Regulation of delta FosB and FosB-like proteins by electroconvulsive seizure and cocaine treatments.

Regulation of delta FosB and FosB-like proteins by electroconvulsive seizure and cocaine treatments.
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DOI:
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发表时间:
1995-11
影响因子:
3.6
通讯作者:
J. Chen;H. E. Nye;M. Kelz;N. Hiroi;Y. Nakabeppu;B. Hope;E. Nestler
J. Chen;H. E. Nye;M. Kelz;N. Hiroi;Y. Nakabeppu;B. Hope;E. Nestler
中科院分区:
医学3区
文献类型:
--
作者:
J. Chen;H. E. Nye;M. Kelz;N. Hiroi;Y. Nakabeppu;B. Hope;E. Nestler

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先前的研究表明,c-Fos和几种Fos样蛋白或Fos相关抗原(Fos相关抗原)在脑中被急性诱导,以响应各种各样的刺激。相反,几种刺激诱导明显不同的Fos样蛋白,称为慢性Fras,慢性给药后。我们发现,三角洲FosB,FosB的截短剪接变异体,响应像其他急性FRAS:它是快速和短暂的急性电惊厥发作(ECS)后,在大脑皮层和纹状体急性可卡因后,但不积累慢性ECS或可卡因治疗。尽管慢性Fras与δ FosB在免疫化学上相关,但它们可以基于它们的时间特性与δ FosB区分开,因为它们仅在慢性ECS和可卡因处理后诱导。此外,慢性Fras和δ FosB可以通过它们在一维和二维凝胶电泳上的迁移模式来区分。因此,慢性Fras似乎是新的FosB相关蛋白。我们还提供了证据表明,慢性FRAS异源二聚体主要与Jun-D和Jun-B,而不是c-Jun。AP-1复合物含有慢性FRAS作为AP-1介导的转录负调控因子的可能性进行了讨论。
Previous work has shown that c-Fos and several Fos-like proteins or Fras (Fos-related antigens) are induced acutely in brain in response to a wide variety of stimuli. In contrast, several stimuli induce apparently distinct Fos-like proteins, termed chronic Fras, after chronic administration. We show that delta FosB, a truncated splice variant of FosB, responds like the other acute Fras: it is induced rapidly and transiently in cerebral cortex after acute electroconvulsive seizure (ECS) and in striatum after acute cocaine but does not accumulate after chronic ECS or cocaine treatment. Although the chronic Fras are immunochemically related to delta FosB, they can be distinguished from delta FosB based on their temporal properties in that they are induced after chronic ECS and cocaine treatments only. Moreover, the chronic Fras and delta FosB can be distinguished by their migration patterns on one- and two-dimensional gel electrophoresis. The chronic Fras, therefore, appear to be novel FosB-related proteins. We also provide evidence that the chronic Fras heterodimerize primarily with Jun-D and Jun-B, as opposed to c-Jun. The possibility that AP-1 complexes containing the chronic Fras function as negative regulators of AP-1 mediated transcription is discussed.