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

我们已经研究了IKK/NF-κB信号轴在iPS细胞重编程中的作用。我们发现，Yamanaka 4因子的异位表达诱导了IKKβ激酶的活性，这依赖于ATM。此外，IKKβ基因的破坏降低了重编程效率，而IKKβ的组成活性形式IKKβ^(EE)与山中4因子的共表达促进了重编程效率。我们发现，在重新编程过程中，IKKβ的中断增加了衰老细胞的数量。综上所述，我们的结果表明，IKKβ通过以Anat M依赖的方式对抗山中因子异位表达引起的细胞衰老，从而增强细胞重新编程。

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.