Genetic relationships between A20/TNFAIP3, chronic inflammation and autoimrnune disease
(2011) BIOCHEMICAL SOCIETY TRANSACTIONS. 39. p.1086-1091- abstract
- A20 [also known as TNFAIP3 (tumour necrosis factor a-induced protein 3)] restricts and terminates inflammatory responses through modulation of the ubiquitination status of central components in NF-kappa B (nuclear factor kappa B), IRF3 (interferon regulatory factor 3) and apoptosis signalling cascades. The phenotype of mice with full or conditional A20 deletion illustrates that A20 expression is essential to prevent chronic inflammation and autoimmune pathology. In addition, polymorphisms within the A20 genomic locus have been associated with multiple inflammatory and autoimmune disorders, including SLE (systemic lupus erythaematosis), RA (rheumatoid arthritis), Crohn's disease and psoriasis. A20 has also been implicated as a tumour suppressor in several subsets of B-cell lymphomas. The present review outlines recent findings that illustrate the effect of A20 defects in disease pathogenesis and summarizes the identified A20 polymorphisms associated with different immunopathologies.
Please use this url to cite or link to this publication:
http://hdl.handle.net/1854/LU-1892640
- author
- Lars Vereecke UGent, Rudi Beyaert UGent and Geert van Loo UGent
- organization
- year
- 2011
- type
- journalArticle (original)
- publication status
- published
- subject
- keyword
- GENOME-WIDE ASSOCIATION, JAPANESE POPULATION, MULTIPLE AUTOIMMUNE-DISEASES, SYSTEMIC-LUPUS-ERYTHEMATOSUS, NF-KAPPA-B, RHEUMATOID-ARTHRITIS, SUSCEPTIBILITY LOCI, A20 DEFICIENCY, CELIAC-DISEASE, CELL LYMPHOMA, A20, autoimmunity, B-cell, inflammatory bowel disease (IBD), nuclear factor kappa B (NF-kappa B), tumour necrosis factor alpha-induced protein 3 (TNFAIP3)
- journal title
- BIOCHEMICAL SOCIETY TRANSACTIONS
- Biochem. Soc. Trans.
- volume
- 39
- pages
- 1086 - 1091
- Web of Science type
- Article
- Web of Science id
- 000293814800043
- JCR category
- BIOCHEMISTRY & MOLECULAR BIOLOGY
- JCR impact factor
- 3.711 (2011)
- JCR rank
- 94/286 (2011)
- JCR quartile
- 2 (2011)
- ISSN
- 0300-5127
- DOI
- 10.1042/BST0391086
- project
- Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
- language
- English
- UGent publication?
- yes
- classification
- A1
- copyright statement
- I have transferred the copyright for this publication to the publisher
- id
- 1892640
- handle
- http://hdl.handle.net/1854/LU-1892640
- date created
- 2011-08-25 16:46:23
- date last changed
- 2016-12-19 15:41:56
@article{1892640, abstract = {A20 [also known as TNFAIP3 (tumour necrosis factor a-induced protein 3)] restricts and terminates inflammatory responses through modulation of the ubiquitination status of central components in NF-kappa B (nuclear factor kappa B), IRF3 (interferon regulatory factor 3) and apoptosis signalling cascades. The phenotype of mice with full or conditional A20 deletion illustrates that A20 expression is essential to prevent chronic inflammation and autoimmune pathology. In addition, polymorphisms within the A20 genomic locus have been associated with multiple inflammatory and autoimmune disorders, including SLE (systemic lupus erythaematosis), RA (rheumatoid arthritis), Crohn's disease and psoriasis. A20 has also been implicated as a tumour suppressor in several subsets of B-cell lymphomas. The present review outlines recent findings that illustrate the effect of A20 defects in disease pathogenesis and summarizes the identified A20 polymorphisms associated with different immunopathologies.}, author = {Vereecke, Lars and Beyaert, Rudi and van Loo, Geert}, issn = {0300-5127}, journal = {BIOCHEMICAL SOCIETY TRANSACTIONS}, keyword = {GENOME-WIDE ASSOCIATION,JAPANESE POPULATION,MULTIPLE AUTOIMMUNE-DISEASES,SYSTEMIC-LUPUS-ERYTHEMATOSUS,NF-KAPPA-B,RHEUMATOID-ARTHRITIS,SUSCEPTIBILITY LOCI,A20 DEFICIENCY,CELIAC-DISEASE,CELL LYMPHOMA,A20,autoimmunity,B-cell,inflammatory bowel disease (IBD),nuclear factor kappa B (NF-kappa B),tumour necrosis factor alpha-induced protein 3 (TNFAIP3)}, language = {eng}, pages = {1086--1091}, title = {Genetic relationships between A20/TNFAIP3, chronic inflammation and autoimrnune disease}, url = {http://dx.doi.org/10.1042/BST0391086}, volume = {39}, year = {2011}, }
- Chicago
- Vereecke, Lars, Rudi Beyaert, and Geert van Loo. 2011. “Genetic Relationships Between A20/TNFAIP3, Chronic Inflammation and Autoimrnune Disease.” Biochemical Society Transactions 39: 1086–1091.
- APA
- Vereecke, L., Beyaert, R., & van Loo, G. (2011). Genetic relationships between A20/TNFAIP3, chronic inflammation and autoimrnune disease. BIOCHEMICAL SOCIETY TRANSACTIONS, 39, 1086–1091.
- Vancouver
- 1.Vereecke L, Beyaert R, van Loo G. Genetic relationships between A20/TNFAIP3, chronic inflammation and autoimrnune disease. BIOCHEMICAL SOCIETY TRANSACTIONS. 2011;39:1086–91.
- MLA
- Vereecke, Lars, Rudi Beyaert, and Geert van Loo. “Genetic Relationships Between A20/TNFAIP3, Chronic Inflammation and Autoimrnune Disease.” BIOCHEMICAL SOCIETY TRANSACTIONS 39 (2011): 1086–1091. Print.