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anti-Mouse (Murine) BCL3 Antibodies:
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Human Polyclonal BCL3 Primary Antibody for EIA, FACS - ABIN950634
Kabuta, Hakuno, Cho, Yamanaka, Chida, Asano, Wada, Takahashi: Insulin receptor substrate-3, interacting with Bcl-3, enhances p50 NF-kappaB activity. in Biochemical and biophysical research communications 2010
Show all 3 references for ABIN950634
Human Monoclonal BCL3 Primary Antibody for EIA - ABIN950628
Mitchell, Hildeman, Kedl, Teague, Schaefer, White, Zhu, Kappler, Marrack: Immunological adjuvants promote activated T cell survival via induction of Bcl-3. in Nature immunology 2001
Show all 2 references for ABIN950628
Human Monoclonal BCL3 Primary Antibody for FACS - ABIN950630
Watanabe, Iwamura, Shinoda, Fujita: Regulation of NFKB1 proteins by the candidate oncoprotein BCL-3: generation of NF-kappaB homodimers from the cytoplasmic pool of p50-p105 and nuclear translocation. in The EMBO journal 1997
Show all 2 references for ABIN950630
Human Polyclonal BCL3 Primary Antibody for FACS, IF - ABIN653286
Folco, Rocha, López-Ilasaca, Libby: Adiponectin inhibits pro-inflammatory signaling in human macrophages independent of interleukin-10. in The Journal of biological chemistry 2009
Show all 2 references for ABIN653286
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 Antibodies)/STAT3 (show STAT3 Antibodies) 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 Antibodies) homodimers.
Low expression of IL-6 (show IL6 Antibodies) and TNF-alpha (show TNF Antibodies) correlates with the presence of the nuclear regulators of NF-kappaB (show NFKB1 Antibodies), IkappaBNS (show NFKBID Antibodies) 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 Antibodies) homodimers and in particular with ankyrin repeats (ANK) 1 (show ANK1 Antibodies), 6, and 7, and the N-terminal region of Bcl-3.
The presence of a p50 (show LSP1 Antibodies)/Bcl-3 complex in nuclear extracts from cells of metastatic lung tissues.
In SOD1 (show SOD1 Antibodies) and Neurotomized mice the results of this studysuggest LC3 (show MAP1LC3A Antibodies), Fn14 (show TNFRSF12A Antibodies), Bcl3 and Gadd45a (show GADD45A Antibodies) 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 Antibodies) cell plasticity and promoted pathogenicity by blocking conversion to Th17-like cells, revealing a unique type of regulation that shapes adaptive immunity.
miR (show MLXIP Antibodies)-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 Antibodies)-19b
Study confirmed that BCL-3 is overexpressed in hepatocellular carcinoma (HCC (show FAM126A Antibodies)) tissues and correlated with adverse clinicopathological features and poorer prognosis. BCL-3 can promote the growth of HCC (show FAM126A Antibodies) cells by promoting cell viability, proliferation and cell cycle progression through regulation of CCND1 (show CCND1 Antibodies) 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 Antibodies) 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 Antibodies) 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 Antibodies) directs adaptive T helper cell type-2immunity to fucose-expressing pathogens via an IKKepsilon (show IKBKE Antibodies)-CYLD (show CYLD Antibodies)-dependent signalling pathway leading to Bcl3 activation.
data show that BCL-3 makes extensive contacts with p50 (show CD40 Antibodies) homodimers and in particular with ankyrin repeats (ANK) 1 (show ANK1 Antibodies), 6, and 7, and the N-terminal region of Bcl-3.
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