• Title/Summary/Keyword: Suppressor

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microRNA-29b: an Emerging Player in Human Cancer

  • Liu, Hao;Wang, Bin;Lin, Jie;Zhao, Liang
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.21
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    • pp.9059-9064
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    • 2014
  • MicroRNAs (miRNAs) are ubiquitously expressed small, non-coding RNAs that negatively regulate gene expression at a post transcriptional/translational level. They have emerging as playing crucial roles in cancer at all stages ranging from initiation to metastasis. As a tumor suppressor miRNA, aberrant expression of microRNA-29b (miR-29b) has been detected in various types of cancer, and its disturbance is related with tumor development and progression. In this review, we summarize the latest findings with regard to the tumor suppressor signatureof miR-29b and its regulatory mechanisms. Our review highlights the diverse relationships between miR-29b and its target genes in malignant tumors.

Coaxial-type Transient Voltage Suppressor for Antenna Circuit Protection (안테나용 동축형 과도전압 차단장치)

  • 송재용;이종혁;길경석;배정철
    • Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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    • 2000.05a
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    • pp.489-492
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    • 2000
  • This paper describes a new transient voltage suppressor(TVS) with a low insertion loss and a very wide frequency bandwidth to protect antenna circuit from transient voltages. Conventional protection devices have some problems such as low frequency bandwidth and high insertion loss. In order to improve these limitations, a coaxal type TVS, which consists of a gas tube is developed. The performance of the proposed transient voltage suppressor is tested by using a combination surge generator specified in IEC 61000-4-5 standard and by using a network analyzer of 40 MHz ∼ 5GHz bandwidth. From the experimental results, it is confirmed that the proposed TVS has an enough protection performance in low insertion loss and in wide frequency bandwidth

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Tumour Suppressor Mechanisms in the Control of Chromosome Stability: Insights from BRCA2

  • Venkitaraman, Ashok R.
    • Molecules and Cells
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    • v.37 no.2
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    • pp.95-99
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    • 2014
  • Cancer is unique amongst human diseases in that its cellular manifestations arise and evolve through the acquisition of somatic alterations in the genome. In particular, instability in the number and structure of chromosomes is a near-universal feature of the genomic alterations associated with epithelial cancers, and is triggered by the inactivation of tumour suppressor mechanisms that preserve chromosome integrity in normal cells. The nature of these mechanisms, and how their inactivation promotes carcinogenesis, remains enigmatic. I will review recent work from our laboratory on the tumour suppressor BRCA2 that addresses these issues, focusing on new insights into cancer pathogenesis and therapy that are emerging from improved understanding of the molecular basis of chromosomal instability in BRCA2-deficient cancer cells.

Targeting Tumor Metastasis by Regulating Nm23 Gene Expression

  • Prabhu, V. Vinod;Siddikuzzaman, Siddikuzzaman;Grace, V.M. Berlin;Guruvayoorappan, C.
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.8
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    • pp.3539-3548
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    • 2012
  • The Nm23 gene is a metastatic suppressor identified in a melanoma cell line and expressed in different tumors where their levels of expression are associated with reduced or increased metastatic potential. Nm23 is one of the over 20 metastasis suppressor genes (MSGs) confirmed in vivo. It is highly conserved from yeast to human, implying a critical developmental function. Tumors with alteration of the p53 gene and reduced expression of the Nm23 gene are more prone to metastasis. Nm23-H1 has 3'-5' exonuclease activity. This review focuses on the role of Nm23 in cancer progression and also a potential novel target for cancer therapy.

Tumor suppressor $p16^{INK4a}$ in Cancer

  • Lee, Mee-Hyun;Choi, Bu-Young;Surh, Young-Joon
    • Environmental Mutagens and Carcinogens
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    • v.25 no.3
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    • pp.87-96
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    • 2005
  • [ $p16^{INK4a}$ ] is a tumor suppressor that belongs to the INK4 family of the cyclin D-dependent kinases (cdk) inhibitors. It plays regulatory roles in cell proliferation and in tumorigenesis by interacting with Rb signaling. Abnormally elevated $p16^{INK4a}$ protein expression causes cell cycle arrest (G1/S transition) and loss of cyclin-cdk activity. In many cancers, $p16^{INK4a}$ is altered by mutation, deletion, and promoter methylation. This review summarizes the function of p16 as an important regulator of cancer pathobiology and a promising target fer developing cancer therapeutic and chemopreventive agents.

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A Study on the Slide Suppressor Wall Method Reinforced with Nailing System (Nailing System으로 보강된 억지벽체공법에 관한 연구)

  • 김홍택;강인규
    • Geotechnical Engineering
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    • v.11 no.1
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    • pp.79-100
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    • 1995
  • This paper proposes a stabilizing method against landslide using slide suppressor wall reinforced with soil nails. Included are a procedure to predict earth pressures acting on the concrete panel and a method of analysis of stabilizing pile. Based on the proposed procedure, the efficient installation type and inclusion angle of nails are analyzed. Also, optimum location of the slide suppressor wall composed of concrete panel and stabilizing pile is analyzed. Finally the comparison with a method proposed by Wright is made, and the effect of interactions between stabilizing piles is examined, throughout the design example.

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Exploring the Potential of Glycolytic Modulation in Myeloid-Derived Suppressor Cells for Immunotherapy and Disease Management

  • Jisu Kim;Jee Yeon Choi;Hyeyoung Min;Kwang Woo Hwang
    • IMMUNE NETWORK
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    • v.24 no.3
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    • pp.26.1-26.19
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    • 2024
  • Recent advancements in various technologies have shed light on the critical role of metabolism in immune cells, paving the way for innovative disease treatment strategies through immunometabolism modulation. This review emphasizes the glucose metabolism of myeloid-derived suppressor cells (MDSCs), an emerging pivotal immunosuppressive factor especially within the tumor microenvironment. MDSCs, an immature and heterogeneous myeloid cell population, act as a double-edged sword by exacerbating tumors or mitigating inflammatory diseases through their immune-suppressive functions. Numerous recent studies have centered on glycolysis of MDSC, investigating the regulation of altered glycolytic pathways to manage diseases. However, the specific changes in MDSC glycolysis and their exact functions continue to be areas of ongoing discussion yet. In this paper, we review a range of current findings, including the latest research on the alteration of glycolysis in MDSCs, the consequential functional alterations in these cells, and the outcomes of attempts to modulate MDSC functions by regulating glycolysis. Ultimately, we will provide insights into whether these research efforts could be translated into clinical applications.

Study on a Suppressor System for Segregation-Distorter Action in Natural Populations of Drosophila melanogaster in Korea (한국산 초파리의 자연집단에 있어서의 SD 요소에 대한 억제요인에 대하여)

  • Chung, Yong-Jai;Kang, Soon-Ja
    • The Korean Journal of Zoology
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    • v.12 no.1
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    • pp.22-28
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    • 1969
  • In order to see if any suppressor system for the SD action was involved in natural populations of D. melanogaster samples from the populations of nine localities in Korea, Choonchun, Yusoo, Namhai, Shinchon(Seoul), Kwangjoo(Kyunggi), Koonsan, Kwangjoo(Chunnam), Jejoo and Pusan were analyzed by using the mating scheme for locating the suppressor on chromosome pairs. And also two kinds of recombinant SD lines R-1, the American line and $R(SD^NH -1)-1$, the Japanese one were used in order to see any difference of the response of the suppressor for differently originated SD. The results of the experiment are given below. (1) The suppressor system was involved in all lines of natural populations from nine localities of Korea. (2) Most of the suppressors were found to be located on the X chromosome and only a few lines from three populations showed to carry the suppressors on the second chromosome and on the third or fourth chromosoem. (3) The response of the suppressor for differently originated SD lines showed no significant difference.

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Loss of Heterozygosity and Microsatellite Instability at Multiple Tumor Suppressor Genes in Gastric Carcinomas (위암에서 여러 종양억제유전자 부위의 이형접합성 소실과 현미 부수체 불안정성)

  • Cho Young Gu;Kim Chang Jae;Park Cho Hyun;Kim Young Sil;Kim Su Young;Nam Suk Woo;Lee Sug Hyung;Yoo Nam Jin;Lee Jung Young;Park Won Sang
    • Journal of Gastric Cancer
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    • v.3 no.4
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    • pp.214-220
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    • 2003
  • Purpose: The aim of this study was to investigate the frequency of loss of heterozygosity and the microsatellite instability at multiple tumor suppressor gene loci in gastric adenocarcinomas. Materials and Methods: Loss of heterozygosity and the microsatellite instability at several tumor suppressor gene loci were analyzed in 29 primary gastric carcinomas by using microdissection and the polymerase chain reaction. Results: Twenty-three ($79\%$) of the 29 cases demonstrated loss of heterozygosity at one or more loci. The frequency of loss of heterozygosity at the p53 locus was the highest ($63\%$) and those at the VHL, APC, p16, Rb, MEN1, BRCA1, DPC4, 3p21, and 16p13 region were $41\%,\;36\%,\;19\%,\;29\%,\;33\%,\;26\%,\;21\%,\;32\%,\;and\;11\%$, respectively. Compared with histological type, loss of heterozygosity was more common in diffuse-type gastric cancer (P<0.01). Interestingly, 9 of 10 tumors with allelic deletion at the p53 locus showed loss of heterozygosity at other tumor suppressor gene loci. The microsatellite instability was also detected in 6 ($20\%$) of the 29 cases at one or more loci. Conclusion: These data suggest that frequent loss of heterozygosity and the microsatellite instability at multiple tumor suppressor genes might be required for the development and the progression of gastric carcinomas and that p53 allelic loss may be the most frequent event in the development of gastric carcinomas.

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Crystal Structure of the PTEN Tumor Suppressor: Implications for Its Phosphoinositide Phosphatase Activity and Membrane Association

  • Lee, Jie-Oh;Haijuan Yang;Nikola Pavletich
    • Proceedings of the Korean Biophysical Society Conference
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    • 2001.06a
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    • pp.20-20
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    • 2001
  • The PTEN tumor suppressor is mutated in diverse human cancers and in hereditary cancer predisposition syndromes. PTEN is a phosphatase that can act on both polypeptide and phosphoinositide substrates in vitro. The PTEN structure reveals a phosphatase domain similar to protein phosphatases but having an enlarged active site important for the accommodation of the phosphoinositide substrate.(omitted)

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