Metalloprotease type III effectors that specifically cleave JNK and NF-κB.
EMBO J
; 30(1): 221-31, 2011 Jan 05.
Article
em En
| MEDLINE
| ID: mdl-21113130
ABSTRACT
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.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
NF-kappa B
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Proteínas de Escherichia coli
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Proteínas Quinases JNK Ativadas por Mitógeno
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Infecções por Escherichia coli
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Escherichia coli Enteropatogênica
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Interações Hospedeiro-Patógeno
Limite:
Humans
Idioma:
En
Ano de publicação:
2011
Tipo de documento:
Article