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首页> 外文期刊>The European Journal of Neuroscience >Proteasome-dependent and -independent mechanisms for FosB destabilization: identification of FosB degron domains and implications for DeltaFosB stability.
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Proteasome-dependent and -independent mechanisms for FosB destabilization: identification of FosB degron domains and implications for DeltaFosB stability.

机译：蛋白酶体依赖性和非依赖性FosB失稳机制：鉴定FosB degron域及其对DeltaFosB稳定性的影响。

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摘要

The transcription factor DeltaFosB (Delta FosB) accumulates in a region-specific manner in the brain during chronic exposure to stress, drugs of abuse or other chronic stimuli. Once induced, DeltaFosB persists in the brain for at least several weeks following cessation of the chronic stimulus. The biochemical basis of the persistent expression of DeltaFosB has remained unknown. Here, we show that the FosB C-terminus, absent in DeltaFosB as a result of alternative splicing, contains two degron domains. Pulse-chase experiments of C-terminal truncation mutants of full-length FosB indicate that removal of its most C-terminal degron increases its half-life approximately fourfold, and prevents its proteasome-mediated degradation and ubiquitylation, properties similar to DeltaFosB. In addition, removal of a second degron domain, which generates DeltaFosB, further stabilizes FosB approximately twofold, but in a proteasome-independent manner. These data indicate that alternative splicing specifically removes two destabilizing elements from FosB in order to generate a longer-lived transcription factor, DeltaFosB, in response to chronic perturbations to the brain.
机译：在长期暴露于压力，滥用药物或其他慢性刺激过程中，转录因子DeltaFosB（Delta FosB）以特定区域的方式在大脑中积累。一旦被诱导，DeltaFosB在慢性刺激停止后在大脑中持续存在至少几周。 DeltaFosB持续表达的生化基础仍然未知。在这里，我们显示，由于选择性剪接，DeltaFosB中不存在的FosB C末端包含两个degron域。全长FosB的C端截短突变体的脉冲追踪实验表明，去除其最C端的degron可以将其半衰期延长约四倍，并防止其蛋白酶体介导的降解和泛素化，其性质类似于DeltaFosB。此外，去除产生DeltaFosB的第二个degron域，进一步使FosB稳定了大约两倍，但不依赖蛋白酶体。这些数据表明，选择性剪接可从FosB中特异性去除两个不稳定元素，从而响应大脑的长期扰动而产生寿命更长的转录因子DeltaFosB。

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