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Thus, we concluded that fine-tuning expression of Bcl-3 is needed for proper CD4 (show CD4 Proteins)(+) T-cell development and is required to sustain Th17-cell mediated pathology.
Bcl-3 suppressed colorectal tumor formation: Bcl-3-deficient mice were relatively protected from DSS (show PMP22 Proteins)-induced epithelial damage and developed more polyps after AOM (show COL2A1 Proteins)/DSS (show PMP22 Proteins) treatment, although polyp size was unaffected.
this study implicates the intracellular protein (show CKAP2 Proteins), BCL3, as a key mediator of the IL-10 (show IL10 Proteins)-induced immunosuppressive macrophage phenotype
These results establish that Bcl3 positively regulates pluripotency genes and thus shed light on the mechanism of Bcl3 as a downstream molecule of LIF (show LIF Proteins)/STAT3 (show STAT3 Proteins) signaling in pluripotency maintenance.
Bcl3 reduces the inflammatory response in pancreas/biliary tissue by blocking ubiquitination and proteasome-mediated degradation of nuclear factor-kappaB p50 (show NFKB1 Proteins) homodimers.
Low expression of IL-6 (show IL6 Proteins) and TNF-alpha (show TNF Proteins) correlates with the presence of the nuclear regulators of NF-kappaB (show NFKB1 Proteins), IkappaBNS (show NFKBID Proteins) and BCL-3, in the uterus of mice.
These findings demonstrate that Bcl-3 is required in dendritic cells to prime protective T-cell-mediated immunity to T. gondii
data show that BCL-3 makes extensive contacts with p50 (show LSP1 Proteins) homodimers and in particular with ankyrin repeats (ANK) 1, 6, and 7, and the N-terminal region of Bcl-3.
The presence of a p50 (show LSP1 Proteins)/Bcl-3 complex in nuclear extracts from cells of metastatic lung tissues.
In SOD1 (show SOD1 Proteins) and Neurotomized mice the results of this studysuggest LC3 (show MAP1LC3A Proteins), Fn14 (show TNFRSF12A Proteins), Bcl3 and Gadd45a (show GADD45A Proteins) as candidate genes involved in the maintenance of the severe atrophic state.
Akt2 (show AKT2 Proteins), Erk2 (show MAPK1 Proteins), and IKK1 (show CHUK Proteins)/2 phosphorylate Bcl3, converting Bcl3 into a transcriptional coregulator by facilitating its recruitment to DNA.
Bcl-3 knockdown enhanced the degradation of Smad3 (show SMAD3 Proteins) but not Smad2 (show SMAD2 Proteins) following TGFbeta (show TGFB1 Proteins) treatment.
We have shown for the first time that BCL-3 promotes the growth of colorectal cancer cells through activation of the AKT (show AKT1 Proteins) pathway, increasing tumour cell yield both in vitro and in vivo.
BCL3 serves as an oncogene (show RAB1A Proteins) in glioma by modulating proliferation, cell cycle progression and apoptosis, and its oncogenic effects are mediated by the STAT3 (show STAT3 Proteins) signaling pathway.
miR (show MLXIP Proteins)-19b silencing promoted cell proliferation and cell cycle progression in gastric cancer cells and BCL3 was identified as a direct target of miR (show MLXIP Proteins)-19b
Study confirmed that BCL-3 is overexpressed in hepatocellular carcinoma (HCC (show FAM126A Proteins)) tissues and correlated with adverse clinicopathological features and poorer prognosis. BCL-3 can promote the growth of HCC (show FAM126A Proteins) cells by promoting cell viability, proliferation and cell cycle progression through regulation of CCND1 (show CCND1 Proteins) expression.
Variant of BCL3 gene is strongly associated with five-year survival of non-small-cell lung cancer patients
Subcellular localization of Bcl-3 could be a potential-early diagnostic marker in colon cancer.
Bcl-3 is involved in the development of Tfh cells and the pathogenesis of RA, presumably by inducing IL-21 (show IL17C Proteins) production.
This gene is a proto-oncogene candidate. It is identified by its translocation into the immunoglobulin alpha-locus in some cases of B-cell leukemia. The protein encoded by this gene contains seven ankyrin repeats, which are most closely related to those found in I kappa B proteins. This protein functions as a transcriptional co-activator that activates through its association with NF-kappa B homodimers. The expression of this gene can be induced by NF-kappa B, which forms a part of the autoregulatory loop that controls the nuclear residence of p50 NF-kappa B.
B-cell CLL/lymphoma 3
, B-cell leukemia/lymphoma 3
, B-cell lymphoma 3 protein homolog
, B-cell lymphoma 3 protein
, B-cell lymphoma 3-encoded protein
, chronic lymphatic leukemia protein
, proto-oncogene BCL3