TNF-α mediated NF-kappaB activation is constantly extended by transglutaminase 2

Kang Seo Park, Dae Seok Kim, Chunkyu Ko, Sang Jin Lee, Seung Hyun Oh, Soo Youl Kim

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


Increased levels of transglutaminase 2 (TGase 2) expression have been reported in many inflammatory diseases, as well as in drug resistant cancer cells. Previous reports have shown that TGase 2 is capable of inducing nuclear factor-kappaB (NF-kappaB) activation via depletion of inhibitor of kappaB (I-kappaB)α through polymerization in the absence of I-kappaBalpha kinase activation. This raises the question of whether increased expression of TGase 2 can extend NF-kappaB activation mediated by a canonical activation pathway. In the TGase 2-inducible EcR23/TG cell line, TGase 2 over-expression resulted in sustained activation of NF-κB in the presence of TNF-alpha, for up to 24 hrs, while in the absence of TGase 2 induction, NF-kappaB activity was restored to basal levels within 6 hrs of TNF-alpha treatment. In mice injected with an adenovirus vector expressing TGase 2, NF-kappaB was constitutively activated for up to 5 days, whereas Adeno/GFP-injected mice exhibited attenuated activation of NF-kappaB in response to TNF-α stress. Thus, the presence of increased levels of TGase 2 may exacerbate NF-κB activation in inflammatory states.

Original languageEnglish (US)
Pages (from-to)341-354
Number of pages14
JournalFrontiers in Bioscience - Elite
Volume3 E
Issue number1
StatePublished - Jan 1 2011
Externally publishedYes


  • I-κBα
  • Inflammation
  • NF-κB
  • Review
  • TNF-α
  • Transglutaminase 2

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)


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