BCL10-Bridging CARDs to immune activation.
Front. Immunol. 9, 1539 (2018)
Since the B-cell lymphoma/leukemia 10 (BCL10) protein was first described in 1999, numerous studies have elucidated its key functions in channeling adaptive and innate immune signaling downstream of CARMA/caspase-recruitment domain (CARD) scaffold proteins. While T and B cell antigen receptor (TCR/BCR) signaling induces the recruitment of BCL10 bound to mucosa-associated lymphoid tissue (MALT) 1 to the lymphocyte-specific CARMA1/CARD11-BCL10-MALT1 (CBM-1) signalosome, alternative CBM complexes utilize different CARMA/CARD scaffolds in distinct innate or inflammatory pathways. BCL10 constitutes the smallest subunit in all CBM signalosomes, containing a 233 amino acid coding for N-terminal CARD as well as a C-terminal Ser/Thr-rich region. BCL10 forms filaments, thereby aggregating into higher-order clusters that mediate and amplify stimulation-induced signals, ultimately leading to MALT1 protease activation and canonical NF-kappa B and JNK signaling. BCL10 additionally undergoes extensive post-translational regulation involving phosphorylation, ubiquitination, MALT1-catalyzed cleavage, and degradation. Through these feedback and feed-forward events, BCL10 integrates positive and negative regulatory processes that govern the function as well as the dynamic assembly, disassembly, and destruction of CBM complexes. Thus, BCL10 is a critical regulator for activation as well as termination of immune cell signaling, revealing that its role extends far beyond that of a mere linking factor in CBM complexes.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Review
Typ der Hochschulschrift
Herausgeber
Schlagwörter
Adaptive Immunity ; T Cell Signaling ; Innate Immunity ; Nf-kappa B ; B-cell Lymphoma/leukemia 10 ; Cbm Complex; Nf-kappa-b; Caspase Recruitment Domain; T-cell-receptor; Lymphoid-tissue Lymphomas; Containing Protein; Signaling Pathway; Paracaspase Malt1; Carma1-bcl10-malt1 Complex; Cytokine Production; Negative Regulator
Keywords plus
Sprache
englisch
Veröffentlichungsjahr
2018
Prepublished im Jahr
HGF-Berichtsjahr
2018
ISSN (print) / ISBN
1664-3224
e-ISSN
1664-3224
ISBN
Bandtitel
Konferenztitel
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Konferenzort
Konferenzband
Quellenangaben
Band: 9,
Heft: JUL,
Seiten: 1539
Artikelnummer: ,
Supplement: ,
Reihe
Verlag
Frontiers
Verlagsort
Avenue Du Tribunal Federal 34, Lausanne, Ch-1015, Switzerland
Tag d. mündl. Prüfung
0000-00-00
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Gutachter
Prüfer
Topic
Hochschule
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Veröffentlichungsdatum
0000-00-00
Anmeldedatum
0000-00-00
Anmelder/Inhaber
weitere Inhaber
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Priorität
Begutachtungsstatus
Peer reviewed
Institut(e)
Research Unit Signaling and Translation (SAT)
POF Topic(s)
30203 - Molecular Targets and Therapies
Forschungsfeld(er)
Enabling and Novel Technologies
PSP-Element(e)
G-509800-002
Förderungen
Copyright
Erfassungsdatum
2018-06-27