Matches in UGent Biblio for { <https://biblio.ugent.be/publication/2999688#aggregation> ?p ?o. }
Showing items 1 to 38 of
38
with 100 items per page.
- aggregation classification "A1".
- aggregation creator B372141.
- aggregation creator B372142.
- aggregation creator B372143.
- aggregation creator B372144.
- aggregation creator B372145.
- aggregation creator B372146.
- aggregation creator person.
- aggregation date "2012".
- aggregation format "application/pdf".
- aggregation hasFormat 2999688.bibtex.
- aggregation hasFormat 2999688.csv.
- aggregation hasFormat 2999688.dc.
- aggregation hasFormat 2999688.didl.
- aggregation hasFormat 2999688.doc.
- aggregation hasFormat 2999688.json.
- aggregation hasFormat 2999688.mets.
- aggregation hasFormat 2999688.mods.
- aggregation hasFormat 2999688.rdf.
- aggregation hasFormat 2999688.ris.
- aggregation hasFormat 2999688.txt.
- aggregation hasFormat 2999688.xls.
- aggregation hasFormat 2999688.yaml.
- aggregation isPartOf urn:issn:0028-0836.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "NLRP6 negatively regulates innate immunity and host defence against bacterial pathogens".
- aggregation abstract "Members of the intracellular nucleotide-binding and oligomerization domain (NOD)-like receptor (NLR) family contribute to immune responses through activation of nuclear factor-kappa B (NF-kappa B), type I interferon and inflammasome signalling(1). Mice lacking the NLR family member NLRP6 were recently shown to be susceptible to colitis and colorectal tumorigenesis(2-4), but the role of NLRP6 in microbial infections and the nature of the inflammatory signalling pathways regulated by NLRP6 remain unclear. Here we show that Nlrp6-deficient mice are highly resistant to infection with the bacterial pathogens Listeria monocytogenes, Salmonella typhimurium and Escherichia coli. Infected Nlrp6-deficient mice had increased numbers of monocytes and neutrophils in circulation, and NLRP6 signalling in both haematopoietic and radioresistant cells contributed to increased susceptibility. Nlrp6 deficiency enhanced activation of mitogen-activated protein kinase (MAPK) and the canonical NF-kappa B pathway after Toll-like receptor ligation, but not cytosolic NOD1/2 ligation, in vitro. Consequently, infected Nlrp6-deficient cells produced increased levels of NF-kappa B-and MAPK-dependent cytokines and chemokines. Thus, our results reveal NLRP6 as a negative regulator of inflammatory signalling, and demonstrate a role for this NLR in impeding clearance of both Gram-positive and -negative bacterial pathogens.".
- aggregation authorList BK673092.
- aggregation endPage "393".
- aggregation issue "7411".
- aggregation startPage "389".
- aggregation volume "488".
- aggregation aggregates 2999708.
- aggregation isDescribedBy 2999688.
- aggregation similarTo nature11250.
- aggregation similarTo LU-2999688.