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-κB 是一组蛋白质复合体的统称，主要包含 RelA (p65)、 RelB 、 c-Rel 、 p50 / p105 (NF-κB1) 和 p52 / p100 (NF-κB2) 等亚单位。 在未被激活状态下，NF-κB 位于细胞质中，与抑制蛋白 IκB 绑定，从而被保持在非活化状态。

Our results demonstrate two separate functions of the IKK complex in NFκB activation in cells with constitutive Akt activity: the phosphorylation and consequent degradation of IκB and the phosphorylation of p65. The data further support the conclusion that NFκB activity is essential for PI3K- and Akt-induced oncogenic transformation.

2019年7月17日 · In a rat model of HPH, we found that Akt/mTOR signaling was activated and the level of phosphorylated NF-κB (p65) was subsequently increased, indicating that crosstalk occurs between mTORC1 and...

2016年5月25日 · Vav1 controls downstream p65 phosphorylation and NF-κB activation. Synergistic signalling is defective in X-linked lymphoproliferative disease (XLP1) NK cells entailing 2B4 dysfunction and...

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）…

2007年6月11日 · Expression of the NF- κ B subunit p65 is sufficient for EMT induction, validating this signalling module during EMT. NF- κ B pathway activation is associated with tumour progression and...

2001年6月1日 · We propose two mechanisms for Akt-mediated NF-κB activation: 1) Akt expression alone utilizes IKKβ in a p38-dependent manner, which requires serines 529 and 536 of RelA/p65 to directly stimulate NF-κB activity, and 2) Akt signaling in response to IL-1 exposure stimulates NF-κB by activating p38 in a manner dependent on IKKα.

2003年10月20日 · Elevated expression of p65/RelA stimulates both phosphorylation and expression of Akt in NIH3T3 cells and primary endothelial cells. Both effects of p65 on Akt are blocked by transcriptional and translational inhibitors, suggesting the need for new gene expression. Elevated p65 expression leads to an activation of PI-3 kinase and PDK1.

Ang II decreased phospho‑Akt, phospho‑p65 NF‑κB, nephrin, and podocin and increased caspase‑9 expression, while podocyte apoptosis was promoted. LY294002 further enhanced Ang II‑induced downregulation of Akt and p65 NF‑κB activation, as well as upregulation of caspase‑9 mRNA and protein, and promoted the apoptosis of podocytes.