| This study demonstrates that interaction with p50 is necessary and sufficient for the anti-inflammatory properties of Bcl-3 and further highlights the importance of p50 homodimer stability in the control of NF-kappaB target gene expression. | Inhibition of transcription by B cell Leukemia 3 (Bcl-3) protein requires interaction with nuclear factor κB (NF-κB) p50.
Collins PE, Kiely PA, Carmody RJ., Free PMC Article | 06/28/2014 |
| The overexpression of the transcription factor Bcl-3 inhibits germinal center formation. | Overexpression of Bcl-3 inhibits the development of marginal zone B cells.
Hövelmeyer N, Wörns MA, Reissig S, Adams-Quack P, Leclaire J, Hahn M, Wörtge S, Nikolaev A, Galle PR, Waisman A. | 04/26/2014 |
| Bcl-3 is a regulator of B cell fate determination, restricting the marginal zone path and favoring the follicular pathway, at least in part, via increased signal-specific survival of the latter. | The tumor promoter and NF-κB modulator Bcl-3 regulates splenic B cell development.
Zhang X, Paun A, Claudio E, Wang H, Siebenlist U., Free PMC Article | 02/22/2014 |
| Bcl3 knockout mice are resistant to disuse muscle atrophy. | The ChIP-seq-defined networks of Bcl-3 gene binding support its required role in skeletal muscle atrophy.
Jackman RW, Wu CL, Kandarian SC., Free PMC Article | 06/8/2013 |
| acute alcohol treatment induces molecular signatures of TLR4/LPS tolerance through the induction of Bcl-3 | Induction of Bcl-3 by acute binge alcohol results in toll-like receptor 4/LPS tolerance.
Bala S, Tang A, Catalano D, Petrasek J, Taha O, Kodys K, Szabo G., Free PMC Article | 11/3/2012 |
| showed increased Bcl-3 binding to kappaB sites in unloaded muscle and thus were direct targets of Bcl-3 | Identification of genes that elicit disuse muscle atrophy via the transcription factors p50 and Bcl-3.
Wu CL, Kandarian SC, Jackman RW., Free PMC Article | 08/6/2011 |
| Bcl-3 is critically involved in lung defense against Klebsiella pneumoniae, modulating functions of several cells to facilitate efficient clearance of bacteria. | The IκB family member Bcl-3 coordinates the pulmonary defense against Klebsiella pneumoniae infection.
Pène F, Paun A, Sønder SU, Rikhi N, Wang H, Claudio E, Siebenlist U., Free PMC Article | 04/30/2011 |
| In a model of transplant-mediated lung ischemia reperfusion injury, expression of Bcl3 in recipients inhibited emergency granulopoiesis and limited acute graft damage. | Bcl3 prevents acute inflammatory lung injury in mice by restraining emergency granulopoiesis.
Kreisel D, Sugimoto S, Tietjens J, Zhu J, Yamamoto S, Krupnick AS, Carmody RJ, Gelman AE., Free PMC Article | 02/5/2011 |
| Bcl-3 prevents autoimmune diabetes by inhibiting inflammatory chemokine and cytokine gene transcription. | Roles of Bcl-3 in the pathogenesis of murine type 1 diabetes.
Ruan Q, Zheng SJ, Palmer S, Carmody RJ, Chen YH., Free PMC Article | 10/30/2010 |
| Biochemical purification of interacting partners of BCL-3 led to the identification of CtBP as a molecule required for the ability of BCL-3 to repress gene transcription. | The repressing function of the oncoprotein BCL-3 requires CtBP, while its polyubiquitination and degradation involve the E3 ligase TBLR1.
Keutgens A, Shostak K, Close P, Zhang X, Hennuy B, Aussems M, Chapelle JP, Viatour P, Gothot A, Fillet M, Chariot A., Free PMC Article | 08/23/2010 |
| over-expression of Bcl-3 slows T cell activation very early in T cell responses to antigen, both in vitro and in vivo. | Transgenic Bcl-3 slows T cell proliferation.
Bassetti MF, White J, Kappler JW, Marrack P., Free PMC Article | 01/21/2010 |
| enhanced lipopolysaccharide-induced IL-23p19 gene expression in IL-10(-/-) mice is due to impaired Bcl3 expression leading to diminished p50 and enhanced RelA recruitment to the IL-23p19 promoter | Impaired Bcl3 up-regulation leads to enhanced lipopolysaccharide-induced interleukin (IL)-23P19 gene expression in IL-10(-/-) mice.
Mühlbauer M, Chilton PM, Mitchell TC, Jobin C., Free PMC Article | 01/21/2010 |
| we identified Bcl-3 as a regulator of immunologic tolerance to self | A role for the IkappaB family member Bcl-3 in the control of central immunologic tolerance.
Zhang X, Wang H, Claudio E, Brown K, Siebenlist U., Free PMC Article | 01/21/2010 |
| NF-kappaB p50 ubiquitination blockade by Bcl-3 limits the strength of toll-like receptor responses and maintains innate immune homeostasis | Negative regulation of toll-like receptor signaling by NF-kappaB p50 ubiquitination blockade.
Carmody RJ, Ruan Q, Palmer S, Hilliard B, Chen YH. | 01/21/2010 |
| an essential function of Bcl-3 during an innate immune response against bacteria is to inhibit transcription of the IL-10 gene in macrophages. | The IkappaB protein Bcl-3 negatively regulates transcription of the IL-10 gene in macrophages.
Riemann M, Endres R, Liptay S, Pfeffer K, Schmid RM. | 01/21/2010 |
| Bim-independent pathway to activated T cell death | The NF-kappaB regulator Bcl-3 and the BH3-only proteins Bim and Puma control the death of activated T cells.
Bauer A, Villunger A, Labi V, Fischer SF, Strasser A, Wagner H, Schmid RM, Häcker G., Free PMC Article | 01/21/2010 |
| These data indicate that, depending on the external signals, Cyld can negatively regulate different NF-kappaB pathways; inactivation of TRAF2 controls survival and inflammation, while inhibition of Bcl-3 controls proliferation and tumor growth. | Cyld inhibits tumor cell proliferation by blocking Bcl-3-dependent NF-kappaB signaling.
Massoumi R, Chmielarska K, Hennecke K, Pfeifer A, Fässler R. | 01/21/2010 |
| Bcl-3 acts as a member of a critical survival signaling pathway in activated T-cells. | CD8 T cells require Bcl-3 for maximal gamma interferon production upon secondary exposure to antigen.
Chilton PM, Mitchell TC., Free PMC Article | 01/21/2010 |
| Bcl-3 is required for condensation of fibrin by activated platelets, demonstrating functional significance for mTOR-regulated synthesis of the protein | mTOR-dependent synthesis of Bcl-3 controls the retraction of fibrin clots by activated human platelets.
Weyrich AS, Denis MM, Schwertz H, Tolley ND, Foulks J, Spencer E, Kraiss LW, Albertine KH, McIntyre TM, Zimmerman GA., Free PMC Article | 01/21/2010 |
| Physiologically mediated shifts in the balance between Bcl-3 and RelB in the nuclei of activated CD4+ T cells might regulate the balance between Th1 and Th2 cell responses. | Opposing roles for RelB and Bcl-3 in regulation of T-box expressed in T cells, GATA-3, and Th effector differentiation.
Corn RA, Hunter C, Liou HC, Siebenlist U, Boothby MR. | 01/21/2010 |
| Experiments presented here indicate that Bcl-3 is inducible by DNA damage and is required for the induction of Hdm2 gene expression and the suppression of persistent p53 activity | Expression of the Bcl-3 proto-oncogene suppresses p53 activation.
Kashatus D, Cogswell P, Baldwin AS., Free PMC Article | 01/21/2010 |
| IL-10-induced Bcl-3 inhibited LPS-induced production of TNF-alpha, but not IL-6, in macrophages; nuclear translocation of NF-kappaB p65 was not impaired; DNA binding by NF-kappaB p50/p65 was profoundly inhibited. | IL-10-inducible Bcl-3 negatively regulates LPS-induced TNF-alpha production in macrophages.
Kuwata H, Watanabe Y, Miyoshi H, Yamamoto M, Kaisho T, Takeda K, Akira S. | 01/21/2010 |