Investigating the role of IKK/NF-・B signaling axis on the cellular reprogramming

我们研究了IKK/NF-κB信号轴在细胞重编程为iPS细胞中的作用。我们发现Yamanaka 4因子的异位表达依赖于ATM诱导IKKβ激酶活性。此外，Ikkβ基因的破坏降低了重编程效率，而IKKβ^（EE）（IKKβ的组成性活性形式）与Yamanaka 4因子的共表达促进了重编程效率。我们发现Ikkβ的破坏增加了重编程过程中衰老细胞的数量。总的来说，我们的研究结果表明，IKKβ增强细胞重编程通过拮抗细胞衰老引起的异位表达Yamanaka因子在anATM依赖的方式。

We have investigated the role, if any, of IKK/NF-κB signaling axis in cellular reprogramming into iPS cells. We found that ectopic expr ession of Yamanaka 4 factors induced the IKKβ kinase activity depending on ATM. Moreover, disruption of Ikkβ gene reduced the reprogramming efficiency, whereas co-expr ession of IKKβ^(EE), a constitutive active form of IKKβ, with Yamanaka 4 factors promoted the efficiency. We found disruption of Ikkβ elevated the number of senescent cells during the reprogramming. Collectively, our results indicate that IKKβ potentiates cellular reprogramming by antagonizing the cellular senescence evoked by the ectopic expression of Yamanaka factors in anAT M-dependent manner.