단백체를 이용한 애기장대 Cytokinin 유도 단백질의 분석

양영실,차준영,네티 엘마와티,정민희,배동원,이창원,손대영 Plant molecular biology and biotechnology research 2005 Plant molecular biology and biotechnology research Vol.2005 No.

Cytokinins are essential plant hormones that play crucial roles in various aspects of plant growth and development. To better understand the molecular mechanisms of cytokinin action, we identified cytokinin related proteins by a proteomic approach. Proteins extracted from control and trans-zeatin treated Arabidopsis seedlings were separated and analyzed by two dimensional gel analysis. Differentially expressed protein spots were identified with peptide mass fingerprinting based on matrix assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry and database searching. We obtained ten up-regulated and one down-regulated proteins upon t-zeatin treatment. The expression of the following proteins was induced; pollen allergen like protein, L-ascorbate peroxidase, tetrapyrrole methylase family protein, SGT1 protein homolog, disease resistance related protein, maternal embryogenesis control protein, paxneb related protein, gluthathione S-transferase and IAA amino acid hydrolase homolog.

퉁퉁마디로부터 색소체 외막 단백질 유전자의 분리 및 발현분석

네티 엘마와티,차준영,양영실,정민희,신동진,이병현,이곤호,손대영 Plant molecular biology and biotechnology research 2004 Plant molecular biology and biotechnology research Vol.2004 No.-

Complementary DNA encoding chloroplast outer envelope membrane protein (OEP) from the halophyte Salicornia herbacea has been cloned and sequenced. The full length cDNA is 596 bp and encodes a polypeptide of 91 amino acid residues with a molecular mass of 8.9 kDa. The expression level of ShOEP increased by salt, drought and ABA treatments. ShOEP expression was largely induced in roots and shoots by high salts. The biological function of ShOEP was examined by yeast complementation. ShOEP can suppress Na+ sensitivity of yeast mutant (cnbΔ) in the presence of salt. These results suggest that ShOEP is a salt inducible gene and may have functions in the regulation of plant salt stress.

Hiwi Knockdown Inhibits the Growth of Lung Cancer in Nude Mice

Liang, Dong,Dong, Min,Hu, Lin-Jie,Fang, Ze-Hui,Xu, Xia,Shi, En-Hui,Yang, Yi-Ju Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.2

Hiwi, a human homologue of the Piwi family, plays an important role in stem cell self-renewal and is overexpressed in various human tumors. This study aimed to determine whether an RNA interference-based strategy to suppress Hiwi expression could inhibit tumor growth in a xenograft mouse model. A rare population of $SSC^{lo}\;Alde^{br}$ cells was isolated and identified as lung cancer stem cells in our previous study. Plasmids containing U6 promoter-driven shRNAs against Hiwi or control plasmids were successfully established. The xenograft tumor model was generated by subcutaneously inoculating with lung cancer stem cell $SSC^{lo}\;Alde^{br}$ cells. After the tumor size reached about 8 mm in diameter, shRNA plasmids were injected into the mice via the tail vein three times a week for two weeks, then xenograft tumor growth was assessed. In nude mice, intravenously delivery of Hiwi shRNA plasmids significantly inhibited tumor growth compared to treatment with control scrambled shRNA plasmids or the vehicle PBS. No mice died during the experiment and no adverse events were observed in mice administered the plasmids. Moreover, delivery of Hiwi shRNA plasmids resulted in a significant suppressed expression of Hiwi and ALDH-1 in xenograft tumor samples, based on immunohistochemical analysis. Thus, shRNA-mediated Hiwi gene silencing in lung cancer stem cells by an effective in vivo gene delivery strategy appeared to be an effective therapeutic approach for lung cancer, and may provide some useful clues for RNAi gene therapy in solid cancers.

MicroRNA-27a Inhibits Cell Migration and Invasion of Fibroblast-Like Synoviocytes by Targeting Follistatin-Like Protein 1 in Rheumatoid Arthritis

Dong-liang Shi,Gui-rong Shi,Jing Xie,Xu-zhao Du,Hao Yang 한국분자세포생물학회 2016 Molecules and cells Vol.39 No.8

Fibroblast-like synoviocytes (FLS) with aberrant expres-sion of microRNA (miRNA) are critical pathogenic regula-tors in rheumatoid arthritis (RA). Previous studies have found that overexpression or silencing of miRNA can contribute to the development of miRNA-based therapeutics in arthritis models. In this study, we explored the effects of miR-27a on cell migration and invasion in cultured FLS from RA patients. We found that miR-27a was markedly downregulated in the serum, synovial tissue, and FLS of RA patients. Meanwhile, the expression of follistatin-like protein 1 (FSTL1) was upregulated, which suggests that FSTL1 plays a key role in RA development. The results of a Transwell assay showed that miR-27a inhibited FLS migration and invasion. However, miR-27a inhibition promoted the migration and invasion of FLS. In addition, the down-regulated expression of matrix metalloproteinases (MMP2, MMP9, and MMP13) and Rho family proteins (Rac1, Cdc42, and RhoA) was detected after treatment with miR-27a in RA-FLS by quantitative reverse transcription-PCR and western blot analysis. Then, a luciferase reporter assay validated that miR-27a targeted the 3-untranslated region (3-UTR) of FSTL1. Moreover, miR-27a caused a significant decrease of FSTL1. In addition, the expression of TLR4 and NFκB was inhibited by miR-27a but increased by FSTL1 overexpression. In conclusion, we found that miR-27a inhibited cell migration and invasion of RA-FLS by targeting FSTL1 and restraining the TLR4/NFκB pathway.

MicroRNA-27a Inhibits Cell Migration and Invasion of Fibroblast-Like Synoviocytes by Targeting Follistatin-Like Protein 1 in Rheumatoid Arthritis

Shi, Dong-liang,Shi, Gui-rong,Xie, Jing,Du, Xu-zhao,Yang, Hao Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.8

Fibroblast-like synoviocytes (FLS) with aberrant expression of microRNA (miRNA) are critical pathogenic regulators in rheumatoid arthritis (RA). Previous studies have found that overexpression or silencing of miRNA can contribute to the development of miRNA-based therapeutics in arthritis models. In this study, we explored the effects of miR-27a on cell migration and invasion in cultured FLS from RA patients. We found that miR-27a was markedly downregulated in the serum, synovial tissue, and FLS of RA patients. Meanwhile, the expression of follistatin-like protein 1 (FSTL1) was upregulated, which suggests that FSTL1 plays a key role in RA development. The results of a Transwell assay showed that miR-27a inhibited FLS migration and invasion. However, miR-27a inhibition promoted the migration and invasion of FLS. In addition, the down-regulated expression of matrix metalloproteinases (MMP2, MMP9, and MMP13) and Rho family proteins (Rac1, Cdc42, and RhoA) was detected after treatment with miR-27a in RA-FLS by quantitative reverse transcription-PCR and western blot analysis. Then, a luciferase reporter assay validated that miR-27a targeted the 3-untranslated region (3'-UTR) of FSTL1. Moreover, miR-27a caused a significant decrease of FSTL1. In addition, the expression of TLR4 and $NF{\kappa}B$ was inhibited by miR-27a but increased by FSTL1 overexpression. In conclusion, we found that miR-27a inhibited cell migration and invasion of RA-FLS by targeting FSTL1 and restraining the $TLR4/NF{\kappa}B$ pathway.

Loss of RTN3 phenocopies chronic kidney disease and results in activation of the IGF2-JAK2 pathway in proximal tubular epithelial cells

Fan Liang-Liang,Du Ran,Liu Ji-Shi,Jin Jie-Yuan,Wang Chen-Yu,Dong Yi,He Wan-Xia,Yan Ri-Qiang,Xiang Rong 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-

Reticulon 3 (RTN3) is an endoplasmic reticulum protein that has previously been shown to play roles in neurodegenerative diseases, but little is known about its function in the kidneys. The aim of the present study was to clarify the roles of RTN3 in chronic kidney disease (CKD) and kidney fibrosis. In this study, RTN3 levels were measured in kidney tissues from healthy controls and CKD or kidney fibrosis patients. An RTN3-null mouse model was generated to explore the pathophysiological roles of RTN3 in the kidneys. The underlying mechanisms were studied in primary proximal tubular epithelial cells and HEK293 cells in vitro. The results showed that (1) a reduction in RTN3 in mice induces CKD and kidney fibrosis; (2) decreased RTN3 expression is found in patients with CKD; (3) RTN3 plays critical roles in regulating collagen biosynthesis and mitochondrial function; and (4) mechanistically, RTN3 regulates these phenotypes by interacting with GC-Rich Promoter Binding Protein 1 (GPBP1), which activates the IGF2-JAK2-STAT3 pathway. Our study indicates that RTN3 might play crucial roles in CKD and kidney fibrosis and that a reduction in RTN3 in the kidneys might be a risk factor for CKD and kidney fibrosis.

Measure Correlation Analysis of Network Flow Based On Symmetric Uncertainty

( Shi Dong ),( Wei Ding ),( Liang Chen ) 한국인터넷정보학회 2012 KSII Transactions on Internet and Information Syst Vol.6 No.6

In order to improve the accuracy and universality of the flow metric correlation analysis, this paper firstly analyzes the characteristics of Internet flow metrics as random variables, points out the disadvantages of Pearson Correlation Coefficient which is used to measure the correlation between two flow metrics by current researches. Then a method based on Symmetrical Uncertainty is proposed to measure the correlation between two flow metrics, and is extended to measure the correlation among multi-variables. Meanwhile, the simulation and polynomial fitting method are used to reveal the threshold value between different correlation degrees for SU method. The statistical analysis results on the common flow metrics using several traces show that Symmetrical Uncertainty can not only represent the correct aspects of Pearson Correlation Coefficient, but also make up for its shortcomings, thus achieve the purpose of measuring flow metric correlation quantitatively and accurately. On the other hand, reveal the actual relationship among fourteen common flow metrics.

Anti-neuroinflammatory Effects of 12-Dehydrogingerdione in LPS-Activated Microglia through Inhibiting Akt/IKK/NF-κB Pathway and Activating Nrf-2/HO-1 Pathway

Dong Zhao,Ming-Yao Gu,Jiu Liang Xu,Li Jun Zhang,Shi Yong Ryu,양현옥 한국응용약물학회 2019 Biomolecules & Therapeutics(구 응용약물학회지) Vol.27 No.1

Ginger, one of worldwide consumed dietary spice, is not only famous as food supplements, but also believed to exert a variety of remarkable pharmacological activity as herbal remedies. In this study, a ginger constituent, 12-dehydrogingerdione (DHGD) was proven that has comparable anti-inflammatory activity with positive control 6-shogaol in inhibiting LPS-induced interleukin (IL)-6, tumor necrosis factor (TNF)-α, prostaglandin (PG) E2, nitric oxide (NO), inducible NO synthase (iNOS) and cyclooxygenase (COX)-2, without interfering with COX-1 in cultured microglial cells. Subsequent mechanistic studies indicate that 12-DHGD may inhibit neuro-inflammation through suppressing the LPS-activated Akt/IKK/NF-κB pathway. Furthermore, 12-DHGD markedly promoted the activation of NF-E2-related factor (Nrf)-2 and heme oxygenase (HO)-1, and we demonstrated that the involvement of HO-1 on the production of pro-inflammatory mediators such as NO and TNF-α by using a HO-1 inhibitor, Zinc protoporphyrin (Znpp). These results indicate that 12-DHGD may protect against neuro-inflammation by inhibiting Akt/IKK/IκB/NF-κB pathway and promoting Nrf-2/HO-1 pathway.

Adaptive Synchronization of Leader-Follower Networked Systems against Communication Attenuation and Actuators Faults

Liang Dong,Jian-Hui Wang,Shu-Sheng Gu,Yuan-Bo Shi,Fang-Mei Zhao 제어·로봇·시스템학회 2016 International Journal of Control, Automation, and Vol.14 No.6

This paper addresses the adaptive asymptotic synchronization problem of a class of leader-follower largescale networked systems against communicated signal attenuation and actuator bias faults. Adaptive mechanismsare constructed to estimate each unknown faulty factor of communications and actuators on-line. Based on theestimations, an adaptive compensation controller is designed to automatically remove the unexpected impacts ofcommunication and actuator faults. Through the adaptive adjustment parameters and Lyapunov functions, theachievement of asymptotic synchronization of the leader-follower large-scale networked system with the improperactuator and faulty transmitted signals is obtained. Finally, the synchronization results are validated by a multiplevehicle large-scale device.

β3GnT8 Regulates Laryngeal Carcinoma Cell Proliferation Via Targeting MMPs/TIMPs and TGF-β1

Hua, Dong,Qin, Fang,Shen, Li,Jiang, Zhi,Zou, Shi-Tao,Xu, Lan,Cheng, Zhi-Hong,Wu, Shi-Liang Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.5

Previous evidence showed ${\beta}1$, 3-N-acetylglucosaminyltransferase 8 (${\beta}3GnT8$), which can extend polylactosamine on N-glycans, to be highly expressed in some cancer cell lines and tissues, indicating roles in tumorigenesis. However, so far, the function of ${\beta}3GnT8$ in laryngeal carcinoma has not been characterized. To test any contribution, Hep-2 cells were stably transfected with sense or interference vectors to establish cell lines that overexpressed or were deficient in ${\beta}3GnT8$. Here we showed that cell proliferation was increased in ${\beta}3GnT8$ overexpressed cells but decreased in ${\beta}3GnT8$ knockdown cells using MTT. Furthermore, we demonstrated that change in ${\beta}3GnT8$ expression had significant effects on tumor growth in nude mice.We further provided data suggesting that overexpression of ${\beta}3GnT8$ enhanced the expression of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) at both the mRNA and protein levels, associated with shedding of tissue inhibitors of metalloproteinase TIMP-2. In addition, it caused increased production of transforming growth factor beta 1 (TGF-${\beta}1$), whereas ${\beta}3GnT8$ gene knockdown caused the reverse effect. The results may indicate a novel mechanism by which effects of ${\beta}3GnT8$ in regulating cellular proliferation are mediated, at least in partvia targeting MMPs/TIMPs and TGF-${\beta}1$ in laryngeal carcinoma Hep-2 cells. The finding may lay a foundation for further investigations into the ${\beta}3GnT8$ as a potential target for therapy of laryngeal carcinoma.