• Microbiology and Biotechnology Letters
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• v.25 no.2
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• pp.137-143
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• 1997

Porcine transforming growth factor-$\beta$1 (TGF-$\beta$1) was expressed in Escherichia coli using cDNA of TGF-$\beta$1 and glutathione S-transferase (GST) fusion vector pGEX-1$\lambda$T. An ApoI-Tth111I fragment of cDNA which correspond to the amino acid residues from 123 to 390 of the precursor TGF-$\beta$1 was inserted into EcoRI-Tth111I digested pGEM#-l$\lambda$T and the recombined plasmid was named pGET-12. Gene products from the cloned regions of the recombinant plasmids pGET-12 was not detected in soluble fraction of cell free extract but detected in insoluble fraction. The solubilization of insoluble gene product was achieved by the treatment of N-laurylsarcosine. Molecular weight of partially purified proteins determined by electrophoresis was same as expected from cloned fragment. The ELISA test results of the purified proteins showed that immunologically detectable epitope was preserved in recombinant protein.

• The Korean Journal of Zoology
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• v.38 no.1
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• pp.20-25
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• 1995

계배 limb bud 간충직 연골원성 세포로부터 연골세포로의 분화에 미치는 transforming growth factor-f2(TGF-$\beta$2)의 영향을 알아보기 위하여, Hamburger-Hamilton stages 23/24의 간충직 세포들을 미세배양법으로 배양하면서. TGF-$\beta$2의 농도 및 처리시간에 따른 연골세포의 분화에 미치는 영향을 조사하였다 그 결과 TGF-$\beta$2는 배양 첫 24시간 동안 1-2 ng/ml의 농도로 처리하였을 때 가장 효과적으로 연골세포의 분화를 촉진하였으며, 또한 TGF-$\beta$2의 처리군에서 배양 3일째에 tsss) sulfate의 glycosaminoglvcan으로의 유입량이 현저히 증가함을 보였다 한편. 배양 48시간내에TGF-$\beta$2를 처리한 경우 분화를 촉진 유도한 반면, 배양 48시간 이후에 처리하였을 때에는 분화 촉진 효과가 나타나지 않았다. 이상의 결과로부터 TGF-$\beta$2는 연골원 세포의 분화 초기단계에 세포외기질의 합성을 촉진시켜 세포응축을 유발하고. 세포-세포 및 세포-세포외기질의 상호작용을 증대시킴으로써 연골세포로의 분화를 촉진시킬 것으로 추정되었다.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.142-142
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• 2003

Transforming growth factor (TGF)-${\beta}$, a hormonally active polypeptide found in normal and transformed tissue, is a potent regulator of cell growth and differentiation. In this study, we examined the effect of TGF-${\beta}$ on invasion and motility of MCF10A human breast epithelial cells. TGF-${\beta}$ induced migration and invasive phenotype of the parental MCF10A cells in a dose-dependent manner.(omitted)

• Journal of Cancer Prevention
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• v.23 no.4
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• pp.162-169
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• 2018

$TGF-{\beta}$ signaling plays a tumor suppressive role in normal and premalignant cells but promotes tumor progression during the late stages of tumor development. The $TGF-{\beta}$ signaling pathway is tightly regulated at various levels, including transcriptional and post-translational mechanisms. Ubiquitination of signaling components, such as receptors and Smad proteins is one of the key regulatory mechanisms of $TGF-{\beta}$ signaling. Tripartite motif (TRIM) family of proteins is a highly conserved group of E3 ubiquitin ligase proteins that have been implicated in a variety of cellular functions, including cell growth, differentiation, immune response, and carcinogenesis. Recent emerging studies have shown that some TRIM family proteins function as important regulators in tumor initiation and progression. This review summarizes current knowledge of TRIM family proteins regulating the $TGF-{\beta}$ signaling pathway with relevance to cancer.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2019.10a
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• pp.70-70
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• 2019

Hepatic fibrosis is a common chronic liver diseases, characterized by the excessive deposition of extracellular matrix (ECM). Activation of hepatic stellate cells (HSC) is proliferative and fibrogenic and accumulating ECM. Transforming growth factor $(TGF)-{\beta}1$ is a critical mediator of HSC activation and ECM accumulation leading to fibrosis. Tenebrio molitor (TM), known as yellow mealworms, is reported in many countries as the nutritional value of foods. Our study has aims of finding liver function improvement effect of S. cerevisiae fermented Tenebrio molitor (SCTM) in vitro model. SCTM regulates $TGF-{\beta}1$ induced hepatic fibrosis via regulation of the $TGF-{\beta}1/Smad$ signaling. Also, we compared the components increased by yeast fermentation. It is possible to make a useful insect-derived alternative food in the improvement of hepatic liver disease.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.152.2-153
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• 2003

${\beta}Although$ it has been demonstrated that $p2l^{WAFl/Cip1}$, a well known cell cycle inhibitor, could be induced by $TGF-{\beta}$ in a p53-independent manner, the detailed signal transduction pathways still remain poorly understood. In this study, we show that ERK is required for $TGF-{\beta}$ induction of $p21^{WAF1/Cip1}$, but JNK or p38 MAPK is not. ERK activation by $TGF-{\beta}$ significantly attenuated by treatment with ROS scavenger such as NAC or catalase, indicating that ROS, mainly $H_2O_2$, generation by $TGF-{\beta}$ might stimulate ERK signaling pathway to require the induction of $p21^{WAF1/Cip1}$. (omitted)

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.846-860
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• 1998

Background: Endotoxin (LPS : lipopolysaccharide), a potent activator of immune system, can induce acute and chronic inflammation through the production of cytokines by a variety of cells, such as monocytes, endothelial cells, lymphocytes, eosinophils, neutrophils and fibroblasts. LPS stimulate the mononucelar cells by two different pathway, the CD14 dependent and independent way, of which the former has been well documented, but not the latter. LPS binds to the LPS-binding protein (LBP), in serum, to make the LPS-LBP complex which interacts with CD14 molecules on the mononuclear cell surface in peripheral blood or is transported to the tissues. In case of high concentration of LPS, LPS can stimulate directly the macrophages without LBP. We investigated to detect the generation of proinflammatory cytokines such as interleukin 1 (IL-1), IL-6 and TNF-$\alpha$ and fibrogenic cytokine, TGF-$\beta$, by peripheral blood mononuclear cells (PBMC) after LPS stimulation under serum-free conditions, which lacks LBPs. Methods : PBMC were obtained by centrifugation on Ficoll Hypaque solution of peripheral venous bloods from healthy normal subjects, then stimulated in the presence of LPS (0.1 ${\mu}g/mL$ to 100 ${\mu}g/mL$ ). The activities of IL-1, IL-6, TNF, and TGF-$\beta$ were measured by bioassaies using cytokines - dependent proliferating or inhibiting cell lines. The cellular sources producing the cytokines was investigated by immunohistochemical stains and in situ hybridization. Results : PBMC started to produce IL-6, TNF-$\alpha$ and TGF-$\beta$ in 1 hr, 4 hrs and 8hrs, respectively, after LPS stimulation. The production of IL-6, TNF-$\alpha$ and TGF-$\beta$ continuously increased 96 hrs after stimulation of LPS. The amount of production was 19.8 ng/ml of IL-6 by $10^5$ PBMC, 4.1 ng/mL of TNF by $10^6$ PBMC and 34.4 pg/mL of TGF-$\beta$ by $2{\times}10^6$ PBMC. The immunoreactivity to IL-6, TNF-$\alpha$ and TGF-$\beta$ were detected on monocytes in LPS-stimulated PBMC. Some of lymphocytes showed positive immunoreactivity to TGF-$\beta$. Double immunohistochemical stain showed that IL-1$\beta$, IL-6, TNF-$\alpha$ expression was not associated with CD14 postivity on monocytes. IL-1$\beta$, IL-6, TNF-$\alpha$ and TGF-$\beta$mRNA expression were same as observed in immunoreactivity for each cytokines. Conclusion: When monocytes are stimulated with LPS under serum-free conditions, IL-6 and TNF-$\alpha$ are secreted in early stage of inflammation. In contrast, the secretion of TGF-$\beta$ arise in the late stages and that is maintained after 96 hrs. The main cells releasing IL-1$\beta$, IL-6, TNF-$\alpha$ and TGF-$\beta$ are monocytes, but also lymphocytes can secret TGF-$\beta$.

• Journal of Microbiology and Biotechnology
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• v.12 no.1
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• pp.65-70
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• 2002

A TGF-${\beta}1$/GFP monomeric fusion protein was cloned from pPK9A and pGFP-Cl plasmid by PCR amplification. The fusion protein was expressed in a $Bac-To-Bac^{TM}$ baculovirus expression system. A 45 kDa fusion protein was purified using an Ni-NTA column with 300 mM imidazol from a cell lysate infected with recombinant viruses for 72 h post-infection. The fusion protein cross-reacted with the commercial $TGF-{\beta}1$ polyclonal Ab as well as Ab raised against a precursor, monomeric $TGF-{\beta}1$, and GFP. The binding activity of the fusion protein with a $TGF-{\beta}1$ receptor was examined. Fluorescence was observed in Mv1Lu cells, yet not in insect cells treated with the fusion protein. No fluorescence was detected in Mv1Lu cells incubated with the fusion protein treated with Ab prior to the binding reaction, or with GFP alone, thereby indicating that the binding of the fusion protein was specific to $TGF-{\beta}1$ with a receptor.

• IMMUNE NETWORK
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• v.14 no.5
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• pp.237-240
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• 2014

Endoglin (also known as CD105 or TGF-${\beta}$ type III receptor) is a co-receptor involved in TGF-${\beta}$ signaling. In atherosclerosis, TGF-${\beta}$ signaling is crucial in regulating disease progression owing to its anti-inflammatory effects as well as its inhibitory effects on smooth muscle cell proliferation and migration. Endoglin is a regulator of TGF-${\beta}$ signaling, but its role in atherosclerosis has yet to be defined. This review focuses on the roles of the various forms of endoglin in atherosclerosis. The expression of the two isoforms of endoglin (long-form and short-form) is increased in atherosclerotic lesions, and the expression of the soluble forms of endoglin is upregulated in sera of patients with hypercholesterolemia and atherosclerosis. Interestingly, long-form endoglin shows an atheroprotective effect via the induction of eNOS expression, while short-form and soluble endoglin enhance atherogenesis by inhibiting eNOS expression and TGF-${\beta}$ signaling. This review summarizes evidence suggesting that the different forms of endoglin have distinct roles in atherosclerosis.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.20 no.4
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• pp.334-340
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• 1998

Stimulatory effects of epidermal growth factor (EGF) and transforming growth $factor-{\alpha}$($TGF-{\alpha}$) on the growth of squamous cancer cell lines established from human oral cancer tissue with moderate differentiation were studied in vitro. After culturing in serum-free media for 24 hours, growth factors-EGF only, $TGF-{\alpha}$ only and EGF, $TGF-{\alpha}$ together-were added to the media and numbers of cells were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and compared with the control at 96, 144 hours. Each of EGF and $TGF-{\alpha}$ showed statistically significant stimulatory effects on the growth of cells respectively. Dose-dependent relationship of the stimulatory effects were not clearly demonstrated. The effects of EGF were higher than those of $TGF-{\alpha}$ and combinative administration showed higher effects than those of single uses. In conclusion, EGF may play an important and major role in differentiation and growth of human oral squamous cancer cells. $TGF-{\alpha}$, produced from cells activated by EGF, also can stimulate the cell growth and could be an alternative ligand for EGF receptor.