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2018 ; 9
(ä): 1539
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BCL10 - Bridging CARDs to Immune Activation
#MMPMID30022982
Gehring T
; Seeholzer T
; Krappmann D
Front Immunol
2018[]; 9
(ä): 1539
PMID30022982
show ga
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-?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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