• Korean Journal of Microbiology
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• v.30 no.5
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• pp.347-354
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• 1992

New regulatory, loci which participate in the regulation of anaerobic inducible gene expression in Salmonella typhimurium were identified. We observed the regulatory network of new regulator mutations to various anaerobic inducible gene (1). Some anaerobic inducible lac fusions were also induced at low pH condition which was severe environment to withstand for its virulence at the place like phagolysosome. Sic oxygen-regulated regulatory mutants (oxr) isolated by Tn10 mutagenesis were divided into two groups. Five of them were found to show negative effect on the regulation of anaerobic gene expression, while on e showed positive effect on the regulation. Genetic loci of four oxr were identified with 54 Mud-P22 lysogens covering the whole chromosome of S. typhimurium, in the nearby region of map unit 87 min (oxr101), 63 min (oxr104), 97 min (oxr 105), and 57 min (oxr 106), respectively. Two oxr mutants were subjected to two-dimensional polyacrylamide electrophoretic analysis of anaerobic inducible proteins for searching the control circuitry of our oxr mutants.

• Archives of Pharmacal Research
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• v.22 no.1
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• pp.1-8
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• 1999

Transforming growth factor-$\beta$ (TGF-$\beta$) is the prototypical multifunctional cytokine, participating in the regulation of vital cellular activities such as proliferation and differentiations as well as a number of basic physiological functions. The effects of TGF-$\beta$ are critically dependent on the expression and distribution of a family of TGF-$\beta$ receptors, the TGF-$\beta$ types I, II, and III. It is now known that a wide variety of human pathology can be caused by aberrant expression and function of these receptors. the coding sequence of the type II receptor (RII) appears to render it uniquely susceptible to DNA replication errors in the course of normal cell division. By virtue of its key role in the regulation of cell proliferation, TGF-$\beta$ RII should be considered as a tumor suppressor gene. High levels of mutation in the TGF-$\beta$ RII gene have been observed in a wide range of primarily epithelial malignancies, including colon and gastric cancer. It appears likely that mutation of the TGF-$\beta$ RII gene may be a very critical step in the pathway of carcinogenesis.

• Reproductive and Developmental Biology
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• v.34 no.2
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• pp.103-109
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• 2010

Functional regulation of a specific tissue or organ is controlled by a number of ways, including local cell-cell interaction. Of several forms of cell-cell junctional complexes, gap junctions are caught a great attention due to a formation of direct linkage between neighboring cells. Gap junctions are consisted of connexin (Cx) isoforms. In the present study, we evaluated expressional profiling of Cx isoforms in the rat initial segment (IS) of the male reproductive tract at different postnatal ages. The presence and expression of 13 Cx isoform mRNAs were determined by semi-quantitative real-time PCR analyses. A total of 8 Cx isoform mRNAs were detected in the IS of the male rats during postnatal development. The highest level of Cx30.3 mRNA was found at 5 months of age, while abundance of Cx31 mRNA was the highest at 1 year of age. Expression of Cx31.1 gene was relatively consistent during the postnatal development. Fluctuation of Cx32 and 37 gene expression was observed during the postnatal period. Significant elevation of Cx40 mRNA abundance was detected at 25 days of age and older ages. Expression patterns of Cx43 and 45 genes were similar with the highest level at 2 weeks of age, followed by gradual decreases at older ages. These results indicate differential regulation on expression of Cx isoforms in the rat IS during postnatal development. A complicated regulation of gene expression of Cx isoforms in the IS at different postnatal ages is suggested.

• BMB Reports
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• v.46 no.2
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• pp.92-96
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• 2013

The breast cancer susceptibility gene BRCA1 encodes a nuclear protein, which functions as a tumor suppressor and is involved in gene transcription and DNA repair processes. Many families with inherited breast and ovarian cancers have mutations in the BRCA1 gene. However, only a few studies have reported on the mechanism underlying the regulation of BRCA1 expression in humans. In this study, we investigated the transcriptional regulation of BRCA1 in HeLa cells treated with etoposide. We found that three Egr-1-binding sequences (EBSs) were located at -1031, -1005, and -385 within the enhancer region of the BRCA1 gene. Forced expression of Egr-1 stimulated the BRCA1 promoter activity. EMSA data showed that Egr-1 bound directly to the EBS within the BRCA1 gene. Knockdown of Egr-1 through the expression of a small hairpin RNA (shRNA) attenuated etoposide-induced BRCA1 promoter activity. We conclude that Egr-1 targets the BRCA1 gene in HeLa cells exposed to etoposide.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.1
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• pp.37-44
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• 2017

Regulation of vascular smooth muscle cell (VSMC) phenotype plays an essential role in many cardiovascular diseases. In the present study, we provide evidence that $kr{\ddot{u}}ppel$-like factor 8 (KLF8) is essential for tumor necrosis factor ${\alpha}$ ($TNF{\alpha}$)-induced phenotypic conversion of VSMC obtained from thoracic aorta from 4-week-old SD rats. Stimulation of the contractile phenotype of VSMCs with $TNF{\alpha}$ significantly reduced the VSMC marker gene expression and KLF8. The gene expression of KLF8 was blocked by $TNF{\alpha}$ stimulation in an ERK-dependent manner. The promoter region of KLF8 contained putative Sp1, KLF4, and $NF{\kappa}B$ binding sites. Myocardin significantly enhanced the promoter activity of KLF4 and KLF8. The ectopic expression of KLF4 strongly enhanced the promoter activity of KLF8. Moreover, silencing of Akt1 significantly attenuated the promoter activity of KLF8; conversely, the overexpression of Akt1 significantly enhanced the promoter activity of KLF8. The promoter activity of SMA, $SM22{\alpha}$, and KLF8 was significantly elevated in the contractile phenotype of VSMCs. The ectopic expression of KLF8 markedly enhanced the expression of SMA and $SM22{\alpha}$ concomitant with morphological changes. The overexpression of KLF8 stimulated the promoter activity of SMA. Stimulation of VSMCs with $TNF{\alpha}$ enhanced the expression of KLF5, and the promoter activity of KLF5 was markedly suppressed by KLF8 ectopic expression. Finally, the overexpression of KLF5 suppressed the promoter activity of SMA and $SM22{\alpha}$, thereby reduced the contractility in response to the stimulation of angiotensin II. These results suggest that cross-regulation of KLF family of transcription factors plays an essential role in the VSMC phenotype.

• Proceedings of the Zoological Society Korea Conference
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• 1995.10b
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• pp.82-82
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• 1995

Regulation of enzyme synthesis by transcriptional and translational control systems provides rather stable adaptation to change of amino acid level in the growth medium, while manipulation of enzyme activity through endproduct feedback inhibition represents rather short-term and reversible ways of adjusting metabolic fluctuation of amino acid level. Various control mechanisms interplay to regulate genes encoding enzymes for amino acid biosynthesis in the yeast, Sacchromyces cerevisiae. When amino acids are in short supply, genes under a cross-pathway regulatory mechanism Or general amino acid control (general control) increase their action, in which Gcn4p is the major positive regulator of gene expression. When cells are cultured in minimal medium, basal level expression is also regulated by supplementary control elements, where inorganic phosphate level is additionally involved. Most of amino acid biosynthetic genes are also regulated by the level of endproduct of the pathway. This pathway-specific regulatory mechanism is called specific amino acid control (specific controD, under which gene expression is reduced when endproduct is present in the medium. Derepression of a gene through general control can be usually overridden by repression through specific control, where the endproduct level of that particular pathway is high and not limiting. In this presentation, regulatory factors for basal level expression and general control of yeast amino acid biosynthesis will be discussed, m addition to pathway-specific repression patterns and interaction between CrOSS- and specific-control mechanisms. Preliminary results are also presented from the investigation of the cloned genes in the threonine biosynthetic pathway of the yeast. yeast.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.34 no.5
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• pp.518-524
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• 2008

Chromosome 18q alteration plays a key role in colorectal tumorigenesis, and loss of heterozygosity at 18q is associated with a poor prognosis in colon cancer. DCC(Deleted in Colorectal Cancer) is a putative tumor- suppressor gene at 18q21 that encodes a transmembrane protein with structural similarity to neural cell adhesion molecule that is involved in both epithelial and neuronal cell differentiation. DCC is implicated in regulation of cell growth, survival and proliferation. Thus, tumor progression in squamous cell carcinoma, stomach cancer, colorectal cancer correlates with downregulation of DCC expression. The mechanism for DCC suppression is associated with hypermethylation of the DCC gene promoter region. Hence, the goal of this study is to identify the promoter methylation responsible for the down-regulation of DCC expression in oral squamous cell carcinoma. 12 of tissue specimens for the study are excised and gathered from 12 patients who are diagnosed as SCC in department of OMS, dental hospital, dankook university. To find expression of DCC in each tissue samples, immunohistochemical staining, RT-PCR gene analysis and methylation specific PCR are processed. The results are as follows. 1. In the DCC gene RT-PCR analysis, 5(41.6%) of 12 specimens of oral squamous cell carcinoma did not expressed DCC gene. 2. In the promoter methylation specific PCR analysis, 5(41.6%) of 12 specimens showed promoter methylation of DCC gene. 3. In the immunohistochemical staining of poor differentiated and invasive oral squamous cell carcinoma, loss of DCC expression was observed. These findings suggest that methylation of the DCC gene may play a role in loss of gene expression in invasive oral squamous cell carcinoma.

• Asian-Australasian Journal of Animal Sciences
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• v.17 no.12
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• pp.1635-1640
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• 2004

Two experiments were conducted to evaluate developmental gene expression of antimicrobial peptide PR-39 and effect of zinc oxide on gene regulation of PR-39 in piglets using semi-quantitative RT-PCR analysis. In experiment 1, fifteen female Tai-Hu pigs (a local breed in China) in five groups, each of three pigs at 1, 14, 28, 42 and 56 days of age were used to determine effect of age and weaning on mRNA expression of PR-39. In experiment 2, nine groups of pigs (total seventy-two female 36 days-age weanling Tai-Hu piglets) were assigned to three treatments (${ZnO}_0$, ${ZnO}_{100}$ and ${ZnO}_{3000}$). The feeding experimental period lasted 15 days. After feeding experiment, nine pigs with three animals in each treatment were chosen to determine the effect of ZnO on PR-39 mRNA expression of pigs. The results showed that PR-39 mRNA levels increased steadily in postnatal day 1-28 (preweaning), and weaning significantly decreased PR-39 mRNA expression of piglets (p<0.05). ${ZnO}_{3000}$ (3,000 mg zinc/kg diet) significantly increased PR-39 mRNA expression (p<0.05) when piglets were feed ${ZnO}_{3000}$ diet for 15 days. ${ZnO}_{100}$ (100 mg zinc/kg diet) also increased PR-39 gene expression, but the result was not statistically significant (p>0.05). The result was in accordance with the effect of ${ZnO}_{3000}$ and ${ZnO}_{100}$ on weight gain of piglets and prevention of diarrhea.

• BMB Reports
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• v.53 no.1
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• pp.3-9
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• 2020

The mitochondrial genome encodes 13 proteins that are components of the oxidative phosphorylation system (OXPHOS), suggesting that precise regulation of these genes is crucial for maintaining OXPHOS functions, including ATP production, calcium buffering, cell signaling, ROS production, and apoptosis. Furthermore, heteroplasmy or mis-regulation of gene expression in mitochondria frequently is associated with human mitochondrial diseases. Thus, various approaches have been developed to investigate the roles of genes encoded by the mitochondrial genome. In this review, we will discuss a wide range of techniques available for investigating the mitochondrial genome, mitochondrial transcription, and mitochondrial translation, which provide a useful guide to understanding mitochondrial gene expression.

• Biomedical Science Letters
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• v.12 no.3
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• pp.131-137
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• 2006

RGS is a negative regulator of G-protein signaling and can be identified by the presence of a conserved $120{sim}125$ amino acid motif, which is referred to as the RGS box. A number of RGSs are induced in response to a wide variety of stimuli. Increased levels of RGSs lead to significant decreases in GPCR responsiveness. To obtain further evidence of a role of RGS proteins in rat C6 astrocytoma cells, we first determined the expression profile of RGS-specific mRNA in C6 cells using reverse transcription-polymerase chain reaction (RT-PCR) with a poly dT18 primer and transcript-specific primers. We found that RGS2, RGS3, RGS6, RGS9, RGS10, RGS12, and RGS16 were differentially expressed in C6 astrocytoma cells. The highest expression rate was found for RGS3, followed by RGS16, RGS10 and RGS9, whereas the expression level for RGS2 was barely detectable. We next assessed whether forskolin regulated the expression of RGSs expressed in C6 astrocytoma cells. The present study found that forskolin dose-dependently stimulated the expression of RGS2 transcripts. This up-regulation of RGS2 gene was abrogated by H-89, potent and broad-spectrum protein kinase A (PKA) inhibitors. Actinomycin D completely inhibited the up-regulation of RGS2 gene induced by forskolin $(10{\mu}M)$, indicating that the regulation of RGS2 gene is controlled at the transcriptional level. In addition, forskolin did significantly activate transcriptional cAMP response element (CRE) in either HEK 293 cells or C6 cells and did not modulate the $NF-{\kappa}B$ and AP-l activity as measured by luciferase reporter gene assay. Finally, forskolin induced the expression of RGS2 mRNA in C6 astrocytoma cells, which depend on the PKA pathway and CRE transcriptional pathways.