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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 (Montrer CD4 Protéines)(+) 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 (Montrer PMP22 Protéines)-induced epithelial damage and developed more polyps after AOM (Montrer COL2A1 Protéines)/DSS (Montrer PMP22 Protéines) treatment, although polyp size was unaffected.
this study implicates the intracellular protein (Montrer CKAP2 Protéines), BCL3, as a key mediator of the IL-10 (Montrer IL10 Protéines)-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 (Montrer LIF Protéines)/STAT3 (Montrer STAT3 Protéines) 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 (Montrer NFKB1 Protéines) homodimers.
Low expression of IL-6 (Montrer IL6 Protéines) and TNF-alpha (Montrer TNF Protéines) correlates with the presence of the nuclear regulators of NF-kappaB (Montrer NFKB1 Protéines), IkappaBNS (Montrer NFKBID Protéines) 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 (Montrer LSP1 Protéines) 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 (Montrer LSP1 Protéines)/Bcl-3 complex in nuclear extracts from cells of metastatic lung tissues.
Bcl-3 participates in the IL-22 (Montrer IL22 Protéines)-induced expression of STAT3 (Montrer STAT3 Protéines)-dependent late-response genes, and the combination of IL-22 (Montrer IL22 Protéines) and IL-17 (Montrer IL17A Protéines)-induced psoriasis-related gene expression.
B-cell leukemia protein 3 (Montrer HSPB3 Protéines) (Bcl3) expressed in response to cytokine TWEAK (Montrer TNFSF12 Protéines) stimulation (experimental kidney injury) decreases TWEAK (Montrer TNFSF12 Protéines)-induced inflammatory and lethal responses.
Four gene signature (PTEN, PIK3C2A (Montrer PIK3C2A Protéines), ITPA (Montrer ITPA Protéines) and BCL3) is an independent prognostic factors of both overall survival and disease-free survival in clear-cell renal-cell carcinoma (Montrer MOK Protéines).
Akt2 (Montrer AKT2 Protéines), Erk2 (Montrer MAPK1 Protéines), and IKK1 (Montrer CHUK Protéines)/2 phosphorylate Bcl3, converting Bcl3 into a transcriptional coregulator by facilitating its recruitment to DNA.
Bcl-3 knockdown enhanced the degradation of Smad3 (Montrer SMAD3 Protéines) but not Smad2 (Montrer SMAD2 Protéines) following TGFbeta (Montrer TGFB1 Protéines) treatment.
We have shown for the first time that BCL-3 promotes the growth of colorectal cancer cells through activation of the AKT (Montrer AKT1 Protéines) pathway, increasing tumour cell yield both in vitro and in vivo.
BCL3 serves as an oncogene (Montrer RAB1A Protéines) in glioma by modulating proliferation, cell cycle progression and apoptosis, and its oncogenic effects are mediated by the STAT3 (Montrer STAT3 Protéines) signaling pathway.
miR (Montrer MLXIP Protéines)-19b silencing promoted cell proliferation and cell cycle progression in gastric cancer cells and BCL3 was identified as a direct target of miR (Montrer MLXIP Protéines)-19b
Study confirmed that BCL-3 is overexpressed in hepatocellular carcinoma (HCC (Montrer FAM126A Protéines)) tissues and correlated with adverse clinicopathological features and poorer prognosis. BCL-3 can promote the growth of HCC (Montrer FAM126A Protéines) cells by promoting cell viability, proliferation and cell cycle progression through regulation of CCND1 (Montrer CCND1 Protéines) 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