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Monoclonal BCL3 Primary Antibody for ELISA, WB - ABIN533917
Nolan, Fujita, Bhatia, Huppi, Liou, Scott, Baltimore: The bcl-3 proto-oncogene encodes a nuclear I kappa B-like molecule that preferentially interacts with NF-kappa B p50 and p52 in a phosphorylation-dependent manner. in Molecular and cellular biology 1993
Show all 3 Pubmed References
KLF9 and BCL3 as transcription factors that enhance reprogramming of primordial germ cells
a sufficient concentration of Bcl3 in mouse embryonic stem cells plays a critical role in the maintenance of pluripotency and the self-renewal.
Thus, we concluded that fine-tuning expression of Bcl-3 is needed for proper CD4(+) 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-induced epithelial damage and developed more polyps after AOM/DSS treatment, although polyp size was unaffected.
this study implicates the intracellular protein, BCL3, as a key mediator of the IL-10-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/STAT3 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 homodimers.
Low expression of IL-6 and TNF-alpha correlates with the presence of the nuclear regulators of NF-kappaB, 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 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/Bcl-3 complex in nuclear extracts from cells of metastatic lung tissues.
In SOD1 and Neurotomized mice the results of this studysuggest LC3, Fn14, Bcl3 and Gadd45a 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 cell plasticity and promoted pathogenicity by blocking conversion to Th17-like cells, revealing a unique type of regulation that shapes adaptive immunity.
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.
The overexpression of the transcription factor Bcl-3 inhibits germinal center formation.
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.
Bcl3 knockout mice are resistant to disuse muscle atrophy.
acute alcohol treatment induces molecular signatures of TLR4/LPS tolerance through the induction of Bcl-3
Data suggest that B cell lymphoma 3 (Bcl-3) may be a potential clinical biomarker for diagnosis, treatment, and prognosis of patients with BL1-subtype triple-negative breast cancer (TNBC).
This work identifies PD-L1 as a novel target of Bcl3, and links Bcl3 to IFN-gamma signaling and PD-L1-mediated immune escape.
BCL-3 transcription is regulated directly by NF-KB signaling in colorectal cancer
Bcl3 overexpression could be a surrogate biomarker for NF-kappaB activation in Barrett's epithelial cells leading to deregulation of NF-kappaB-inducible gene expression, inferring resistance to apoptosis through the activation of anti-apoptotic genes such as Survivin.
Data show that B-cell CLL-lymphoma 3 (Bcl-3) expression levels in colonic T cells correlate with disease manifestation in patients with inflammatory bowel disease.
Bcl-3 participates in the IL-22-induced expression of STAT3-dependent late-response genes, and the combination of IL-22 and IL-17-induced psoriasis-related gene expression.
B-cell leukemia protein 3 (Bcl3) expressed in response to cytokine TWEAK stimulation (experimental kidney injury) decreases TWEAK-induced inflammatory and lethal responses.
Four gene signature (PTEN, PIK3C2A, ITPA and BCL3) is an independent prognostic factors of both overall survival and disease-free survival in clear-cell renal-cell carcinoma.
Akt2, Erk2, and IKK1/2 phosphorylate Bcl3, converting Bcl3 into a transcriptional coregulator by facilitating its recruitment to DNA.
Bcl-3 knockdown enhanced the degradation of Smad3 but not Smad2 following TGFbeta treatment.
We have shown for the first time that BCL-3 promotes the growth of colorectal cancer cells through activation of the AKT pathway, increasing tumour cell yield both in vitro and in vivo.
BCL3 serves as an oncogene in glioma by modulating proliferation, cell cycle progression and apoptosis, and its oncogenic effects are mediated by the STAT3 signaling pathway.
miR-19b silencing promoted cell proliferation and cell cycle progression in gastric cancer cells and BCL3 was identified as a direct target of miR-19b
Study confirmed that BCL-3 is overexpressed in hepatocellular carcinoma (HCC) tissues and correlated with adverse clinicopathological features and poorer prognosis. BCL-3 can promote the growth of HCC cells by promoting cell viability, proliferation and cell cycle progression through regulation of CCND1 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 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 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.
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