simple animal may provide broad insight into vertebrate stem cells (e.g., hematopoietic stem cells) and their cell fate specification.

Functional Characterization of cAMP-Regulated Gene, CAR1, in Cryptococcus neoformans

  • Jung, Kwang-Woo;Maeng, Shin-Ae;Bahn, Yong-Sun
    • Mycobiology
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    • v.38 no.1
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    • pp.26-32
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    • 2010
  • The cyclic AMP (cAMP) pathway plays a major role in growth, sexual differentiation, and virulence factor synthesis of pathogenic fungi. In Cryptococcus neoformans, perturbation of the cAMP pathway, such as a deletion in the gene encoding adenylyl cyclase (CAC1), causes defects in the production of virulence factors, including capsule and melanin production, as well as mating. Previously, we performed a comparative transcriptome analysis of the Ras- and cAMP- pathway mutants, which revealed 163 potential cAMP-regulated genes (38 genes at a 2-fold cutoff). The present study characterized the role of one of the cAMP pathway-dependent genes (serotype A identification number CNAG_ 06576.2). The expression patterns were confirmed by Northern blot analysis and the gene was designated cAMP-regulated gene 1 (CAR1). Interestingly, deletion of CAR1 did not affect biosynthesis of any virulence factors and the mating process, unlike the cAMP-signaling deficient cac1$\Delta$ mutant. Furthermore, the car1$\Delta$ mutant exhibited wild-type levels of the stress-response phenotype against diverse environmental cues, indicating that Car1, albeit regulated by the cAMP-pathway, is not essential to confer a cAMP-dependent phenotype in C. neoformans.

A Study on NOx Removal Efficiency Depending on Electrode Configurations of Silent Discharges (무성방전 플라즈마 전극구조에 대한 질소산화물 제거효율 연구)

  • Hyung-Taek Kim;Young-Sik Chung;Myung-Whan Whang;Elena. A. Filimonova
    • Journal of the Korean Society of Safety
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    • v.17 no.3
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    • pp.112-117
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    • 2002
  • A comparative investigation of an experimental and a simulation of chemical kinetics for NOx removal from silent(dielectric-barrier) discharges is presented. Several types of dielectric-barrier discharges were implemented depending upon the configuration of electrodes. The simulation was based on an approximate mathematical model for plasma cleaning of waste gas. The influence of non-uniform distributions of species due to the production of primary active particles in the streamer channel was taken into account. A comparison of observed experimental to the calculated removal efficiency of NOx showed acceptable agreement.

Intracranial Germ Cell Tumor in the Molecular Era

  • Phi, Ji Hoon;Wang, Kyu-Chang;Kim, Seung-Ki
    • Journal of Korean Neurosurgical Society
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    • v.61 no.3
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    • pp.333-342
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    • 2018
  • Intracranial germ cell tumors (iGCTs) are a heterogeneous group of tumors with peculiar characteristics clearly distinguished from other brain tumors of neuroepithelial origin. Diverse histology, similarity to gonadal GCT, predilection to one sex, and geographic difference in incidence all present enigmas and fascinating challenges. The treatment of iGCT has advanced for germinoma to date; thus, clinical attention has shifted from survival to long-term quality of life. However, for non-germinomatous GCT, current protocols provide only modest improvement and more innovative therapies are needed. Recently, next-generation sequencing studies have revealed the genomic landscape of iGCT. Novel mutations in the KIT-RAS-MAPK and AKT-MTOR pathways were identified. More importantly, methylation profiling revealed a new method to assess the pathogenesis of iGCT. Molecular research will unleash new knowledge on the origin of iGCT and solve the many mysteries that have lingered on this peculiar neoplasm for a long time.

Carcinogenic Role of Tumor Necrosis Factor-α Inducing Protein of Helicobacter pylori in Human Stomach

  • Suganuma, Masami;Kuzuhara, Takashi;Yamaguchi, Kensei;Fujiki, Hirota
    • BMB Reports
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    • v.39 no.1
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    • pp.1-8
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    • 2006
  • Helicobacter pylori is the definitive carcinogen for stomach cancer and is known to induce proinflammatory cytokines, such as tumor necrosis factor-$\alpha$ (TNF-$\alpha$) and interleukin-1(IL-1) in the stomach. Based on our findings that TNF-$\alpha$ is an endogenous tumor promoter, we identified the TNF-$\alpha$ inducing protein (Tip$\alpha$) gene family, and confirmed Tip$\alpha$ and HP-MP1 as new carcinogenic proteins of H. pylori. Tip$\alpha$ protein is unique to H. pylori, and this paper shows the strong tumor promoting activity of Tip$\alpha$ gene family, in cooperation with Ras protein and its mechanisms of action in relation to NF-${\kappa}B$ activation, and discusses the carcinogenic role of Tip$\alpha$ in stomach cancer. Our recent finding showing that penicillin-binding proteins of other bacteria are weak homologues of Tip$\alpha$ is also discussed.