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首页> 外文期刊>Cell death and differentiation >The PIDDosome, DNA-damage-induced apoptosis and beyond.
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The PIDDosome, DNA-damage-induced apoptosis and beyond.

机译:PIDDosome,DNA损伤诱导的细胞凋亡及其他。

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摘要

P53-induced protein with a death domain (PIDD) was cloned as a death domain (DD)-containing protein whose expression is induced by p53. It was later described as the core of a molecular platform-activating caspase-2, named the PIDDosome. These first results pointed towards a role for PIDD in apoptosis, in response to DNA damage. Identification of new PIDDosome complexes involved in DNA repair and nuclear factor-kappaB signaling challenged this early concept. PIDD functions are growing as new complexes and new interaction partners are being discovered, and as additional functions are being revealed. A fascinating feature of PIDD lies within its complex and tight regulation mechanisms, which allow the molecule to fine-tune its different functions: from transcriptional regulation to the expression of different isoforms, and from the interaction with regulatory proteins to an ingenious post-translational cleavage mechanism generating various active fragments with specific functions. Further studies still need to be carried out to provide answers to many unresolved issues and to reconcile conflicting results. This review aims at providing an overview of the current PIDD knowledge status.
机译:将具有死亡结构域(PIDD)的P53诱导的蛋白克隆为包含表达被p53诱导的死亡结构域(DD)的蛋白。后来被描述为分子平台激活caspase-2的核心,称为PIDDosome。这些最初的结果指出了PIDD在响应DNA损伤时在凋亡中的作用。鉴定涉及DNA修复和核因子-κB信号转导的新PIDDosome复合物对这一早期概念提出了挑战。随着发现新的复合体和新的交互伙伴以及发现其他功能,PIDD功能正在不断增长。 PIDD的一个令人着迷的特征在于其复杂而严密的调节机制,该机制使分子可以微调其不同功能:从转录调节到不同同工型的表达,从与调节蛋白的相互作用到巧妙的翻译后切割产生具有特定功能的各种活性片段的机制。为了解决许多未解决的问题并调和矛盾的结果,仍需要进行进一步的研究。这篇综述旨在概述当前的PIDD知识状态。

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