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BCL10 forms CARMA1-BCL10-MALT1-TRAF6 signalosome and BCL10 polymerizes in a unidirectional manner.
The results suggest that the involvement of BCL10 in DNA damage-induced NF-kappaB (显示 NFKB1 蛋白) is through the recruitment of TRAF6 (显示 TRAF6 蛋白).
results define molecular determinants that control the production of Lin(Ub)n-Bcl10, an important signaling intermediate in TCR and oncogenic CARD11 (显示 CARD11 蛋白) signaling.
Psoriasis mutations disrupt CARD14 (显示 CARD14 蛋白) autoinhibition promoting BCL10-MALT1 (显示 MALT1 蛋白)-dependent NF-kappaB (显示 NFKB1 蛋白) activation
BCL10 promoted DNA double-strand breaks repair, enhancing cell survival after DNA damage.
Data show that caspase recruitment domain-containing protein 11 (显示 CARD11 蛋白)/B-cell CLL/lymphoma 10/mucosa-associated lymphoid tissue lymphoma translocation gene 1 (显示 MALT1 蛋白) signaling drives lymphoproliferation (显示 FAS 蛋白) through NF-kappa B (显示 NFKB1 蛋白) and c-Jun N-terminal kinase activation.
BCL10 is not essential for actin polymerization after fibroblast FcgammaR stimulation.
characterization of zebrafish (Danio rerio) Bcl10
we identified BCL10 as a bona fide target of BCR (显示 BCR 蛋白)-induced linear ubiquitylation and demonstrated an important role of the linear ubiquitin ligase HOIP (显示 RNF31 蛋白) in BCR (显示 BCR 蛋白)-induced phosphorylation
The results of this study indicate that inherited BCL10 deficiency should be considered in patients with combined immunodeficiency with B cell, T cell, and fibroblast defects.
Data show that BCL10 was located in cytoplasm in Pig Kidney Epithelial (PK15) cells.
Data found that, BCL10 expressed in high level in swine spleen, and with a modest level in thymus, brain and lymph node; low level mRNA was expressed in liver and not detectable level in kidney.
IKKbeta is involved in membrane fusion, and serves as a critical protein kinase required for initial formation and the regulation of the CARMA1/MALT1/Bcl10/CBM complex in platelets.
high fat diet (HFD) and zinc deficiency synergistically induce obesity-related cardiac hypertrophy (ORCH), by increasing oxidative stress-mediated activation of BCL10/CARD9 (显示 CARD9 蛋白)/p38 MAPK (显示 MAPK14 蛋白) signalling. Zinc supplement ameliorates ORCH through activation of metallothionein (显示 MT 蛋白) to repress oxidative stress-activated BCL10 expression and p38 MAPK (显示 MAPK14 蛋白) activation.
Inherited BCL10 deficiency impairs hematopoietic and nonhematopoietic immunity.
cell receptor-dependent activation of mTOR signaling in T cells is mediated by Carma1 and MALT1, but not Bcl10.
Trehalose 6,6'-dimycolate-induced Mincle (显示 CLEC4E 蛋白) expression is dependent on Dectin-3-mediated NF-kappaB (显示 NFKB1 蛋白) activation through the CARD9 (显示 CARD9 蛋白)-BCL10-MALT1 (显示 MALT1 蛋白) complex.
Bcl10 mediates angiotensin II-induced cardiac damage and electrical remodeling.
TCR-stimulated activation of NF-kappaB requires the assembly of cytosolic p62-Bcl10-Malt1-IKK signalosomes, which may ensure highly regulated activation of NF-kappaB in response to TCR engagement.
Bcl10 is an essential regulator for A20 (显示 TNFAIP3 蛋白) gene expression.
Data indicate that caspase recruitment domain-containing protein 11 (CARD11 (显示 CARD11 蛋白)) is involved in the pathogenesis of collagen-induced arthritis (CIA (显示 NCOA5 蛋白)) by formation of the CARD11 (显示 CARD11 蛋白)/Bcl10 complex and enhancement of the Th17 cell response.
Findings demonstrate a Bcl10 requirement for maximum development of carrageenan-induced inflammation and lack of complete suppression by IL-10 (显示 IL10 蛋白) of carrageenan-induced inflammation.
This gene was identified by its translocation in a case of mucosa-associated lymphoid tissue (MALT) lymphoma. The protein encoded by this gene contains a caspase recruitment domain (CARD), and has been shown to induce apoptosis and to activate NF-kappaB. This protein is reported to interact with other CARD domain containing proteins including CARD9, 10, 11 and 14, which are thought to function as upstream regulators in NF-kappaB signaling. This protein is found to form a complex with MALT1, a protein encoded by another gene known to be translocated in MALT lymphoma. MALT1 and this protein are thought to synergize in the activation of NF-kappaB, and the deregulation of either of them may contribute to the same pathogenetic process that leads to the malignancy.
B-cell lymphoma/leukemia 10
, CARD containing molecule enhancing NF-kB
, CARD-containing apoptotic signaling protein
, CARD-containing molecule enhancing NF-kappa-B
, CARD-containing proapoptotic protein
, CED-3/ICH-1 prodomain homologous E10-like regulator
, caspase-recruiting domain-containing protein
, cellular homolog of vCARMEN
, mammalian CARD-containing adapter molecule E10
, B-cell leukemia/lymphoma 10
, B-cell lymophoma 10 protein
, B-cell CLL/lymphoma 10
, B cell lymphoma/leukemia 10
, CARD-like apoptotic protein