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c-Fos 缺乏会抑制由固定应激诱导的部分而非全部神经递质生物合成酶的 mRNA 表达。

c-Fos deficiency inhibits induction of mRNA for some, but not all, neurotransmitter biosynthetic enzymes by immobilization stress.

作者信息

Serova L I, Saez E, Spiegelman B M, Sabban E L

机构信息

Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla 10595, USA.

出版信息

J Neurochem. 1998 May;70(5):1935-40. doi: 10.1046/j.1471-4159.1998.70051935.x.

DOI:10.1046/j.1471-4159.1998.70051935.x
PMID:9572277
Abstract

Recent studies indicated that c-Fos protein may be mediating stress-elicited transcriptional activation of genes involved in neurotransmitter biosynthesis. However, direct evidence for c-Fos mediating these changes in gene expression has been lacking. Mice with disrupted c-fos gene (+/- or -/- genotypes) were used to examine the effect of immobilization stress on a group of stress-responsive genes. In male adrenals, c-Fos was found not essential for stress-elicited activation of expression of tyrosine hydroxylase, dopamine beta-hydroxylase (DBH), phenylethanolamine N-methyltransferase, or neuropeptide Y. In females, immobilization failed to induce adrenal DBH in the c-Fos-deficient mice. In brainstem, c-Fos was indispensable for elevation of DBH mRNA in both genders. The gene, gender, and tissue specificity in the requirement for c-Fos points to diversity in adaptation mechanisms to stress.

摘要

近期研究表明,c-Fos蛋白可能介导应激引发的参与神经递质生物合成的基因的转录激活。然而,一直缺乏c-Fos介导这些基因表达变化的直接证据。利用c-fos基因破坏的小鼠(+/-或-/-基因型)来检测固定应激对一组应激反应基因的影响。在雄性肾上腺中,发现c-Fos对于应激引发的酪氨酸羟化酶、多巴胺β-羟化酶(DBH)、苯乙醇胺N-甲基转移酶或神经肽Y表达的激活并非必需。在雌性中,固定应激未能在c-Fos缺陷小鼠中诱导肾上腺DBH。在脑干中,c-Fos对于两性中DBH mRNA的升高是不可或缺的。c-Fos需求中的基因、性别和组织特异性表明了应激适应机制的多样性。

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