Matches in UGent Biblio for { <https://biblio.ugent.be/publication/1887628#aggregation> ?p ?o. }
Showing items 1 to 40 of
40
with 100 items per page.
- aggregation classification "A1".
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation date "2011".
- aggregation format "application/pdf".
- aggregation hasFormat 1887628.bibtex.
- aggregation hasFormat 1887628.csv.
- aggregation hasFormat 1887628.dc.
- aggregation hasFormat 1887628.didl.
- aggregation hasFormat 1887628.doc.
- aggregation hasFormat 1887628.json.
- aggregation hasFormat 1887628.mets.
- aggregation hasFormat 1887628.mods.
- aggregation hasFormat 1887628.rdf.
- aggregation hasFormat 1887628.ris.
- aggregation hasFormat 1887628.txt.
- aggregation hasFormat 1887628.xls.
- aggregation hasFormat 1887628.yaml.
- aggregation isPartOf urn:issn:0261-4189.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "T-cell receptor-induced JNK activation requires proteolytic inactivation of CYLD by MALT1".
- aggregation abstract "The paracaspase mucosa-associated lymphoid tissue 1 (MALT1) is central to lymphocyte activation and lymphomagenesis. MALT1 mediates antigen receptor signalling to NF-kappa B by acting as a scaffold protein. Furthermore, MALT1 has proteolytic activity that contributes to optimal NF-kappa B activation by cleaving the NF-kappa B inhibitor A20. Whether MALT1 protease activity is involved in other signalling pathways, and the identity of the relevant substrates, is unknown. Here, we show that T-cell receptors (TCR) activation, as well as overexpression of the oncogenic API2-MALT1 fusion protein, results in proteolytic inactivation of CYLD by MALT1, which is specifically required for c-jun N-terminal kinase (JNK) activation and the inducible expression of a subset of genes. These results indicate a novel role for MALT1 proteolytic activity in TCR-induced JNK activation and reveal CYLD cleavage as the underlying mechanism.".
- aggregation authorList BK480112.
- aggregation endPage "1752".
- aggregation issue "9".
- aggregation startPage "1742".
- aggregation volume "30".
- aggregation aggregates 3146868.
- aggregation aggregates 3146869.
- aggregation isDescribedBy 1887628.
- aggregation similarTo emboj.2011.85.
- aggregation similarTo LU-1887628.