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      • KCI등재

        The USP21/YY1/SNHG16 axis contributes to tumor proliferation, migration, and invasion of non-small-cell lung cancer

        Pei Xu,Haibo Xiao,Qi Yang,Rui Hu,Lianyong Jiang,Rui Bi,Xueyan Jiang,Lei Wang,Ju Mei,Fangbao Ding,Jianbing Huang 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-

        Deubiquitinases (DUBs) and noncoding RNAs have been the subjects of recent extensive studies regarding their roles in lung cancer, but the mechanisms involved are largely unknown. In our study, we used The Cancer Genome Atlas data set and bioinformatics analyses and identified USP21, a DUB, as a potential contributor to oncogenesis in nonsmall-cell lung cancer (NSCLC). We further demonstrated that USP21 was highly expressed in NSCLCs. We then conducted a series of in vitro and in vivo assays to explore the effect of USP21 on NSCLC progression and the underlying mechanism involved. USP21 promoted NSCLC cell proliferation, migration, and invasion and in vivo tumor growth by stabilizing a well-known oncogene, Yin Yang-1 (YY1), via mediating its deubiquitination. Furthermore, YY1 transcriptionally regulates the expression of SNHG16. Moreover, StarBase bioinformatics analyses predicted that miR4500 targets SNHG16 and USP21. A series of in vitro experiments indicated that SNHG16 increased the expression of USP21 through miR-4500. In summary, the USP21/YY1/SNHG16 axis plays a role in promoting the progression of NSCLC. Therefore, the USP21/YY1/SNHG16/miR-4500 axis may be a potential therapeutic target in NSCLC treatment.

      • KCI등재

        One-step Purification and Immobilization of His-tagged Protein via Ni2+-functionalized Fe3O4@Polydopamine Magnetic Nanoparticles

        Jianbing Yang,Kefeng Ni,Dongzhi Wei,Yuhong Ren 한국생물공학회 2015 Biotechnology and Bioprocess Engineering Vol.20 No.5

        Ni2+-functionalized Fe3O4@polydopamine magnetic nanoparticles (Ni2+-PD-MNPs) were designed and synthesized by in situ coating of magnetic nanoparticles with polydopamine, followed by conjugation of Ni2+ to the polydopamine film. The Ni2+-PD-MNPs were used to purify His-tagged red fluorescent protein (His-RFP) via affinity interaction between Ni2+ and the His-tag. The results showed that the Ni2+-PD-MNPs had extraordinary selectivity for His-RFP purification. In addition, a Histagged transaminase (ω-transaminase BJ110) was selectively immobilized onto the Ni2+-PD-MNPs without purification, and the immobilized enzyme showed improved specific activity, as well as enhanced stability and reusability.

      • KCI등재

        Altered microRNA Expression Profiles of Extracellular Vesicles in Nasal Mucus From Patients With Allergic Rhinitis

        Geping Wu,Guanghai Yang,Ruxin Zhang,Guangyin Xu,Ling Zhang,Wu Wen,Jianbing Lu,Jianyong Liu,Yan Yu 대한천식알레르기학회 2015 Allergy, Asthma & Immunology Research Vol.7 No.5

        Purpose: Allergic rhinitis (AR) is an inflammatory disorder of the upper airway. Exosomes or extracellular vesicles are nanosized vesicles of endosomal origin released from inflammatory and epithelial cells that have been implicated in allergic diseases. In this study, we characterized the microRNA (miRNA) content of exosomes in AR. Methods: Extracellular vesicles were isolated from nasal mucus from healthy control subjects (n=10) and patients with severe AR (n=10). Vesicle RNA was analyzed by using a TaqMan microRNA assays Human Panel-Early Access kit (Applied Biosystems, Foster City, CA, USA) containing probes for 366 human miRNAs, and selected findings were validated with quantitative RT-PCR. Target prediction and pathway analysis for the differentially expressed miRNAs were performed using DIANA-mirPath. Results: Twenty-one vesicle miRNAs were up -regulated and 14 miRNAs were under-regulated significantly (P<0.05) in nasal mucus from AR patients when compared to healthy controls. Bioinformatic analysis by DIANA-mirPath demonstrated that 32 KEGG biological processes were significantly enriched (P<0.05, FDR corrected) among differentially expressed vesicle miRNA signatures. Among them, the B-cell receptor signaling pathway (P=3.709E-09), the natural killer cell-mediated cytotoxicity (P=8.466E-05), the T-cell receptor signaling pathway (P=0.00075), the RIG-I-like receptor signaling pathway (P=0.00127), the Wnt signaling pathway (P=0.00130), endocytosis (P=0.00440), and salivary secretion (P=0.04660) were the most prominent pathways enriched in quantiles with differential vesicle miRNA patterns. Furthermore, miR-30-5p, miR-199b-3p, miR-874, miR-28-3p, miR-203, and miR-875-5p, involved in B-cell receptor and salivary secretion signaling pathways, were selected for validation using independent samples from 44 AR patients and 20 healthy controls. MiR-30-5p and miR-199b-3p were significantly increased in extracellular vesicles from nasal mucus when compared to healthy controls, while miR-874 and miR-28-3p were significantly down-regulated. In addition, miRNA-203 was significantly increased in AR patients, while miRNA-875-5p was found to be significantly decreased in AR patients. Conclusions: This study demonstrated that vesicle miRNA may be a regulator for the development of AR.

      • A Vibration Signal Analysis Method based on Enforced De-Noising and Modified EMD

        He jun,Qinghua Zhang,Guoxi Sun,Ji-cheng Yang,Jianbin Xiong 보안공학연구지원센터(IJSIP) 2015 International Journal of Signal Processing, Image Vol.8 No.1

        To deal with the noise from rotating machinery vibration signal and analysis the fault signal, a rotating machinery fault diagnosis method based on enforced de-noising and modified EMD is proposed. Firstly, fault signals were de-noised by the wavelet with enforced threshold in order to filter the noises in the high frequency, and then the EMD method used to decompose the fault signals into a finite number of stationary intrinsic mode function (IMFs), then the linear correlation coefficient between two sets of data is proposed to select the useful IMF. In order to restrain the endpoint effect of EMD, in this paper, the cosine window function is employ to the fault signals, and then the envelope error of the fault signals is controlled at the both endpoints of the vibration signals. Experimental results shows: this proposed method can extract the fault information effectively, with overcoming the drawbacks of EMD well.

      • KCI등재

        Genome-Wide Association Analysis to Search for New Loci Associated with Lifelong Premature Ejaculation Risk in Chinese Male Han Population

        Wang Fei,Luo Defan,Chen Jianxiang,Pan Cuiqing,Wang Zhongyao,Fu Housheng,Xu Jianbing,Yang Meng,Mo Shaowei,Zhuang Liying,Ye Liefu,Wang Weifu 대한남성과학회 2022 The World Journal of Men's Health Vol.40 No.2

        Purpose: Genetic factors play an indispensable role in the pathogenesis of lifelong premature ejaculation (LPE). The suscep-tibility genes/SNPs that have been discovered are very limited and can only explain part of the genetic effects of LPE. There-fore, discovering more genetic polymorphisms associated with the occurrence and development of LPE will help reveal the pathogenesis of LPE. Materials Materials and and Methods:Methods: We conducted a genome-wide association study of LPE in 486 Chinese male Han people (cases and controls). We used Gene Titan multi-channel instrument and Axiom Analysis Suite 6.0 software for genotyping. Imputation was performed by IMPUTE2 software and the 1000 Genomes Project (Phase3) was used as reference for haplotype. Finally, logistic regression analysis was performed on all loci that passed the quality control. The odds ratio and 95% confidence in-terval were calculated to determine the association between each SNPs and Chinese male Han population LPE risk. Results:Results: The results showed that a total of 33 genetic variants in 13 genes (LACTBL1 , SSBP3 , ACOT11 , LINC02486 , TMEM154, LINC01098, NONE, HCG27, HLA-C, TNFSF8, TNC, FAM53B, SULF2) have a suggestively significant genome-wide association with LPE risk (p<5×10-6). Conclusions:Conclusions: This study is the first to conduct a GWAS on LPE in Chinese male Han population 33 genetic polymorphisms have a suggestive genome-wide association with LPE risk. This study have provided data supplement for the genetic loci of LPE risk, and laid a scientific foundation for the pathogenesis and the targeted therapy of LPE.

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