• Journal of the Optical Society of Korea
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• v.12 no.2
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• pp.107-111
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• 2008

We demonstrated single-molecule fluorescence resonance energy transfer (FRET) from single donor-acceptor dye pair attached to a DNA with a setup based on a confocal microscope. Singlestrand DNAs were immobilized on a glass surface with suitable inter-dye distance. Energy transfer efficiency between the donor and the acceptor dyes attached to the DNA was measured with different lengths of DNA. Photobleaching of single dye molecule was observed and used as a sign of single-molecule detection. We could achieve high enough signal-to-noise ratio to detect the fluorescence from a single-molecule, which allows real-time observation of the distance change between single dye pairs in nanometer scale.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.22
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• pp.9791-9795
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• 2014

To study the gene expression change and possible signal pathway during androgen-dependent prostate cancer (ADPC) becoming androgen-independent prostate cancer (AIPC), an LNCaP cell model of AIPC was established using flutamide in combination with androgen-free environment inducement, and differential expression genes were screened by microarray. Then the biological process, molecular function and KEGG pathway of differential expression genes are analyzed by Molecule Annotation System (MAS). By comparison of 12,207 expression genes, 347 expression genes were acquired, of which 156 were up-ragulated and 191 down-regulated. After analyzing the biological process and molecule function of differential expression genes, these genes are found to play crucial roles in cell proliferation, differntiation, cell cycle control, protein metabolism and modification and other biological process, serve as signal molecules, enzymes, peptide hormones, cytokines, cytoskeletal proteins and adhesion molecules. The analysis of KEGG show that the relevant genes of AIPC transformation participate in glutathione metabolism, cell cycle, P53 signal pathway, cytochrome P450 metabolism, Hedgehog signal pathway, MAPK signal pathway, adipocytokines signal pathway, PPAR signal pathway, TGF-${\beta}$ signal pathway and JAK-STAT signal pathway. In conclusion, during the process of ADPC becoming AIPC, it is not only one specific gene or pathway, but multiple genes and pathways that change. The findings above lay the foundation for study of AIPC mechanism and development of AIPC targeting drugs.

• Proceedings of the Korean Society for Applied Microbiology Conference
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• 2003.06a
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• pp.159-160
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• 2003

• BMB Reports
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• v.56 no.2
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• pp.126-131
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• 2023

The abnormal accumulation and aggregation of the misfolded α-synuclein protein is the neuropathological hallmark of all α-synucleinopathies, including Parkinson's disease. The secreted proteins known as netrins (netrin-1, netrin-3, and netrin-4) are related to laminin and have a role in the molecular pathway for axon guidance and cell survival. Interestingly, only netrin-1 is significantly expressed in the substantia nigra (SN) of healthy adult brains and its expression inversely correlates with that of α-synuclein, which prompted us to look into the role of α-synuclein and netrin-1 molecular interaction in the future of dopaminergic neurons. Here, we showed that netrin-1 and α-synuclein directly interacted in pre-formed fibrils (PFFs) generation test, real time binding assay, and co-immunoprecipitation with neurotoxin treated cell lysates. Netrin-1 deficiency appeared to activate the dopaminergic neuronal cell death signal pathway via α-synuclein aggregation and hyperphosphorylation of α-synuclein S129. Taken together, netrin-1 can be a promising therapeutic molecule in Parkinson's disease.

• BMB Reports
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• v.32 no.2
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• pp.103-111
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• 1999

Hh proteins represent a new signaling paradigm in metazoan development. In species ranging from fruit flies to humans, Hh proteins mediate multiple processes vital to appropriate pattern formation in the developing embryo. Hh proteins undergo an autoprocessing event in which the full-length protein is cleaved into N-terminal and C-terminal domains (Hh-N and Hh-C, respectively), and a cholesterol moiety becomes covalently attached to Hh-N. All known signaling activities of Hh proteins are mediated by Hh-N while both the cleavage and cholesterol transfer reactions are mediated by Hh-C. The cholesterol attached to Hh-N is required to retrict the range of Hh signaling and may be involved in ensuring appropriate reception of the Hh signal in target tissues. Disruptions of Hh signaling pathways lead to severe developmental defects in newborns and cancers in adults. While studies of Hh proteins have yielded a wealth of new insight into the molecular mechanisms of metazoan development, many outstanding questions concerning Hh signaling mechanisms ensure that unraveling the secrets of this molecule will keep scientists well entertained for the foreseeable future.

• Biomolecules & Therapeutics
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• v.31 no.4
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• pp.388-394
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• 2023

Nitric oxide (NO) is a signaling molecule that plays a crucial role in numerous cellular physiological processes. In the skin, NO is produced by keratinocytes, fibroblasts, endothelial cells, and immune cells and is involved in skin functions such as vasodilation, pigmentation, hair growth, wound healing, and immune responses. NO modulates both innate and adaptive immune responses. As a signaling molecule and cytotoxic effector, NO influences the function of immune cells and production of cytokines. NO is a key mediator that protects against or contributes to skin inflammation. Moreover, NO has been implicated in skin sensitization, a process underlying contact dermatitis. It modulates the function of dendritic cells and T cells, thereby affecting the immune response to allergens. NO also plays a role in contact dermatitis by inducing inflammation and tissue damage. NO-related chemicals, such as nitrofatty acids and nitric oxide synthase (NOS) inhibitors, have potential therapeutic applications in skin conditions, including allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD). Further research is required to fully elucidate the therapeutic potential of NO-related chemicals and develop personalized treatment strategies for skin conditions.

• BMB Reports
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• v.32 no.3
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• pp.215-225
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• 1999

Phytochromes (with gene family members phyA, B, C, D, and E) are a wavelength-dependent light sensor or switch for gene regulation that underscore a number of photo responsive developmental and morphogenic processes in plants. Recently, phytochrome-like pigment proteins have also been discovered in prokaryotes, possibly functioning as an auto-phosphorylating/phosphate-relaying two-component signaling system (Yeh et al., 1997). Phytochromes are photochromically convertible between the light sensing Pr and regulatory active Pfr forms. Red light converts Pr to Pfr, the latter having a "switch-on" conformation. The Pfr form triggers signal transduction pathways to the downstream responses including the expression of photosynthetic and other growth-regulating genes. The components involved in and the molecular mechanisms of the light signal transduction pathways are largely unknown, although G-proteins, protein kinases, and secondary messengers such as $Ca^{2+}$ ions and cGMP are implicated. The 124-127 kDa phytochromes form homodimeric structures. The N-terminal half contains the tetrapyrrolic phytochromobilin for red/far-red light absorption. The C-terminal half includes both a dimerization motif and regulatory box where the red light signal perceived by the chromophore-domain is recognized and transduced to initiate the signal transduction cascade. A working model for the inter-domain signal communication within the phytochrome molecule is proposed in this Review.

• Journal of Photoscience
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• v.7 no.3
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• pp.79-86
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• 2000

Phytochromes are red and far-red light absorbing photoreceptors for photomorphogenesis in plants. The red/far wavelength reversible biliproteins are made up of two structural domains. The light-perceiving function of the photoreceptor resides in the N-terminal domain, whereas the signal transducing regulatory function is located within the C-terminal domain. The characteristic role of the phytochromes as phtosensory molecular switches is derived from the phototransformation between two distinct spectral forms, the red light absorbing Pr and the far-red light absorbing Pfr forms. The photoinduced Pr Pfr phototransformation accompanies subtle conformational changes throughout the phytochrome molecule. The conformational signals are subsequently transmitted to the C-terminal domain through various inter-domain crosstalks and induce the interaction of the activated C-terminal domain with phytochrome interacting factors. Thus the inter-domain crosstalks play critical roles in the photoactivation of the phytochromes. Posttranslational modifications, such as the phosphorylation of Ser-598, are also involved in this process through conformational changes and by modulating inter-domain signaling.

• YAKHAK HOEJI
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• v.60 no.3
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• pp.128-134
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• 2016

L1 cell adhesion molecule (L1CAM) is a cell surface molecule to initiate a variety of cellular responses through interacting with other cell adhesion molecules in a homophilic or heterophilic manner. Although its expression was found to be upregulated in some tumor cells, including cholangiocarcinomas, and ovarian cancers, and many studies have investigated the role of L1CAM in these cancers, its role in inflammatory responses has been poorly understood. In this study, we explored the role of L1CAM in macrophage-mediated inflammatory responses. L1CAM significantly suppressed the production of nitric oxide (NO), but induced cell proliferation in RAW264.7 cells. L1CAM expression was detectable, but its expression was markedly decreased by lipopolysaccharide (LPS) in RAW264.7 cells. In addition, the expression of pro-inflammatory genes, such as tumor necrosis factor (TNF)-${\alpha}$, cyclooxygenase (COX)-2, and inducible nitric oxide synthase (iNOS) induced by LPS was dramatically suppressed by L1CAM in RAW264.7 cells. L1CAM inhibited the transcriptional activities of NF-${\kappa}B$ and AP-1 while its cytoplasmic domain deletion form, $L1{\Delta}CD$ did not suppressed their activities in RAW264.7 cells. Moreover, L1CAM suppressed nuclear translocation of p65 and p50 as well as c-Jun, c-Fos and p-ATF2 which are transcription factors of NF-${\kappa}B$ and AP-1, respectively. In conclusion, L1CAM suppressed inflammatory responses in macrophages through inhibiting NF-${\kappa}B$ and AP-1 pathways.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.6
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• pp.541-556
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• 2022

Myocardial fibrosis is a key link in the occurrence and development of diabetic cardiomyopathy. Its etiology is complex, and the effect of drugs is not good. Cardiomyocyte apoptosis is an important cause of myocardial fibrosis. The purpose of this study was to investigate the effect of gaseous signal molecule sulfur dioxide (SO₂) on diabetic myocardial fibrosis and its internal regulatory mechanism. Masson and TUNEL staining, Western-blot, transmission electron microscopy, RT-qPCR, immunofluorescence staining, and flow cytometry were used in the study, and the interstitial collagen deposition, autophagy, apoptosis, and changes in phosphatidylinositol 3-kinase (PI3K)/AKT pathways were evaluated from in vivo and in vitro experiments. The results showed that diabetic myocardial fibrosis was accompanied by cardiomyocyte apoptosis and down-regulation of endogenous SO₂-producing enzyme aspartate aminotransferase (AAT)_1/2. However, exogenous SO₂ donors could up-regulate AAT_1/2, reduce apoptosis of cardiomyocytes induced by diabetic rats or high glucose, inhibit phosphorylation of PI3K/AKT protein, up-regulate autophagy, and reduce interstitial collagen deposition. In conclusion, the results of this study suggest that the gaseous signal molecule SO₂ can inhibit the PI3K/AKT pathway to promote cytoprotective autophagy and inhibit cardiomyocyte apoptosis to improve myocardial fibrosis in diabetic rats. The results of this study are expected to provide new targets and intervention strategies for the prevention and treatment of diabetic cardiomyopathy.