Linked Life Data

19341436

Source:http://linkedlifedata.com/resource/pubmed/id/19341436

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2009-6-11
pubmed:abstractText
In the present study, we show that lethal toxin from Clostridium sordellii (TcsL-82) activates the three MAP kinase pathways, but that only a permeable and specific c-Jun-NH2-terminal kinase (JNK) inhibitor, JNK inhibitor II, prevents toxin-dependent actin depolymerization and cell rounding. We show that JNK activation is dependent on entry of the toxin N-terminal domain into the cytosol as bafilomycin A1, which prevents acidification of endocytic vesicle and subsequent cytosolic translocation of the toxin N-terminal domain, prevents JNK activation. Inhibition of JNK activity delays small GTPase glucosylation generated by N-terminal domain catalytic activity. Using a cell line mutant deficient in UDP-glucose, we observed that activation of JNK occurs even in the absence of small GTPase glucosylation and, thus, is independent of the toxin intrinsic catalytic activity. Facilitation of target glucosylation by JNK activation appeared to be restricted to TcsL-82 and was not a general feature of large clostridial toxins. Indeed, it was not observed with Toxin B from Clostridium difficile although this toxin also activates JNK.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1462-5822
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1102-13
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Activation of a c-Jun-NH2-terminal kinase pathway by the lethal toxin from Clostridium sordellii, TcsL-82, occurs independently of the toxin intrinsic enzymatic activity and facilitates small GTPase glucosylation.
pubmed:affiliation
Institut Pasteur, Paris, France. blandine.geny@pasteur.fr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't