File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Bimp1, a MAGUK Family Member Linking Protein Kinase C Activation to Bcl10-mediated NF-κB Induction

TitleBimp1, a MAGUK Family Member Linking Protein Kinase C Activation to Bcl10-mediated NF-κB Induction
Authors
Issue Date2001
Citation
Journal of Biological Chemistry, 2001, v. 276, n. 33, p. 30589-30597 How to Cite?
AbstractBcl10 and MALT1, products of distinct chromosomal translocations in mucosa-associated lymphoid tissue lymphoma, cooperate in activating NF-κB. Mice lacking Bcl10 demonstrate severe immunodeficiency associated with failure of lymphocytes to activate nuclear factor κB (NF-κB) in response to antigen receptor stimulation and protein kinase C activation. We characterize Bimp1, a new signaling protein that binds Bcl10 and activates NF-κB. Bimp1-mediated NF-κB activation requires Bcl10 and IκB kinases, indicating that Bimp1 acts upstream of these mediators. Bimp1, Bcl10, and MALT1 form a ternary complex, with Bcl10 bridging the Bimp1/MALT1 interaction. A dominant negative Bimp1 mutant inhibits NF-κB activation by anti-CD3 ligation, phorbol ester, and protein kinase C expression. These results suggest that Bimp1 links surface receptor stimulation and protein kinase C activation to Bcl10/MALT1, thus leading to NF-κB induction.
Persistent Identifierhttp://hdl.handle.net/10722/291588
ISSN
2020 Impact Factor: 5.157
2023 SCImago Journal Rankings: 1.766
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMcAllister-Lucas, Linda M.-
dc.contributor.authorInohara, Naohiro-
dc.contributor.authorLucas, Peter C.-
dc.contributor.authorRuland, Jürgen-
dc.contributor.authorBenito, Adalberto-
dc.contributor.authorLi, Qiutang-
dc.contributor.authorChen, Shu-
dc.contributor.authorChen, Felicia F.-
dc.contributor.authorYamaoka, Shoji-
dc.contributor.authorVerma, Inder M.-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorNúñez, Gabriel-
dc.date.accessioned2020-11-17T14:54:41Z-
dc.date.available2020-11-17T14:54:41Z-
dc.date.issued2001-
dc.identifier.citationJournal of Biological Chemistry, 2001, v. 276, n. 33, p. 30589-30597-
dc.identifier.issn0021-9258-
dc.identifier.urihttp://hdl.handle.net/10722/291588-
dc.description.abstractBcl10 and MALT1, products of distinct chromosomal translocations in mucosa-associated lymphoid tissue lymphoma, cooperate in activating NF-κB. Mice lacking Bcl10 demonstrate severe immunodeficiency associated with failure of lymphocytes to activate nuclear factor κB (NF-κB) in response to antigen receptor stimulation and protein kinase C activation. We characterize Bimp1, a new signaling protein that binds Bcl10 and activates NF-κB. Bimp1-mediated NF-κB activation requires Bcl10 and IκB kinases, indicating that Bimp1 acts upstream of these mediators. Bimp1, Bcl10, and MALT1 form a ternary complex, with Bcl10 bridging the Bimp1/MALT1 interaction. A dominant negative Bimp1 mutant inhibits NF-κB activation by anti-CD3 ligation, phorbol ester, and protein kinase C expression. These results suggest that Bimp1 links surface receptor stimulation and protein kinase C activation to Bcl10/MALT1, thus leading to NF-κB induction.-
dc.languageeng-
dc.relation.ispartofJournal of Biological Chemistry-
dc.titleBimp1, a MAGUK Family Member Linking Protein Kinase C Activation to Bcl10-mediated NF-κB Induction-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1074/jbc.M103824200-
dc.identifier.pmid11387339-
dc.identifier.scopuseid_2-s2.0-0035903154-
dc.identifier.volume276-
dc.identifier.issue33-
dc.identifier.spage30589-
dc.identifier.epage30597-
dc.identifier.isiWOS:000170472900003-
dc.identifier.issnl0021-9258-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats