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A20 and CYLD do not share significant overlapping functions during B cell development and activation

(2012) JOURNAL OF IMMUNOLOGY. 189(9). p.4437-4443
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Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
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Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
Abstract
The ubiquitin-editing enzyme A20 (TNFAIP3) and the deubiquitinase CYLD are central negative regulators of NF-kappa B signaling. Both can act by removing nonproteolytic K63-linked polyubiquitin chains from an overlapping set of signaling molecules. In B cells, A20 deficiency results in hyperactivity, loss of immune homeostasis, inflammation, and autoimmunity. The reported consequences of CYLD deficiency are controversial, ranging from an absence of effects to dramatic B cell hyperplasia. These differences could be due to varying compensation for the loss of CYLD function by A20. Therefore, to explore potential overlapping physiological functions between A20 and CYLD, we generated and characterized A20/CYLD double-deficient B cells. Interestingly, the lack of both A20 and CYLD did not exacerbate the developmental defects and hyperresponsive activity of A20-deficient B cells. In addition, the extent of B cell activation after in vitro stimulation with anti-CD40, LPS, and CpG was comparable in B cells lacking A20/CYLD and A20 alone. However, in response to BCR cross-linking, we observed small but reproducible additive effects of the lack of A20 and CYLD. Taken together, our results demonstrate that A20 and CYLD do not share significant functions during B cell development and activation.
Keywords
RHEUMATOID-ARTHRITIS, TUMOR-SUPPRESSOR GENE, UBIQUITIN, TNFAIP3, PROLIFERATION, HOMEOSTASIS, DEFICIENCY, DEUBIQUITINATING ENZYME CYLD, SYSTEMIC-LUPUS-ERYTHEMATOSUS, NF-KAPPA-B

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Citation

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MLA
Chu, Yuanyuan, Valeria Soberon, Laura Glockner, et al. “A20 and CYLD Do Not Share Significant Overlapping Functions During B Cell Development and Activation.” JOURNAL OF IMMUNOLOGY 189.9 (2012): 4437–4443. Print.
APA
Chu, Y., Soberon, V., Glockner, L., Beyaert, R., Massoumi, R., van Loo, G., Krappmann, D., et al. (2012). A20 and CYLD do not share significant overlapping functions during B cell development and activation. JOURNAL OF IMMUNOLOGY, 189(9), 4437–4443.
Chicago author-date
Chu, Yuanyuan, Valeria Soberon, Laura Glockner, Rudi Beyaert, Ramin Massoumi, Geert van Loo, Daniel Krappmann, and Marc Schmidt-Supprian. 2012. “A20 and CYLD Do Not Share Significant Overlapping Functions During B Cell Development and Activation.” Journal of Immunology 189 (9): 4437–4443.
Chicago author-date (all authors)
Chu, Yuanyuan, Valeria Soberon, Laura Glockner, Rudi Beyaert, Ramin Massoumi, Geert van Loo, Daniel Krappmann, and Marc Schmidt-Supprian. 2012. “A20 and CYLD Do Not Share Significant Overlapping Functions During B Cell Development and Activation.” Journal of Immunology 189 (9): 4437–4443.
Vancouver
1.
Chu Y, Soberon V, Glockner L, Beyaert R, Massoumi R, van Loo G, et al. A20 and CYLD do not share significant overlapping functions during B cell development and activation. JOURNAL OF IMMUNOLOGY. 2012;189(9):4437–43.
IEEE
[1]
Y. Chu et al., “A20 and CYLD do not share significant overlapping functions during B cell development and activation,” JOURNAL OF IMMUNOLOGY, vol. 189, no. 9, pp. 4437–4443, 2012.
@article{3063049,
  abstract     = {The ubiquitin-editing enzyme A20 (TNFAIP3) and the deubiquitinase CYLD are central negative regulators of NF-kappa B signaling. Both can act by removing nonproteolytic K63-linked polyubiquitin chains from an overlapping set of signaling molecules. In B cells, A20 deficiency results in hyperactivity, loss of immune homeostasis, inflammation, and autoimmunity. The reported consequences of CYLD deficiency are controversial, ranging from an absence of effects to dramatic B cell hyperplasia. These differences could be due to varying compensation for the loss of CYLD function by A20. Therefore, to explore potential overlapping physiological functions between A20 and CYLD, we generated and characterized A20/CYLD double-deficient B cells. Interestingly, the lack of both A20 and CYLD did not exacerbate the developmental defects and hyperresponsive activity of A20-deficient B cells. In addition, the extent of B cell activation after in vitro stimulation with anti-CD40, LPS, and CpG was comparable in B cells lacking A20/CYLD and A20 alone. However, in response to BCR cross-linking, we observed small but reproducible additive effects of the lack of A20 and CYLD. Taken together, our results demonstrate that A20 and CYLD do not share significant functions during B cell development and activation.},
  author       = {Chu, Yuanyuan and Soberon, Valeria and Glockner, Laura and Beyaert, Rudi and Massoumi, Ramin and van Loo, Geert and Krappmann, Daniel and Schmidt-Supprian, Marc},
  issn         = {0022-1767},
  journal      = {JOURNAL OF IMMUNOLOGY},
  keywords     = {RHEUMATOID-ARTHRITIS,TUMOR-SUPPRESSOR GENE,UBIQUITIN,TNFAIP3,PROLIFERATION,HOMEOSTASIS,DEFICIENCY,DEUBIQUITINATING ENZYME CYLD,SYSTEMIC-LUPUS-ERYTHEMATOSUS,NF-KAPPA-B},
  language     = {eng},
  number       = {9},
  pages        = {4437--4443},
  title        = {A20 and CYLD do not share significant overlapping functions during B cell development and activation},
  url          = {http://dx.doi.org/10.4049/jimmunol.1200396},
  volume       = {189},
  year         = {2012},
}

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