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A20 at the crossroads of cell death, inflammation, and autoimmunity

Arne Martens (UGent) and Geert van Loo (UGent)
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Abstract
A20 is a potent anti-inflammatory protein, acting by inhibiting nuclear factor kappa B (NF-kappa B) signaling and inflammatory gene expression and/or by preventing cell death. Mutations in the A20/TNFAIP3 gene have been associated with a plethora of inflammatory and autoimmune pathologies in humans and in mice. Although the anti-inflammatory role of A20 is well accepted, fundamental mechanistic questions regarding its mode of action remain unclear. Here, we review new findings that further clarify the molecular and cellular mechanisms by which A20 controls inflammatory signaling and cell death, and discuss new evidence for its involvement in inflammatory and autoimmune disease development.
Keywords
NF-KAPPA-B, GENOME-WIDE ASSOCIATION, INDUCED PROTEIN-3 TNFAIP3, MODIFYING ENZYME A20, ZINC-FINGER PROTEIN, LINEAR UBIQUITIN, RESTRICTS, UBIQUITINATION, NLRP3 INFLAMMASOME, DEUBIQUITINASE A20, CROHN-DISEASE

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MLA
Martens, Arne, and Geert van Loo. “A20 at the Crossroads of Cell Death, Inflammation, and Autoimmunity.” COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY, vol. 12, no. 1, 2020.
APA
Martens, A., & van Loo, G. (2020). A20 at the crossroads of cell death, inflammation, and autoimmunity. COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY, 12(1).
Chicago author-date
Martens, Arne, and Geert van Loo. 2020. “A20 at the Crossroads of Cell Death, Inflammation, and Autoimmunity.” COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY 12 (1).
Chicago author-date (all authors)
Martens, Arne, and Geert van Loo. 2020. “A20 at the Crossroads of Cell Death, Inflammation, and Autoimmunity.” COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY 12 (1).
Vancouver
1.
Martens A, van Loo G. A20 at the crossroads of cell death, inflammation, and autoimmunity. COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY. 2020;12(1).
IEEE
[1]
A. Martens and G. van Loo, “A20 at the crossroads of cell death, inflammation, and autoimmunity,” COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY, vol. 12, no. 1, 2020.
@article{8647314,
  abstract     = {A20 is a potent anti-inflammatory protein, acting by inhibiting nuclear factor kappa B (NF-kappa B) signaling and inflammatory gene expression and/or by preventing cell death. Mutations in the A20/TNFAIP3 gene have been associated with a plethora of inflammatory and autoimmune pathologies in humans and in mice. Although the anti-inflammatory role of A20 is well accepted, fundamental mechanistic questions regarding its mode of action remain unclear. Here, we review new findings that further clarify the molecular and cellular mechanisms by which A20 controls inflammatory signaling and cell death, and discuss new evidence for its involvement in inflammatory and autoimmune disease development.},
  articleno    = {a036418},
  author       = {Martens, Arne and van Loo, Geert},
  issn         = {1943-0264},
  journal      = {COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY},
  keywords     = {NF-KAPPA-B,GENOME-WIDE ASSOCIATION,INDUCED PROTEIN-3 TNFAIP3,MODIFYING ENZYME A20,ZINC-FINGER PROTEIN,LINEAR UBIQUITIN,RESTRICTS,UBIQUITINATION,NLRP3 INFLAMMASOME,DEUBIQUITINASE A20,CROHN-DISEASE},
  language     = {eng},
  number       = {1},
  pages        = {18},
  title        = {A20 at the crossroads of cell death, inflammation, and autoimmunity},
  url          = {http://dx.doi.org/10.1101/cshperspect.a036418},
  volume       = {12},
  year         = {2020},
}

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