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RISS 인기검색어
- 검색키워드
- 저자 : Tang Yuchen (검색결과 4 건)
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Wang, Shuang,Zhang, Yuchen,Dai, Wenrui,Lauter, Kristin,Kim, Miran,Tang, Yuzhe,Xiong, Hongkai,Jiang, Xiaoqian Oxford University Press 2016 Bioinformatics Vol.32 No.2
<P>Motivation: Genome-wide association studies (GWAS) have been widely used in discovering the association between genotypes and phenotypes. Human genome data contain valuable but highly sensitive information. Unprotected disclosure of such information might put individual's privacy at risk. It is important to protect human genome data. Exact logistic regression is a bias-reduction method based on a penalized likelihood to discover rare variants that are associated with disease susceptibility. We propose the HEALER framework to facilitate secure rare variants analysis with a small sample size. Results: We target at the algorithm design aiming at reducing the computational and storage costs to learn a homomorphic exact logistic regression model (i.e. evaluate P-values of coefficients), where the circuit depth is proportional to the logarithmic scale of data size. We evaluate the algorithm performance using rare Kawasaki Disease datasets.</P>
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Chongli Xu,Yu Liu,Yuchen Gong,Xinping Duan,Xiaochun Tang,Mingjun Zhang,Daxin Pang,Liqing Yu,Hongwei Zhao,Hongsheng Ouyang 한국유전학회 2015 Genes & Genomics Vol.37 No.2
Although Niemann-Pick C1-Like 1 (NPC1L1)plays a key role in intestinal cholesterol absorption, regulatingcholesterol metabolism and maintaining cholesterolmetabolic homeostasis, the molecular mechanism ofNPC1L1 in lipid-metabolism disorders leading to liverdisease remains largely unknown. Previous studies haveshown that NPC1L1 is related with the development offatty liver. Therefore, we hypothesized that NPC1L1 playsan important role in lipid-metabolism disorders and liverdisease by affecting the transcription of certain genesinvolved in lipid synthesis. To further elucidate the functionof NPC1L1, especially in the liver, we used somaticcellnuclear transfer to establish transgenic pigs thatexpressed human NPC1L1 in their livers. We investigatedsuperoxide dismutase activities and the levels of free fattyacids and malondialdehyde, a biomarker of lipid peroxidation. Superoxide dismutase activities significantlydecreased, and free fatty acid and malondialdehyde levelssignificantly increased in the NPC1L1 transgenic pigs,indicating that the overexpression of NPC1L1 in the liverresulted in severe lipid peroxidation. Our findings suggestthat NPC1L1 plays an important role in lipid-metabolismdisorders and liver disease.
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Liu Na,Feng Yuchen,Liu Huicheng,Wu Wenliang,Liang Yuxia,Li Pingfei,Wei Zhengping,Wu Min,Tang Zhao-Hui,Han Junyan,Cheng Xiang,Liu Zheng,Laurence Arian,Li Huabin,Zhen Guohua,Yang Xiang-Ping 대한천식알레르기학회 2021 Allergy, Asthma & Immunology Research Vol.13 No.3
Purpose Macrophages are important regulators of environmental allergen-induced airway inflammation and asthma. ATP6V0d2 is a subunit of vacuolar ATPase highly expressed in macrophages. However, the functions of ATP6V0d2 in the regulation of pathogenesis of allergic asthma remain unclear. The aim of this study is to determine the function and related molecular mechanisms of macrophage protein ATP6V0d2 in allergic asthma. Methods We compared the disease severity between female C57BL/6 wild-type and ATP6V0d2−/− mice in an ovalbumin (OVA)-induced asthma model. We also investigated the association of expression of ATP6V0d2, PU.1 and CCL17 with disease severity among asthmatic patients. Results The expression of ATP6V0d2 in sputum cells of asthmatic patients and in the lungs of OVA-challenged mice was enhanced compared to healthy subjects and their counterparts, respectively. However, ATP6V0d2-deficient mice exaggerated inflammatory cell infiltration as well as enhanced alternative activated macrophage (AAM) polarization and mucus production in an OVA-induced asthma model. Furthermore, we found that Atp6v0d2 promoted lysosomal degradation of Pu.1, which induced AAM polarization and Ccl17 production. Among asthma patients, ATP6V0d2 expression was inversely associated with disease severity, whereas PU.1 and CCL17 expression was positively associated with disease severity. Conclusions Our results identify macrophage Atp6v0d2, as an induced feedback inhibitor of asthma disease severity by promoting Pu.1 lysosomal degradation, which may in turn leads to reduced AAM polarization and Ccl17 production.
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RhoGDI2 induced malignant phenotypes of pancreatic cancer cells via regulating Snail expression
Yi Bin,Hu You,Zhu Dongming,Yao Jun,Zhou Jian,Zhang Yi,He Zhilong,Zhang Lifeng,Zhang Zixiang,Yang Jian,Tang Yuchen,Huang Yujie,Li Dechun,Liu Qiuhua 한국유전학회 2022 Genes & Genomics Vol.44 No.5
Background: Rho GDP dissociation inhibitor 2 (RhoGDI2) has been shown to contribute to the aggressive phenotypes of human cancers, such as tumor metastasis and chemoresistance. Objective: This study aimed to assess the effects of RhoGDI2 on tumor progression and chemoresistance in pancreatic cancer cells. Methods: The expression of RhoGDI2 in pancreatic cancer cells was detected by Western blot analysis. Gain-of-function and loss-of-function approaches were done to examine the malignant phenotypes of the RhoGDI2-expressing or RhoGDI2-depleting cells. The correlation between RhoGDI2 and Snail was also analyzed. Results: Differential expression of RhoGDI2 protein in pancreatic cancer cell lines was identified. Gain-of-function and loss-of-function experiments showed that RhoGDI2 induced the malignant phenotypes of pancreatic cancer cells, including proliferation, migration, invasion, and gemcitabine (GEM) chemoresistance. The upregulation of RhoGDI2 stimulated the expression of Snail, resulting in the altered expression of epithelial marker E-cadherin and mesenchymal marker Vimentin, which were characteristics of the tumorigenic activity of epithelial-mesenchymal transition. The expression of RhoGDI2 and Snail was upregulated in clinical tumor samples, and higher expression of RhoGDI2 or Snail was significantly associated with poor patient survival in pancreatic ductal adenocarcinoma (PDAC). Conclusion: The findings indicated that RhoGDI2 promoted GEM resistance and tumor progression in pancreatic cancer and that RhoGDI2 might be a potential therapeutic target in patients with PDAC.
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