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142 results on '"Zou, Yongxin"'

9. Study on the influence of polar groups in pour point depressant on flow properties of Karamay crude oil.

Author

Zou, Yongxin, Zheng, Heping, Luo, Xiaowen, and Tang, Jianhua

Subjects
*PETROLEUM, *POINT set theory, *MOLECULAR structure, *PETROLEUM industry, *CONTACT angle
Abstract

Pour point depressant (PPD) is a crucial addition in the petroleum industry which can significantly enhance the flow properties of crude oil by preventing wax from precipitating out of it. The flow assurance effect of PPD on crude oil is impacted by its molecular structure. As a result, we concentrate on the PPD with various molecular structures, such as carboxyl and benzene rings, to investigate its impact on the flow behavior of crude oil. Then, FTIR and contact angle test were used to describe the characteristics of PPD (SAF-n and SAFS-m). The Karamay crude oil was tested using the following items: pour point, rheology, viscosity, viscoelasticity, and POM. When the crude oil was treated with 1000 ppm SAFS-1, the pour point decreased from 12 to −14 °C and the viscosity decreased from 40.1 to 6.3 pa·s at 0 °C. Meanwhile, the results show that the more variety polar groups PPD has, the more its dispersion increases and the stronger its interactions with crude oil are when its molar ratio of non-polar groups are suitable. These effects may be caused by the PPD changing the crystallization characteristics of wax and the aggregate state of resin and asphalt. [ABSTRACT FROM AUTHOR]

Published
2024
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17. Cullin 4B-RING E3 ligase negatively regulates the immunosuppressive capacity of mesenchymal stem cells by suppressing iNOS

Author

Yu, Ruiqi, Han, Hong, Chu, Shuxian, Qin, Liping, Du, Mengying, Ma, Yanyan, Wang, Yufeng, Jiang, Wei, Song, Yu, Zou, Yongxin, Wang, Molin, Liu, Qiao, Jiang, Baichun, Gong, Yaoqin, and Sun, Gongping

Abstract

Mesenchymal stem cells (MSCs) are multipotent stem cells that can exert immunomodulatory capacity upon stimulation with pro-inflammatory cytokines. Our previous work has identified Cullin 4B (CUL4B), a scaffold protein in the CUL4B-RING E3 ligase (CRL4B) complex, as a key regulator in the differentiation of MSCs. Here, we demonstrate the critical role of CUL4B in regulating the immunosuppressive function of MSCs. When stimulated with pro-inflammatory cytokines, MSCs lacking CUL4B display enhanced immunosuppressive capacity, which is mediated by the elevated inducible nitric oxide synthase (iNOS). TGF-β signaling can suppress iNOS by inhibiting its transcription as well as promoting its protein degradation. We show that the CRL4B complex cooperates with PRC2 complex and HDACs to repress transcription of Dlx1and Pmepa1, two inhibitors of TGF-β signaling, leading to decreased expression and accelerated degradation of iNOS. Our study unveils the CRL4B complex as a potential therapeutic target in promoting the immunosuppressive capacity of MSCs.

Published
2024
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21. CUL4B orchestrates mesenchymal stem cell commitment by epigenetically repressing KLF4 and C/EBPδ.

Author

Yu, Ruiqi, Han, Hong, Chu, Shuxian, Ding, Yijun, Jin, Shiqi, Wang, Yufeng, Jiang, Wei, Liu, Yuting, Zou, Yongxin, Wang, Molin, Liu, Qiao, Sun, Gongping, Jiang, Baichun, and Gong, Yaoqin

Subjects
CELL determination, ADIPOGENESIS, BONE growth, BONE marrow, OSTEOCLASTOGENESIS
Abstract

Dysregulated lineage commitment of mesenchymal stem cells (MSCs) contributes to impaired bone formation and an imbalance between adipogenesis and osteogenesis during skeletal aging and osteoporosis. The intrinsic cellular mechanism that regulates MSC commitment remains unclear. Here, we identified Cullin 4B (CUL4B) as a critical regulator of MSC commitment. CUL4B is expressed in bone marrow MSCs (BMSCs) and downregulated with aging in mice and humans. Conditional knockout of Cul4b in MSCs resulted in impaired postnatal skeletal development with low bone mass and reduced bone formation. Moreover, depletion of CUL4B in MSCs aggravated bone loss and marrow adipose accumulation during natural aging or after ovariectomy. In addition, CUL4B deficiency in MSCs reduced bone strength. Mechanistically, CUL4B promoted osteogenesis and inhibited adipogenesis of MSCs by repressing KLF4 and C/EBPδ expression, respectively. The CUL4B complex directly bound to Klf4 and Cebpd and epigenetically repressed their transcription. Collectively, this study reveals CUL4B-mediated epigenetic regulation of the osteogenic or adipogenic commitment of MSCs, which has therapeutic implications in osteoporosis. [ABSTRACT FROM AUTHOR]

Published
2023
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27. Berberine suppresses bladder cancer cell proliferation by inhibiting JAK1-STAT3 signaling via upregulation of miR-17-5p

Author

Xia, Yangyang, primary, Chen, Shouzhen, additional, Cui, Jianfeng, additional, Wang, Yong, additional, Liu, Xiaochen, additional, Shen, Yangli, additional, Gong, Li, additional, Jiang, Xuewen, additional, Wang, Wenfu, additional, Zhu, Yaofeng, additional, Sun, Shuna, additional, Li, Jiangxia, additional, Zou, Yongxin, additional, and Shi, Benkang, additional

Published
2021
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30. Cullin 4b Complex Targets IRGM1 to Regulate Intestinal Stem Cell Stemness and Niche

Author

Fan, Yujia, primary, Huo, Xiaohan, additional, Guo, Beibei, additional, Zhang, Xiaohui, additional, Yang, Yang, additional, Lian, Jiabei, additional, Meng, Xinyuan, additional, Jiang, Baichun, additional, Zou, Yongxin, additional, Guo, Haiyang, additional, Wang, Haitao, additional, Sun, Gongping, additional, Dou, Hao, additional, Shao, Changshun, additional, Gong, Yaoqin, additional, and Hu, Huili, additional

Published
2021
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31. CUL4B facilitates HBV replication by promoting HBx stabilization

Author

Shan, Haixia, primary, Wang, Bo, additional, Zhang, Xiaodong, additional, Song, Hui, additional, Li, Xi, additional, Zou, Yongxin, additional, Jiang, Baichun, additional, Hu, Huili, additional, Dou, Hao, additional, Shao, Changshun, additional, Gao, Lifen, additional, Ma, Chunhong, additional, Yang, Xiaoyun, additional, Liang, Xiaohong, additional, and Gong, Yaoqin, additional

Published
2021
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32. Berberine Suppresses Bladder Cancer Cell Proliferation by Inhibiting JAK1-STAT3 Signaling via Upregulation of miR-17-5p

Author

Xia, Yangyang, primary, Chen, Shouzhen, additional, Cui, Jianfeng, additional, Wang, Yong, additional, Liu, Xiaochen, additional, Shen, Yangli, additional, Gong, Li, additional, Jiang, Xuewen, additional, Wang, Wenfu, additional, Zhu, Yaofeng, additional, Sun, Shuna, additional, Li, Jiaxiang, additional, Zou, Yongxin, additional, and Shi, Benkang, additional

Published
2020
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33. Wogonin Induces Apoptosis and Reverses Sunitinib Resistance of Renal Cell Carcinoma Cells via Inhibiting CDK4-RB Pathway

Author

Wang, Yong, primary, Chen, Shouzhen, additional, Sun, Shuna, additional, Liu, Guangyi, additional, Chen, Lipeng, additional, Xia, Yangyang, additional, Cui, Jianfeng, additional, Wang, Wenfu, additional, Jiang, Xuewen, additional, Zhang, Lei, additional, Zhu, Yaofeng, additional, Zou, Yongxin, additional, and Shi, Benkang, additional

Published
2020
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34. CUL4B Facilitates HBV Replication by Promoting HBx Stabilization

Author

Shan, Haixia, primary, Wang, Bo, additional, Song, Hui, additional, Li, Xi, additional, Zou, Yongxin, additional, Jiang, Baichun, additional, Hu, Huili, additional, Dou, Hao, additional, Shao, Changshun, additional, Gao, Lifen, additional, Ma, chunhong, additional, Liang, Xiaohong, additional, and Gong, Yaoqin, additional

Published
2020
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36. Sp1 and KLF15 regulate basal transcription of the human LRP5 gene

Author

Zou Yongxin, Zhang Xiyu, Jiang Baichun, Yang Yang, Li Jiangxia, and Gong Yaoqin

Subjects
Genetics, QH426-470
Abstract

Abstract Background LRP5, a member of the low density lipoprotein receptor superfamily, regulates diverse developmental processes in embryogenesis and maintains physiological homeostasis in adult organisms. However, how the expression of human LRP5 gene is regulated remains unclear. Results In order to characterize the transcriptional regulation of human LRP5 gene, we cloned the 5' flanking region and evaluated its transcriptional activity in a luciferase reporter system. We demonstrated that both KLF15 and Sp1 binding sites between -72 bp and -53 bp contribute to the transcriptional activation of human LRP5 promoter. Chromatin immunoprecipitation assay demonstrated that the ubiquitous transcription factors KLF15 and Sp1 bind to this region. Using Drosophila SL2 cells, we showed that KLF15 and Sp1 trans-activated the LRP5 promoter in a manner dependent on the presence of Sp1-binding and KLF15-binding motifs. Conclusions Both KLF15 and Sp1 binding sites contribute to the basal activity of human LRP5 promoter. This study provides the first insight into the mechanisms by which transcription of human LRP5 gene is regulated.

Published
2010
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40. MicroRNA-26a/b regulate DNA replication licensing, tumorigenesis, and prognosis by targeting CDC6 in lung cancer

Author

Zhang, Xin, Xiao, Dakai, Wang, Ziyi, Zou, Yongxin, Huang, Liyan, Lin, Weixuan, Deng, Qiuhua, Pan, Hui, Zhou, Jiangfen, Liang, Chun, He, Jianxing, Zhang, Xin, Xiao, Dakai, Wang, Ziyi, Zou, Yongxin, Huang, Liyan, Lin, Weixuan, Deng, Qiuhua, Pan, Hui, Zhou, Jiangfen, Liang, Chun, and He, Jianxing

Abstract

Cancer is characterized by mutations, genome rearrangements, epigenetic changes, and altered gene expression that enhance cell proliferation, invasion, and metastasis. To accommodate deregulated cellular proliferation, many DNA replication-initiation proteins are overexpressed in human cancers. However, the mechanism that represses the expression of these proteins in normal cells and the cellular changes that result in their overexpression are largely unknown. One possible mechanism is through miRNA expression differences. Here, it is demonstrated that miR26a and miR26b inhibit replication licensing and the proliferation, migration, and invasion of lung cancer cells by targeting CDC6. Importantly, miR26a/b expression is significantly decreased in human lung cancer tissue specimens compared with the paired adjacent normal tissues, and miR26a/b downregulation and the consequential upregulation of CDC6 are associated with poorer prognosis of patients with lung cancer. These results indicate that miR26a/b repress replication licensing and tumorigenesis by targeting CDC6.

Published
2014

41. Estrogen receptor α-coupled Bmi1 regulation pathway in breast cancer and its clinical implications

Author

Wang, Huali, Liu, Haijing, Li, Xin, Zhao, Jing, Zhang, Hong, Mao, Jingzhuo, Zou, Yongxin, Zhang, Shuang, Hou, Wei, Hou, Lin, McNutt, Michael A, Zhang, Bo, Wang, Huali, Liu, Haijing, Li, Xin, Zhao, Jing, Zhang, Hong, Mao, Jingzhuo, Zou, Yongxin, Zhang, Shuang, Hou, Wei, Hou, Lin, McNutt, Michael A, and Zhang, Bo

Abstract

Background Bmi1 has been identified as an important regulator in breast cancer, but its relationship with other signaling molecules such as ERα and HER2 is undetermined. Methods The expression of Bmi1 and its correlation with ERα, PR, Ki-67, HER2, p16 INK4a , cyclin D1 and pRB was evaluated by immunohistochemistry in a collection of 92 cases of breast cancer and statistically analyzed. Stimulation of Bmi1 expression by ERα or 17β-estradiol (E2) was analyzed in cell lines including MCF-7, MDA-MB-231, ERα-restored MDA-MB-231 and ERα-knockdown MCF-7 cells. Luciferase reporter and chromatin immunoprecipitation assays were also performed. Results Immunostaining revealed strong correlation of Bmi1 and ERα expression status in breast cancer. Expression of Bmi1 was stimulated by 17β-estradiol in ERα-positive MCF-7 cells but not in ERα-negative MDA-MB-231 cells, while the expression of Bmi1 did not alter expression of ERα. As expected, stimulation of Bmi1 expression could also be achieved in ERα-restored MDA-MB-231 cells, and at the same time depletion of ERα decreased expression of Bmi1. The proximal promoter region of Bmi1 was transcriptionally activated with co-transfection of ERα in luciferase assays, and the interaction of the Bmi1 promoter with ERα was confirmed by chromatin immunoprecipitation. Moreover, in breast cancer tissues activation of the ERα-coupled Bmi1 pathway generally correlated with high levels of cyclin D1, while loss of its activity resulted in aberrant expression of p16 INK4a and a high Ki-67 index, which implied a more aggressive phenotype of breast cancer. Conclusions Expression of Bmi1 is influenced by ERα, and the activity of the ERα-coupled Bmi1 signature impacts p16 INK4a and cyclin D1 status and thus correlates with the tumor molecular subtype and biologic behavior. This demonstrates the important role which is played by ERα-coupled Bmi1 in human breast cancer.

Published
2014

46. CUL4B promotes replication licensing by up-regulating the CDK2-CDC6 cascade

Author

Zou, Yongxin, Mi, Jun, Wang, Wenxing, Lu, Juanjuan, Zhao, Wei, Liu, Zhaojian, Hu, Huili, Yang, Yang, Gao, Xiaoxing, Jiang, Baichun, Shao, Changshun, Gong, Yaoqin, Zou, Yongxin, Mi, Jun, Wang, Wenxing, Lu, Juanjuan, Zhao, Wei, Liu, Zhaojian, Hu, Huili, Yang, Yang, Gao, Xiaoxing, Jiang, Baichun, Shao, Changshun, and Gong, Yaoqin

Abstract

Cullin-RING ubiquitin ligases (CRLs) participate in the regulation of diverse cellular processes including cell cycle progression. Mutations in the X-linked CUL4B, a member of the cullin family, cause mental retardation and other developmental abnormalities in humans. Cells that are deficient in CUL4B are severely selected against in vivo in heterozygotes. Here we report a role of CUL4B in the regulation of replication licensing. Strikingly, CDC6, the licensing factor in replication, was positively regulated by CUL4B and contributed to the loading of MCM2 to chromatin. The positive regulation of CDC6 by CUL4B depends on CDK2, which phosphorylates CDC6, protecting it from APC(CDH1)-mediated degradation. Thus, aside being required for cell cycle reentry from quiescence, CDK2 also contributes to pre-replication complex assembly in G1 phase of cycling cells. Interestingly, the up-regulation of CDK2 by CUL4B is achieved via the repression of miR-372 and miR-373, which target CDK2. Our findings thus establish a CUL4B-CDK2-CDC6 cascade in the regulation of DNA replication licensing.

Published
2013

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