The increased nuclear IκBα in turn removes the NF-κB p65 complex from the DNA terminating its transcriptional activity. 19, 22 As nuclear p65:DNA interaction exhibits fast dissociation kinetics, the newly synthesized IκBα may not only reverse the binding of p65 to DNA, but also capture p65 molecules released from DNA and transport them ...

NF-κB蛋白通常会由p65和p50形成同源/异源二聚体，在胞质中因与抑制蛋白IkB结合形成了三聚体复合物而处于失活状态。 当上游信号因子TNF结合到细胞膜表面受体后，受体构象改变并将信号传递给IKK激酶（IkB kinase）…

包括p65的磷酸化调节和p65的乙酰化调节、p53对转录的竞争性调节，gsk3β对转录的间接调节；nf-κb转录调节中的常见的激酶：pka（蛋白激酶a），msk1和msk2（分裂素和压力激活激酶 ）。

IκB degradation reveals a nuclear localization sequence on NF-κB proteins (e.g., a p50-p65 heterodimer) allowing them to migrate to the nucleus, bind to specific κB-sites and regulate target gene transcription.

NF-κB p65 是NF-κB家族成员之一，NF-κB是一种多效性转录因子，几乎存在于所有细胞类型中，并参与许多生物学过程，例如炎症、免疫、分化、细胞生长、肿瘤发生和凋亡。 NF-κB受翻译后修饰和亚细胞区室化的各种机制以及与其他辅因子或共抑制因子的相互作用的控制。 p65-RelA是哺乳动物NF-κB家族的成员，该家族由5个亚基组成：p50-NF-κB1，p52-NF-κB2，c-Rel，p65-RelA和RelB。

NF-KB p65的问题：总p65不变， 胞浆pp65增加，核内pp65增加这该怎么解释？ IκBα抑制剂（BAY11-7082, 30 mM）效果很明显。 有人做的胞浆pp65是减少的，而我的增加，我是这么解释的：

NF kappa B 信号通路的激活一般分为两种途径：1. 经典的信号通路：IKK---IK--p65。 一般为IKK 磷酸化，引起IK 磷酸化，再引起p65（即NF kappa B分子）磷酸化，释放p65入核，从而调节核内基因表达.2. 非经典的信号通路，具体级联反应记不清了。 你搜一下NF kappa B 这个关键词，然后找出其review，会解释的很清楚。 你的实验方面，IK b磷酸化仅仅提示可能引起p65磷酸化，起码需要补充p65入核的免疫荧光的实验，才能说明p65入核了，严格来说，应该继续做p65的入核 …

Transcription factor NF-KB (p50/p65) is generally localized to the cytoplasm by its inhibitor IKB. Overproduced IKB, free from NF-KB, israpidly degraded. Overexpression of p65 increases endogenous IKB protein in both carcinoma and lymphoid cells by two mechanisms: protein stabilization and increased transcription of IKB mRNA.

IKK activation results in phosphorylation of IκB and p65. IκB phosphorylation leads to its ubiquitin-mediated proteasomal degradation, enabling NF-κB dimers translocation to the nucleus, where they bind to DNA and induce transcription.

1991年3月8日 · DNA binding by truncated p65 is inhibited by IκB, thus mapping the IκB interaction domain to the rel -homologous region and suggesting that IκB exerts its inhibitory effect upon NF-κB primarily through interaction with p65.