Advances in the potential roles of Cullin-RING ligases in regulating autoimmune diseases

被引:8
作者
Zhang, Xiaoying [1 ,2 ]
Liu, Yu'e [3 ]
Zhang, Tong [1 ,2 ]
Tan, Yuying [1 ,2 ]
Dai, Xiangpeng [1 ,2 ]
Yang, Yong-Guang [1 ,2 ,4 ]
Zhang, Xiaoling [1 ,2 ]
机构
[1] Jilin Univ, Hosp 1, Key Lab Organ Regenerat & Transplantat, Minist Educ, Changchun, Peoples R China
[2] Jilin Univ, Hosp 1, Natl Local Joint Engn Lab Anim Models Human Dis, Changchun, Peoples R China
[3] Tongji Univ, Tongji Univ Canc Ctr, Shanghai Peoples Hosp Tongji Univ 10, Sch Med, Shanghai, Peoples R China
[4] Jilin Univ, Int Ctr Future Sci, Changchun, Peoples R China
基金
中国国家自然科学基金;
关键词
Cullin-RING ligases; autoimmune diseases; E3; ligases; ubiquitination; inflammation; E3 UBIQUITIN LIGASE; NF-KAPPA-B; SYSTEMIC-LUPUS-ERYTHEMATOSUS; TRCP-DEPENDENT DEGRADATION; BETA-TRCP; TUMOR-SUPPRESSOR; NEDD8-ACTIVATING ENZYME; PROTEIN STABILITY; SIGNALING PATHWAY; MTOR INHIBITOR;
D O I
10.3389/fimmu.2023.1125224
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Cullin-RING ligases (CRLs) are the largest class of E3 ubiquitin ligases regulating the stability and subsequent activity of a large number of important proteins responsible for the development and progression of various diseases, including autoimmune diseases (AIDs). However, the detailed mechanisms of the pathogenesis of AIDs are complicated and involve multiple signaling pathways. An in-depth understanding of the underlying regulatory mechanisms of the initiation and progression of AIDs will aid in the development of effective therapeutic strategies. CRLs play critical roles in regulating AIDs, partially by affecting the key inflammation-associated pathways such as NF-kappa B, JAK/STAT, and TGF-beta. In this review, we summarize and discuss the potential roles of CRLs in the inflammatory signaling pathways and pathogenesis of AIDs. Furthermore, advances in the development of novel therapeutic strategies for AIDs through targeting CRLs are also highlighted.
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页数:17
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共 184 条
[1]   Multiomics to elucidate inflammatory bowel disease risk factors and pathways [J].
Agrawal, Manasi ;
Allin, Kristine H. ;
Petralia, Francesca ;
Colombel, Jean-Frederic ;
Jess, Tine .
NATURE REVIEWS GASTROENTEROLOGY & HEPATOLOGY, 2022, 19 (06) :399-409
[2]   Mechanism of processing of the NF-κB2 p100 precursor:: identification of the specific polyubiquitin chain-anchoring lysine residue and analysis of the role of NEDD8-modification on the SCFβ-TrCP ubiquitin ligase [J].
Amir, RE ;
Haecker, H ;
Karin, M ;
Ciechanover, A .
ONCOGENE, 2004, 23 (14) :2540-2547
[3]   AMBRA1 Interplay with Cullin E3 Ubiquitin Ligases Regulates Autophagy Dynamics [J].
Antonioli, Manuela ;
Albiero, Federica ;
Nazio, Francesca ;
Vescovo, Tiziana ;
Perdomo, Ariel Basulto ;
Corazzari, Marco ;
Marsella, Claudia ;
Piselli, Pierluca ;
Gretzmeier, Christine ;
Dengjel, Joern ;
Cecconi, Francesco ;
Piacentini, Mauro ;
Fimia, Gian Maria .
DEVELOPMENTAL CELL, 2014, 31 (06) :734-746
[4]   Proteomic screen reveals Fbw7 as a modulator of the NF-κB pathway [J].
Arabi, Azadeh ;
Ullah, Karim ;
Branca, Rui M. M. ;
Johansson, Johan ;
Bandarra, Daniel ;
Haneklaus, Moritz ;
Fu, Jing ;
Aries, Ingrid ;
Nilsson, Peter ;
Den Boer, Monique L. ;
Pokrovskaja, Katja ;
Grander, Dan ;
Xiao, Gutian ;
Rocha, Sonia ;
Lehtio, Janne ;
Sangfelt, Olle .
NATURE COMMUNICATIONS, 2012, 3
[5]   Pathophysiology, Clinical Presentation, and Treatment of Psoriasis A Review [J].
Armstrong, April W. ;
Read, Charlotte .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2020, 323 (19) :1945-1960
[6]   NEDD8 nucleates a multivalent cullin-RING-UBE2D ubiquitin ligation assembly [J].
Baek, Kheewoong ;
Krist, David T. ;
Prabu, J. Rajan ;
Hill, Spencer ;
Kluegel, Maren ;
Neumaier, Lisa-Marie ;
von Gronau, Susanne ;
Kleiger, Gary ;
Schulman, Brenda A. .
NATURE, 2020, 578 (7795) :461-+
[7]   JAK-STAT Signaling as a Target for Inflammatory and Autoimmune Diseases: Current and Future Prospects [J].
Banerjee, Shubhasree ;
Biehl, Ann ;
Gadina, Massimo ;
Hasni, Sarfaraz ;
Schwartz, Daniella M. .
DRUGS, 2017, 77 (05) :521-546
[8]   B cell targeted therapies in autoimmune disease [J].
Barnas, Jennifer L. ;
Looney, Richard John ;
Anolik, Jennifer H. .
CURRENT OPINION IN IMMUNOLOGY, 2019, 61 :92-99
[9]   Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease [J].
Barrett, Jeffrey C. ;
Hansoul, Sarah ;
Nicolae, Dan L. ;
Cho, Judy H. ;
Duerr, Richard H. ;
Rioux, John D. ;
Brant, Steven R. ;
Silverberg, Mark S. ;
Taylor, Kent D. ;
Barmada, M. Michael ;
Bitton, Alain ;
Dassopoulos, Themistocles ;
Datta, Lisa Wu ;
Green, Todd ;
Griffiths, Anne M. ;
Kistner, Emily O. ;
Murtha, Michael T. ;
Regueiro, Miguel D. ;
Rotter, Jerome I. ;
Schumm, L. Philip ;
Steinhart, A. Hillary ;
Targan, Stephan R. ;
Xavier, Ramnik J. ;
Libioulle, Cecile ;
Sandor, Cynthia ;
Lathrop, Mark ;
Belaiche, Jacques ;
Dewit, Olivier ;
Gut, Ivo ;
Heath, Simon ;
Laukens, Debby ;
Mni, Myriam ;
Rutgeerts, Paul ;
Van Gossum, Andre ;
Zelenika, Diana ;
Franchimont, Denis ;
Hugot, Jean-Pierre ;
de Vos, Martine ;
Vermeire, Severine ;
Louis, Edouard ;
Cardon, Lon R. ;
Anderson, Carl A. ;
Drummond, Hazel ;
Nimmo, Elaine ;
Ahmad, Tariq ;
Prescott, Natalie J. ;
Onnie, Clive M. ;
Fisher, Sheila A. ;
Marchini, Jonathan ;
Ghori, Jilur .
NATURE GENETICS, 2008, 40 (08) :955-962
[10]   Transforming Growth Factor-β Signaling in Immunity and Cancer [J].
Batlle, Eduard ;
Massague, Joan .
IMMUNITY, 2019, 50 (04) :924-940