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Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
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CARD14-Mediated Activation of Paracaspase MALT1 in Keratinocytes: Implications for Psoriasis

Elien Van Nuffel1, Anja Schmitt2, Inna S Afonina1

  • 1Unit of Molecular Signal Transduction in Inflammation, Inflammation Research Center, Ghent University-VIB, Ghent, Belgium; Department for Biomedical Molecular Biology, Ghent University, Ghent, Belgium.

The Journal of Investigative Dermatology
|December 13, 2016
PubMed

Insights

Mutations in caspase recruitment domain-containing protein 14 (CARD14) are linked to psoriasis. Pathogenic CARD14 mutations activate MALT1 protease, driving inflammation and psoriasis-associated gene expression.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Immunology

Background:

  • Mutations in CARD14 are associated with psoriasis susceptibility.
  • CARD14 is an intracellular scaffold protein regulating inflammatory gene expression.
  • Recent research elucidates CARD14 signaling mechanisms in keratinocytes.

Purpose of the Study:

  • To review CARD14/MALT1 signaling in keratinocytes.
  • To discuss the molecular impact of psoriasis-associated CARD14 mutations.
  • To explore therapeutic implications for psoriasis.

Main Methods:

  • Literature review of CARD14-mediated signaling pathways.
  • Analysis of molecular mechanisms involving CARD14, BCL10, and MALT1.
  • Summary of current knowledge on CARD14 function in keratinocytes.

Main Results:

  • CARD14 forms a signaling complex with BCL10 and MALT1.
  • Pathogenic CARD14 mutations enhance this complex formation.
  • This leads to MALT1 protease activation and psoriasis-related gene expression.

Conclusions:

  • CARD14/MALT1 signaling is crucial in keratinocytes for psoriasis pathogenesis.
  • Understanding these pathways offers therapeutic targets for psoriasis treatment.

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