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CARD14-mediated activation of paracaspase MALT1 in keratinocytes : implications for psoriasis

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Abstract
Mutations in caspase recruitment domain-containing protein 14 (CARD14) have been linked to susceptibility to psoriasis. CARD14 is an intracellular scaffold protein that regulates proinflammatory gene expression. Recent studies have offered novel insights into the mechanisms of CARD14-mediated signaling in keratinocytes and the molecular impact of psoriasis-associated CARD14 mutations. CARD14 forms a signaling complex with BCL10 and the paracaspase MALT1, and this process is enhanced upon pathogenic CARD14 mutation, culminating in the activation of MALT1 protease activity and psoriasis-associated gene expression. This review summarizes the current knowledge of CARD14/MALT1-mediated signaling in keratinocytes and its therapeutic implications in psoriasis.
Keywords
NF-KAPPA-B, PITYRIASIS-RUBRA-PILARIS, GENERALIZED PUSTULAR PSORIASIS, T-CELL-ACTIVATION, PROTEASE ACTIVITY, CARD14 GENE, PHARMACOLOGICAL, INHIBITION, SIGNALING PATHWAY, CHINESE COHORT, FAMILY MEMBER

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MLA
Van Nuffel, Elien et al. “CARD14-mediated Activation of Paracaspase MALT1 in Keratinocytes : Implications for Psoriasis.” JOURNAL OF INVESTIGATIVE DERMATOLOGY 137.3 (2017): 569–575. Print.
APA
Van Nuffel, E., Schmitt, A., Afonina, I., Schulze-Osthoff, K., Beyaert, R., & Hailfinger, S. (2017). CARD14-mediated activation of paracaspase MALT1 in keratinocytes : implications for psoriasis. JOURNAL OF INVESTIGATIVE DERMATOLOGY, 137(3), 569–575.
Chicago author-date
Van Nuffel, Elien, Anja Schmitt, Inna Afonina, Klaus Schulze-Osthoff, Rudi Beyaert, and Stephan Hailfinger. 2017. “CARD14-mediated Activation of Paracaspase MALT1 in Keratinocytes : Implications for Psoriasis.” Journal of Investigative Dermatology 137 (3): 569–575.
Chicago author-date (all authors)
Van Nuffel, Elien, Anja Schmitt, Inna Afonina, Klaus Schulze-Osthoff, Rudi Beyaert, and Stephan Hailfinger. 2017. “CARD14-mediated Activation of Paracaspase MALT1 in Keratinocytes : Implications for Psoriasis.” Journal of Investigative Dermatology 137 (3): 569–575.
Vancouver
1.
Van Nuffel E, Schmitt A, Afonina I, Schulze-Osthoff K, Beyaert R, Hailfinger S. CARD14-mediated activation of paracaspase MALT1 in keratinocytes : implications for psoriasis. JOURNAL OF INVESTIGATIVE DERMATOLOGY. 2017;137(3):569–75.
IEEE
[1]
E. Van Nuffel, A. Schmitt, I. Afonina, K. Schulze-Osthoff, R. Beyaert, and S. Hailfinger, “CARD14-mediated activation of paracaspase MALT1 in keratinocytes : implications for psoriasis,” JOURNAL OF INVESTIGATIVE DERMATOLOGY, vol. 137, no. 3, pp. 569–575, 2017.
@article{8517340,
  abstract     = {Mutations in caspase recruitment domain-containing protein 14 (CARD14) have been linked to susceptibility to psoriasis. CARD14 is an intracellular scaffold protein that regulates proinflammatory gene expression. Recent studies have offered novel insights into the mechanisms of CARD14-mediated signaling in keratinocytes and the molecular impact of psoriasis-associated CARD14 mutations. CARD14 forms a signaling complex with BCL10 and the paracaspase MALT1, and this process is enhanced upon pathogenic CARD14 mutation, culminating in the activation of MALT1 protease activity and psoriasis-associated gene expression. This review summarizes the current knowledge of CARD14/MALT1-mediated signaling in keratinocytes and its therapeutic implications in psoriasis.},
  author       = {Van Nuffel, Elien and Schmitt, Anja and Afonina, Inna and Schulze-Osthoff, Klaus and Beyaert, Rudi and Hailfinger, Stephan},
  issn         = {0022-202X},
  journal      = {JOURNAL OF INVESTIGATIVE DERMATOLOGY},
  keywords     = {NF-KAPPA-B,PITYRIASIS-RUBRA-PILARIS,GENERALIZED PUSTULAR PSORIASIS,T-CELL-ACTIVATION,PROTEASE ACTIVITY,CARD14 GENE,PHARMACOLOGICAL,INHIBITION,SIGNALING PATHWAY,CHINESE COHORT,FAMILY MEMBER},
  language     = {eng},
  number       = {3},
  pages        = {569--575},
  title        = {CARD14-mediated activation of paracaspase MALT1 in keratinocytes : implications for psoriasis},
  url          = {http://dx.doi.org/10.1016/j.jid.2016.09.031},
  volume       = {137},
  year         = {2017},
}

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