
Negative Regulation of Toll-Like Receptor Signaling by NF-κB p50 ...
2007年8月3日 · We report the identification of B cell leukemia (Bcl)–3 as an essential negative regulator of TLR signaling. By blocking ubiquitination of p50, a member of the nuclear factor (NF)-κB family, Bcl-3 stabilizes a p50 complex that inhibits gene transcription.
Bcl-3 and NFκB p50-p50 Homodimers Act as ... - ScienceDirect
2004年2月27日 · We demonstrate that a predominance of p50-p50 homodimers binding to the IL-2 promoter κB site in tolerant T cells correlated with repression of NFκB-driven transcription. Impaired translocation of the p65 subunit in tolerant T cells was a result from reduced activation of IκB kinase and poor phosphorylation and degradation of cytosolic IκBs.
BCL3 Gene - GeneCards | BCL3 Protein | BCL3 Antibody
2025年3月30日 · In the cytoplasm, inhibits the nuclear translocation of the NF-kappa-B p50 subunit. In the nucleus, acts as transcriptional activator that promotes transcription of NF-kappa-B target genes. Contributes to the regulation of cell proliferation (By similarity).
Bcl3 Phosphorylation by Akt, Erk2, and IKK Is Required for Its ...
2017年8月3日 · These two phosphorylation events are critical for the transcriptional activity of Bcl3 through stabilizion of the Bcl3:p52:DNA (or Bcl3:p50:DNA) ternary complexes. In the absence of these phosphorylation modifications, Bcl3 functions as prototypical IκB protein dissociating p52 and p50 from the p52:DNA (or p50:DNA) complex.
Activation of nuclear factor-kappaB p50 homodimer/Bcl-3
2003年12月1日 · The discrete yet striking NF-kappaB p50 activation in NPC suggests that p50/p50 homodimers may be important factors in the development of NPC and may contribute to oncogenesis through transcriptional up-regulation of target …
Inhibition of Transcription by B Cell Leukemia 3 (Bcl-3) Protein ...
2014年3月7日 · We employed immobilized peptide array technology to define a region of p50 required for the formation of a Bcl-3·p50 homodimer immunosuppressor complex. Our data demonstrate that amino acids 359–361 and 363 of p50 are critical for interaction with Bcl-3 and essential for Bcl-3-mediated inhibition of inflammatory gene expression.
癌蛋白 Bcl-3 可以通过从选定的 kappa B 位点去除抑制性 p50 同源 …
癌蛋白 Bcl-3 可以通过从选定的 kappa B 位点去除抑制性 p50 同源二聚体来促进 NF-kappa B 介导的反式激活。 Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. 以前,我们提出了 Bcl-3 在通过 kappa B 位点通过抵消结合的抑制作用来促进反式激活的作用,NF-kappa B 的 p50 亚基的非反式激活同源二聚体。 这种同源二聚体在例如未受刺激的初级细胞核中很丰富T细胞。 在这里,我 …
BCL-3 and NF-kappaB p50 attenuate lipopolysaccharide-induced …
2004年11月26日 · Following its induction, TNFalpha gene transcription is rapidly attenuated, in part due to the accumulation of NF-kappaB p50 homodimers that bind to three kappaB sites in the TNFalpha promoter. Here we have investigated the inhibitory role of BCL-3, an IkappaB-like protein that interacts exclusively with p50 and p52 homodimers.
Bcl-3 and NFkappaB p50-p50 homodimers act as transcriptional …
2004年2月27日 · We demonstrate that a predominance of p50-p50 homodimers binding to the IL-2 promoter kappaB site in tolerant T cells correlated with repression of NFkappaB-driven transcription. Impaired translocation of the p65 subunit in tolerant T cells was a result from reduced activation of IkappaB kinase and poor phosphorylation and degradation of ...
B 细胞白血病 3 (Bcl-3) 蛋白对转录的抑制需要与核因子 kappaB (NF-kappaB) p50 …
这项研究表明,与 p50 的相互作用对于 Bcl-3 的抗炎特性是必要和充分的,并进一步突出了 p50 同源二聚体稳定性在控制 NF-kappaB 靶基因表达中的重要性。 "点击查看英文标题和摘要"