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Malt1-dependent RelB cleavage promotes canonical NF-kappaB activation in lymphocytes and lymphoma cell lines.

The protease activity of the paracaspase Malt1 contributes to antigen receptor-mediated lymphocyte activation and lymphomagenesis. Malt1 activity is required for optimal NF-κB activation, but little is known about the responsible substrate(s). Here we report that Malt1 cleaved the NF-κB family member RelB after Arg-85. RelB cleavage induced its proteasomal degradation and specifically controlled DNA binding of RelA- or c-Rel-containing NF-κB complexes. Overexpression of RelB inhibited expression of canonical NF-κB target genes and led to impaired survival of diffuse large B-cell lymphoma cell lines characterized by constitutive Malt1 activity. These findings identify a central role for Malt1-dependent RelB cleavage in canonical NF-κB activation and thereby provide a rationale for the targeting of Malt1 in immunomodulation and cancer treatment.

Pubmed ID: 21873235


  • Hailfinger S
  • Nogai H
  • Pelzer C
  • Jaworski M
  • Cabalzar K
  • Charton JE
  • Guzzardi M
  • Décaillet C
  • Grau M
  • Dörken B
  • Lenz P
  • Lenz G
  • Thome M


Proceedings of the National Academy of Sciences of the United States of America

Publication Data

August 30, 2011

Associated Grants


Mesh Terms

  • Caspases
  • Cell Line, Tumor
  • Humans
  • Lymphocyte Activation
  • Lymphocytes
  • Lymphoma, Large B-Cell, Diffuse
  • NF-kappa B
  • Neoplasm Proteins
  • Transcription Factor RelA
  • Transcription Factor RelB