Metalloprotease type III effectors that specifically cleave JNK and NF-κB

Kobi Baruch, Lihi Gur-Arie, Chen Nadler, Simi Koby, Gal Yerushalmi, Yinon Ben-Neriah, Orli Yogev, Eitan Shaulian, Chen Guttman, Raz Zarivach, Ilan Rosenshine*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

164 Scopus citations


Two major arms of the inflammatory response are the NF-κB and c-Jun N-terminal kinase (JNK) pathways. Here, we show that enteropathogenic Escherichia coli (EPEC) employs the type III secretion system to target these two signalling arms by injecting host cells with two effector proteins, NleC and NleD. We provide evidence that NleC and NleD are Zn-dependent endopeptidases that specifically clip and inactivate RelA (p65) and JNK, respectively, thus blocking NF-κB and AP-1 activation. We show that NleC and NleD co-operate and complement other EPEC effectors in accomplishing maximal inhibition of IL-8 secretion. This is a remarkable example of a pathogen using multiple effectors to manipulate systematically the host inflammatory response signalling network.

Original languageAmerican English
Pages (from-to)221-231
Number of pages11
JournalEMBO Journal
Issue number1
StatePublished - 5 Jan 2011


  • JNK
  • NF-κB
  • NleC
  • NleD
  • enteropathogenic E. coli


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