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17 results on '"Zhu, Qingchen"'

2. Biomarkers of aging

Author

Bao, Hainan, Cao, Jiani, Chen, Mengting, Chen, Min, Chen, Wei, Chen, Xiao, Chen, Yanhao, Chen, Yu, Chen, Yutian, Chen, Zhiyang, Chhetri, Jagadish K., Ding, Yingjie, Feng, Junlin, Guo, Jun, Guo, Mengmeng, He, Chuting, Jia, Yujuan, Jiang, Haiping, Jing, Ying, Li, Dingfeng, Li, Jiaming, Li, Jingyi, Liang, Qinhao, Liang, Rui, Liu, Feng, Liu, Xiaoqian, Liu, Zuojun, Luo, Oscar Junhong, Lv, Jianwei, Ma, Jingyi, Mao, Kehang, Nie, Jiawei, Qiao, Xinhua, Sun, Xinpei, Tang, Xiaoqiang, Wang, Jianfang, Wang, Qiaoran, Wang, Siyuan, Wang, Xuan, Wang, Yaning, Wang, Yuhan, Wu, Rimo, Xia, Kai, Xiao, Fu-Hui, Xu, Lingyan, Xu, Yingying, Yan, Haoteng, Yang, Liang, Yang, Ruici, Yang, Yuanxin, Ying, Yilin, Zhang, Le, Zhang, Weiwei, Zhang, Wenwan, Zhang, Xing, Zhang, Zhuo, Zhou, Min, Zhou, Rui, Zhu, Qingchen, Zhu, Zhengmao, Cao, Feng, Cao, Zhongwei, Chan, Piu, Chen, Chang, Chen, Guobing, Chen, Hou-Zao, Chen, Jun, Ci, Weimin, Ding, Bi-Sen, Ding, Qiurong, Gao, Feng, Han, Jing-Dong J., Huang, Kai, Ju, Zhenyu, Kong, Qing-Peng, Li, Ji, Li, Jian, Li, Xin, Liu, Baohua, Liu, Feng, Liu, Lin, Liu, Qiang, Liu, Qiang, Liu, Xingguo, Liu, Yong, Luo, Xianghang, Ma, Shuai, Ma, Xinran, Mao, Zhiyong, Nie, Jing, Peng, Yaojin, Qu, Jing, Ren, Jie, Ren, Ruibao, Song, Moshi, Songyang, Zhou, Sun, Yi Eve, Sun, Yu, Tian, Mei, Wang, Shusen, Wang, Si, Wang, Xia, Wang, Xiaoning, Wang, Yan-Jiang, Wang, Yunfang, Wong, Catherine C. L., Xiang, Andy Peng, Xiao, Yichuan, Xie, Zhengwei, Xu, Daichao, Ye, Jing, Yue, Rui, Zhang, Cuntai, Zhang, Hongbo, Zhang, Liang, Zhang, Weiqi, Zhang, Yong, Zhang, Yun-Wu, Zhang, Zhuohua, Zhao, Tongbiao, Zhao, Yuzheng, Zhu, Dahai, Zou, Weiguo, Pei, Gang, and Liu, Guang-Hui

Published
2023
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8. E3 ligase MKRN3 is a tumor suppressor regulating PABPC1 ubiquitination in non–small cell lung cancer

Author

Li, Ke, primary, Zheng, Xufen, additional, Tang, Hua, additional, Zang, Yuan-Sheng, additional, Zeng, Chunling, additional, Liu, Xiaoxiao, additional, Shen, Yanying, additional, Pang, Yuzhi, additional, Wang, Simin, additional, Xie, Feifei, additional, Lu, Xiaojing, additional, Luo, Yuxiang, additional, Li, Zhang, additional, Bi, Wenbo, additional, Jia, Xiaona, additional, Huang, Tao, additional, Wei, Rongqiang, additional, Huang, Kenan, additional, Chen, Zihao, additional, Zhu, Qingchen, additional, He, Yi, additional, Zhang, Miaoying, additional, Gu, Zhizhan, additional, Xiao, Yichuan, additional, Zhang, Xiaoyang, additional, Fletcher, Jonathan A., additional, and Wang, Yuexiang, additional

Published
2021
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9. BFAR coordinates TGFβ signaling to modulate Th9-mediated cancer immunotherapy

Author

Pei, Siyu, primary, Huang, Mingzhu, additional, Huang, Jia, additional, Zhu, Xiaodong, additional, Wang, Hui, additional, Romano, Simona, additional, Deng, Xiuyu, additional, Wang, Yan, additional, Luo, Yixiao, additional, Hao, Shumeng, additional, Xu, Jing, additional, Yu, Tao, additional, Zhu, Qingchen, additional, Yuan, Jia, additional, Shen, Kunwei, additional, Liu, Zhiqiang, additional, Hu, Guohong, additional, Peng, Chao, additional, Luo, Qingquan, additional, Wen, Zhenzhen, additional, Dai, Dongfang, additional, and Xiao, Yichuan, additional

Published
2021
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10. Cytoplasmic DNA sensing by KU complex in aged CD4+ T cell potentiates T cell activation and aging-related autoimmune inflammation

Author

Wang, Yan, primary, Fu, Zunyun, additional, Li, Xutong, additional, Liang, Yinming, additional, Pei, Siyu, additional, Hao, Shumeng, additional, Zhu, Qingchen, additional, Yu, Tao, additional, Pei, Yifei, additional, Yuan, Jia, additional, Ye, Jialin, additional, Fu, Jiemeng, additional, Xu, Jing, additional, Hong, Jin, additional, Yang, Ruirui, additional, Hou, Hui, additional, Huang, Xinfang, additional, Peng, Chao, additional, Zheng, Mingyue, additional, and Xiao, Yichuan, additional

Published
2021
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11. TRIM24 facilitates antiviral immunity through mediating K63-linked TRAF3 ubiquitination

Author

Zhu, Qingchen, primary, Yu, Tao, additional, Gan, Shucheng, additional, Wang, Yan, additional, Pei, Yifei, additional, Zhao, Qifan, additional, Pei, Siyu, additional, Hao, Shumeng, additional, Yuan, Jia, additional, Xu, Jing, additional, Hou, Fajian, additional, Wu, Xuefeng, additional, Peng, Chao, additional, Wu, Ping, additional, Qin, Jun, additional, and Xiao, Yichuan, additional

Published
2020
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12. Modulation of M2 macrophage polarization by the crosstalk between Stat6 and Trim24

Author

Yu, Tao, primary, Gan, Shucheng, additional, Zhu, Qingchen, additional, Dai, Dongfang, additional, Li, Ni, additional, Wang, Hui, additional, Chen, Xiaosong, additional, Hou, Dan, additional, Wang, Yan, additional, Pan, Qiang, additional, Xu, Jing, additional, Zhang, Xingli, additional, Liu, Junli, additional, Pei, Siyu, additional, Peng, Chao, additional, Wu, Ping, additional, Romano, Simona, additional, Mao, Chaoming, additional, Huang, Mingzhu, additional, Zhu, Xiaodong, additional, Shen, Kunwei, additional, Qin, Jun, additional, and Xiao, Yichuan, additional

Published
2019
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13. Intronic (TTTGA) n insertion in SAMD12 also causes familial cortical myoclonic tremor with epilepsy

Author

Cen, Zhidong, primary, Chen, You, additional, Yang, Dehao, additional, Zhu, Qingchen, additional, Chen, Si, additional, Chen, Xinhui, additional, Wang, Bo, additional, Xie, Fei, additional, Ouyang, Zhiyuan, additional, Jiang, Zhengwen, additional, Fu, Aisi, additional, Hu, Ben, additional, Yin, Houmin, additional, Qiu, Xia, additional, Yu, Feng, additional, Du, Xiaoping, additional, Hao, Weicheng, additional, Liu, Yuxi, additional, Wang, Haotian, additional, Wang, Lebo, additional, Yu, Xiafei, additional, Xiao, Yichuan, additional, Liu, Chunyu, additional, Xiao, Jianfeng, additional, Zhou, Yongxing, additional, Yang, Wei, additional, Zhang, Baorong, additional, and Luo, Wei, additional

Published
2019
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14. Ezh2 competes with p53 to license lncRNA Neat1transcription for inflammasome activation

Author

Yuan, Jia, Zhu, Qingchen, Zhang, Xingli, Wen, Zhenzhen, Zhang, Guiheng, Li, Ni, Pei, Yifei, Wang, Yan, Pei, Siyu, Xu, Jing, Jia, Pan, Peng, Chao, Lu, Wei, Qin, Jun, Cao, Qian, and Xiao, Yichuan

Abstract

Inflammasome contributes to the pathogenesis of various inflammatory diseases, but the epigenetic mechanism controlling its activation remains elusive. Here, we found that the histone methyltransferase Ezh2 mediates the activation of multiple types of inflammasomes in macrophages/microglia independent of its methyltransferase activity and thus promotes inflammasome-related pathologies. Mechanistically, Ezh2 functions through its SANT2 domain to maintain the enrichment of H3K27 acetylation in the promoter region of the long noncoding RNA (lncRNA) Neat1, thereby promoting chromatin accessibility and facilitating p65-mediated transcription of Neat1, which is a critical mediator of inflammasome assembly and activation. In addition, the tumour suppressor protein p53 competes with Ezh2 for the same binding region in the Neat1promoter and thus antagonises Ezh2-induced Neat1transcription and inflammasome activation. Therefore, loss of Ezh2 strongly promotes the binding of p53, which recruits the deacetylase SIRT1 for H3K27 deacetylation of the Neat1promoter and thus suppresses Neat1transcription and inflammasome activation. Overall, our study demonstrates an epigenetic mechanism involved in modulating inflammasome activation through an Ezh2/p53 competition model and highlights a novel function of Ezh2 in maintaining H3K27 acetylation to support lncRNA Neat1transcription.

Published
2022
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15. Chemoradiotherapy-induced ACKR2+tumor cells drive CD8+T cell senescence and cervical cancer recurrence

Author

Dai, Dongfang, Pei, Yifei, Zhu, Biqing, Wang, Deqiang, Pei, Siyu, Huang, Huan, Zhu, Qingchen, Deng, Xiuyu, Ye, Jialin, Xu, Jing, Chen, Xiaoxiang, Huang, Mingzhu, and Xiao, Yichuan

Abstract

Tumor recurrence after chemoradiotherapy is challenging to overcome, and approaches to predict the recurrence remain elusive. Here, human cervical cancer tissues before and after concurrent chemoradiotherapy (CCRT) analyzed by single-cell RNA sequencing reveal that CCRT specifically promotes CD8+T cell senescence, driven by atypical chemokine receptor 2 (ACKR2)+CCRT-resistant tumor cells. Mechanistically, ACKR2 expression is increased in response to CCRT and is also upregulated through the ligation of CC chemokines that are produced by activated myeloid and T cells. Subsequently, ACKR2+tumor cells are induced to produce transforming growth factor β to drive CD8+T cell senescence, thereby compromising antitumor immunity. Moreover, retrospective analysis reveals that ACKR2 expression and CD8+T cell senescence are enhanced in patients with cervical cancer who experienced recurrence after CCRT, indicating poor prognosis. Overall, we identify a subpopulation of CCRT-resistant ACKR2+tumor cells driving CD8+T cell senescence and tumor recurrence and highlight the prognostic value of ACKR2 and CD8+T cell senescence for chemoradiotherapy recurrence.

Published
2024
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16. Intronic (TTTGA)n insertion in SAMD12 also causes familial cortical myoclonic tremor with epilepsy.

Author

Cen, Zhidong, Chen, You, Yang, Dehao, Zhu, Qingchen, Chen, Si, Chen, Xinhui, Wang, Bo, Xie, Fei, Ouyang, Zhiyuan, Jiang, Zhengwen, Fu, Aisi, Hu, Ben, Yin, Houmin, Qiu, Xia, Yu, Feng, Du, Xiaoping, Hao, Weicheng, Liu, Yuxi, Wang, Haotian, and Wang, Lebo

Abstract

Background: Intronic (TTTCA)n insertions in the SAMD12, TNRC6A, and RAPGEF2 genes have been identified as causes of familial cortical myoclonic tremor with epilepsy.Objective: To identify the cause of familial cortical myoclonic tremor with epilepsy pedigrees without (TTTCA)n insertions in SAMD12, TNRC6A, and RAPGEF2.Methods: Repeat-primed polymerase chain reaction, long-range polymerase chain reaction, and Sanger sequencing were performed to identify the existence of a novel (TTTGA)n insertion. Targeted long-read sequencing was performed to confirm the accurate structure of the (TTTGA)n insertion.Results: We identified a novel expanded intronic (TTTGA)n insertion at the same site as the previously reported (TTTCA)n insertion in SAMD12. This insertion cosegregated with familial cortical myoclonic tremor with epilepsy in 1 Chinese pedigree with no (TTTCA)n insertion. In the targeted long-read sequencing of 2 patients and 1 asymptomatic carrier in this pedigree, with 1 previously reported (TTTCA)n -insertion-carrying patient as a positive control, a respective total of 302, 159, 207, and 50 on-target subreads (predicated accuracy: ≥90%) spanning the target repeat expansion region were generated. These sequencing data revealed the accurate repeat expansion structures as (TTTTA)114-123 (TTTGA)108-116 in the pedigree and (TTTTA)38 (TTTCA)479 in (TTTCA)n -insertion-carrying patient.Conclusion: The targeted long-read sequencing helped us to elucidate the accurate structures of the (TTTGA)n and (TTTCA)n insertions. Our finding offers a novel possible cause for familial cortical myoclonic tremor with epilepsy and might shed light on the identification of genetic causes of this disease in pedigrees with no detected (TTTCA)n insertion in the reported causative genes. © 2019 International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Published
2019
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17. Cytoplasmic DNA sensing by KU complex in aged CD4 + T cell potentiates T cell activation and aging-related autoimmune inflammation.

Author

Wang Y, Fu Z, Li X, Liang Y, Pei S, Hao S, Zhu Q, Yu T, Pei Y, Yuan J, Ye J, Fu J, Xu J, Hong J, Yang R, Hou H, Huang X, Peng C, Zheng M, and Xiao Y

Subjects
Animals, Cell Line, Cell Line, Tumor, Cell Nucleus immunology, Cell Proliferation physiology, DNA Repair immunology, HEK293 Cells, Humans, Jurkat Cells, Lymphocyte Activation immunology, Mice, Mice, Inbred C57BL, U937 Cells, Aging immunology, Autoimmune Diseases immunology, CD4-Positive T-Lymphocytes immunology, Cytoplasm immunology, DNA immunology, DNA-Activated Protein Kinase immunology, Inflammation immunology
Abstract

Aging is associated with DNA accumulation and increased homeostatic proliferation of circulating T cells. Although these attributes are associated with aging-related autoimmunity, their direct contributions remain unclear. Conventionally, KU complex, the regulatory subunit of DNA-dependent protein kinase (DNA-PK), together with the catalytic subunit of DNA-PK (DNA-PKcs), mediates DNA damage repair in the nucleus. Here, we found KU complex abundantly expressed in the cytoplasm, where it recognized accumulated cytoplasmic DNA in aged human and mouse CD4 + T cells. This process enhanced T cell activation and pathology of experimental autoimmune encephalomyelitis (EAE) in aged mice. Mechanistically, KU-mediated DNA sensing facilitated DNA-PKcs recruitment and phosphorylation of the kinase ZAK. This activated AKT and mTOR pathways, promoting CD4 + T cell proliferation and activation. We developed a specific ZAK inhibitor, which dampened EAE pathology in aged mice. Overall, these findings demonstrate a KU-mediated cytoplasmic DNA-sensing pathway in CD4 + T cells that potentiates aging-related autoimmunity., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Published
2021
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