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本文引用的文献

1
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.bcl-3原癌基因编码一种核内类IκB分子，该分子以磷酸化依赖的方式优先与NF-κB p50和p52相互作用。
Mol Cell Biol. 1993 Jun;13(6):3557-66. doi: 10.1128/mcb.13.6.3557-3566.1993.
2
KBF1 (p50 NF-kappa B homodimer) acts as a repressor of H-2Kb gene expression in metastatic tumor cells.KBF1（p50核因子κB同型二聚体）在转移性肿瘤细胞中作为H-2Kb基因表达的抑制因子发挥作用。
J Exp Med. 1993 Jun 1;177(6):1651-62. doi: 10.1084/jem.177.6.1651.
3
The oncoprotein Bcl-3 directly transactivates through kappa B motifs via association with DNA-binding p50B homodimers.癌蛋白Bcl-3通过与DNA结合的p50B同型二聚体结合，直接通过κB基序进行反式激活。
Cell. 1993 Mar 12;72(5):729-39. doi: 10.1016/0092-8674(93)90401-b.
4
The NF-kappa B precursor p105 and the proto-oncogene product Bcl-3 are I kappa B molecules and control nuclear translocation of NF-kappa B.核因子-κB前体p105和原癌基因产物Bcl-3是IκB分子，并控制核因子-κB的核转位。
EMBO J. 1993 Jan;12(1):213-22. doi: 10.1002/j.1460-2075.1993.tb05647.x.
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N-myc suppresses major histocompatibility complex class I gene expression through down-regulation of the p50 subunit of NF-kappa B.
EMBO J. 1993 Jan;12(1):195-200. doi: 10.1002/j.1460-2075.1993.tb05645.x.
6
The oncoprotein Bcl-3 can facilitate NF-kappa B-mediated transactivation by removing inhibiting p50 homodimers from select kappa B sites.癌蛋白Bcl-3可通过从特定κB位点去除抑制性p50同二聚体来促进核因子κB介导的反式激活。
EMBO J. 1993 Oct;12(10):3893-901. doi: 10.1002/j.1460-2075.1993.tb06067.x.
7
Regulation of the NF-kappa B/rel transcription factor and I kappa B inhibitor system.核因子-κB/rel转录因子及IκB抑制蛋白系统的调控
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8
Bcl-3, a member of the I kappa B proteins, has distinct specificity towards the Rel family of proteins.Bcl-3是IκB蛋白家族的一员，对Rel蛋白家族具有独特的特异性。
Oncogene. 1993 Aug;8(8):2067-73.
9
The candidate proto-oncogene bcl-3 encodes a transcriptional coactivator that activates through NF-kappa B p50 homodimers.候选原癌基因bcl-3编码一种转录共激活因子，该因子通过核因子κB p50同二聚体激活。
Genes Dev. 1993 Jul;7(7B):1354-63. doi: 10.1101/gad.7.7b.1354.
10
Expression of relB transcripts during lymphoid organ development: specific expression in dendritic antigen-presenting cells.relB转录本在淋巴器官发育过程中的表达：在树突状抗原呈递细胞中的特异性表达。
Development. 1993 Aug;118(4):1221-31. doi: 10.1242/dev.118.4.1221.

胸腺细胞中Bc1-3的组成型表达增加了体内NF-κB1（p50）同二聚体的DNA结合。

Constitutive expression of Bc1-3 in thymocytes increases the DNA binding of NF-kappaB1 (p50) homodimers in vivo.

作者信息

Caamaño J H, Perez P, Lira S A, Bravo R

机构信息

Department of Oncology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543-4000, USA.

出版信息

Mol Cell Biol. 1996 Apr;16(4):1342-8. doi: 10.1128/MCB.16.4.1342.

DOI:10.1128/MCB.16.4.1342
PMID:8657107
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC231118/
Abstract

Previous studies have indicated that Bcl-3 interacts through its ankyrin repeats with the transcriptional factors NF-kappaB1 (p50) and NF-kappaB2 (p52), affecting their biological activities. To further investigate the role of Bcl-3 in vivo and its association with the NF-kappaB proteins, we have generated transgenic mice constitutively expressing Bcl-3 in thymocytes. The results indicate that Bcl-3 is associated with endogenous p50 and p52 in nuclear extracts from transgenic animals. Remarkably, constitutive expression of Bcl-3 in these cells augments the DNA binding activity of p52 homodimers. This effect could be reproduced in vitro and is blocked by anti-Bcl-3 antibodies. We have also shown that Bcl-3 is phosphorylated in thymocytes and that its dephosphorylation greatly decreases the effect on p50 homodimers.

摘要

先前的研究表明，Bcl-3通过其锚蛋白重复序列与转录因子NF-κB1（p50）和NF-κB2（p52）相互作用，影响它们的生物学活性。为了进一步研究Bcl-3在体内的作用及其与NF-κB蛋白的关联，我们构建了在胸腺细胞中组成性表达Bcl-3的转基因小鼠。结果表明，在转基因动物的核提取物中，Bcl-3与内源性p50和p52相关联。值得注意的是，这些细胞中Bcl-3的组成性表达增强了p52同二聚体的DNA结合活性。这种效应在体外可以重现，并且被抗Bcl-3抗体阻断。我们还表明，Bcl-3在胸腺细胞中被磷酸化，其去磷酸化大大降低了对p50同二聚体的影响。