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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 ELISA Kits)/STAT3 (show STAT3 ELISA Kits) 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 ELISA Kits) homodimers.
Low expression of IL-6 (show IL6 ELISA Kits) and TNF-alpha (show TNF ELISA Kits) correlates with the presence of the nuclear regulators of NF-kappaB (show NFKB1 ELISA Kits), IkappaBNS 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 ELISA Kits) homodimers and in particular with ankyrin repeats (ANK) 1 (show ANK1 ELISA Kits), 6, and 7, and the N-terminal region of Bcl-3.
The presence of a p50 (show LSP1 ELISA Kits)/Bcl-3 complex in nuclear extracts from cells of metastatic lung tissues.
In SOD1 (show SOD1 ELISA Kits) and Neurotomized mice the results of this studysuggest LC3 (show MAP1LC3A ELISA Kits), Fn14 (show TNFRSF12A ELISA Kits), Bcl3 and Gadd45a (show GADD45A ELISA Kits) as candidate genes involved in the maintenance of the severe atrophic state.
These findings identify Bcl-3 as a critical player during the later stage of the contact hypersensitivity reaction to limit inflammation via actions in radioresistant cells, including keratinocytes.
The results expose a previously unidentified function for Bcl-3 in dendritic cell survival and the generation of adaptive immunity.
Bcl-3 constrained Th1 (show HAND1 ELISA Kits) cell plasticity and promoted pathogenicity by blocking conversion to Th17-like cells, revealing a unique type of regulation that shapes adaptive immunity.
Study confirmed that BCL-3 is overexpressed in hepatocellular carcinoma (HCC (show FAM126A ELISA Kits)) tissues and correlated with adverse clinicopathological features and poorer prognosis. BCL-3 can promote the growth of HCC (show FAM126A ELISA Kits) cells by promoting cell viability, proliferation and cell cycle progression through regulation of CCND1 (show CCND1 ELISA Kits) 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 ELISA Kits) production.
Suggest the involvement of BCL3 in cardiovascular disease, which could be partly mediated through the influence on metabolic phenotypes.
These findings suggest that the two LMP1 (show PDLIM7 ELISA Kits) signaling domains modulate their combined activity and that the bcl3 transcription factor is likely responsible for some of the unique effects of CTAR1 domain on cellular expression.
DC-SIGN (show CD209 ELISA Kits) directs adaptive T helper cell type-2immunity to fucose-expressing pathogens via an IKKepsilon (show IKBKE ELISA Kits)-CYLD (show CYLD ELISA Kits)-dependent signalling pathway leading to Bcl3 activation.
data show that BCL-3 makes extensive contacts with p50 (show CD40 ELISA Kits) homodimers and in particular with ankyrin repeats (ANK) 1 (show ANK1 ELISA Kits), 6, and 7, and the N-terminal region of Bcl-3.
a delayed (incoherent) feed-forward loop together with differential rates of TNFA (show TNF ELISA Kits) (fast) and BCL3 (slow) mRNA turnover provide robust, pulsatile expression of TNFalpha (show TNF ELISA Kits)
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