Nature Communications (Mar 2018)
Peli1 negatively regulates noncanonical NF-κB signaling to restrain systemic lupus erythematosus
- Junli Liu,
- Xinfang Huang,
- Shumeng Hao,
- Yan Wang,
- Manman Liu,
- Jing Xu,
- Xingli Zhang,
- Tao Yu,
- Shucheng Gan,
- Dongfang Dai,
- Xuan Luo,
- Qingyan Lu,
- Chaoming Mao,
- Yanyun Zhang,
- Nan Shen,
- Bin Li,
- Mingzhu Huang,
- Xiaodong Zhu,
- Jin Jin,
- Xuhong Cheng,
- Shao-Cong Sun,
- Yichuan Xiao
Affiliations
- Junli Liu
- The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
- Xinfang Huang
- Department of Nephrology and Rheumatology, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine
- Shumeng Hao
- The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
- Yan Wang
- The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
- Manman Liu
- Department of Nephrology and Rheumatology, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine
- Jing Xu
- The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
- Xingli Zhang
- The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
- Tao Yu
- The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
- Shucheng Gan
- The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
- Dongfang Dai
- Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University
- Xuan Luo
- Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University
- Qingyan Lu
- Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University
- Chaoming Mao
- Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University
- Yanyun Zhang
- The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
- Nan Shen
- The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
- Bin Li
- Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine
- Mingzhu Huang
- Department of Medical Oncology, Fudan University Shanghai Cancer Center
- Xiaodong Zhu
- Department of Medical Oncology, Fudan University Shanghai Cancer Center
- Jin Jin
- Life Sciences Institute, Zhejiang University
- Xuhong Cheng
- Department of Immunology, MD Anderson Cancer Center, The University of Texas
- Shao-Cong Sun
- Department of Immunology, MD Anderson Cancer Center, The University of Texas
- Yichuan Xiao
- The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
- DOI
- https://doi.org/10.1038/s41467-018-03530-3
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 13
Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disorder mediated by excessive autoantibodies. Here the authors show that an E3 ubiquitin ligase, Peli1, negatively modulates noncanonical NF-κB signaling to restrain lupus-like symptoms in mice, and that Peli1 expression inversely correlates with SLE severity in humans.
