Ebi是TBL1在果蝇中的同系物,调节细胞防御反应和神经元存活之间的平衡。

American journal of neurodegenerative disease Pub Date : 2016-03-01 eCollection Date: 2016-01-01
Young-Mi Lim, Leo Tsuda
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引用次数: 0

摘要

转导蛋白β样1 (TBL1)是一种转录共抑制因子复合物,是迟发性听力障碍的致病因素。转录共抑制因子复合物通过与发散性转录因子形成复合物,在基因表达中发挥关键作用。然而,协同抑制因子复合物如何调控细胞存活仍有待阐明。我们在此证明了ebi, TBL1的果蝇同源物,在存在过多先天免疫信号的情况下抑制光感受器细胞变性。我们还发现,NF-κB和AP-1之间的平衡是应激条件下细胞存活的关键组成部分。鉴于Ebi通过调节NF-κB活性,抑制AP-1诱导的细胞凋亡,在先天免疫应答中发挥重要作用,它可能通过调节NF-κB与AP-1之间的串扰,参与光感受器细胞存活的调控。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Ebi, a Drosophila homologue of TBL1, regulates the balance between cellular defense responses and neuronal survival.

Transducin β-like 1 (TBL1), a transcriptional co-repressor complex, is a causative factor for late-onset hearing impairments. Transcriptional co-repressor complexes play pivotal roles in gene expression by making a complex with divergent transcription factors. However, it remained to be clarified how co-repressor complex regulates cellular survival. We herein demonstrated that ebi, a Drosophila homologue of TBL1, suppressed photoreceptor cell degeneration in the presence of excessive innate immune signaling. We also showed that the balance between NF-κB and AP-1 is a key component of cellular survival under stress conditions. Given that Ebi plays an important role in innate immune responses by regulating NF-κB activity and inhibition of apoptosis induced by associating with AP-1, it may be involved in the regulation of photoreceptor cell survival by modulating cross-talk between NF-κB and AP-1.

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