c-Fos deficiency inhibits induction of mRNA for some, but not all, neurotransmitter biosynthetic enzymes by immobilization stress.
c-Fos deficiency inhibits induction of mRNA for some, but not all, neurotransmitter biosynthetic enzymes by immobilization stress.
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c-Fos 缺乏会抑制某些（但不是全部）神经递质生物合成酶通过固定应激诱导 mRNA。
DOI：
10.1046/j.1471-4159.1998.70051935.x
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发表时间：
1998
影响因子：
4.7
通讯作者：
Sabban,EL
中科院分区：
文献类型：
--
作者：
Serova,LI;Saez,E;Spiegelman,BM;Sabban,EL
最近的研究表明，c-Fos蛋白可能介导应激引起的参与神经递质生物合成的基因的转录激活。然而，缺乏c-Fos介导这些基因表达变化的直接证据。使用c-fosgene（+/-或-/-基因型）被破坏的小鼠来检查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对于应激引起的酪氨酸羟化酶、多巴胺β羟化酶（DBH）、苯乙醇胺N-甲基转移酶或神经肽Y的表达激活不是必需的。在雌性c-Fos-缺陷小鼠中，制动未能诱导肾上腺DBH。在脑干中，c-Fos对于两种性别的DBH mRNA的升高都是不可或缺的。基因、性别和组织对c-Fos需求的特异性表明了应激适应机制的多样性。
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‐fosgene (+/− 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 β‐hydroxylase (DBH), phenylethanolamineN‐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.