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原癌基因c-fos在新生脑组织而非成熟脑组织被破坏时会被高度诱导。

Proto-oncogene c-fos is highly induced by disruption of neonatal but not of mature brain tissue.

作者信息

Ruppert C, Wille W

出版信息

Brain Res. 1987 Apr;388(1):51-6. doi: 10.1016/0169-328x(87)90020-9.

DOI:10.1016/0169-328x(87)90020-9
PMID:3107751
Abstract

The proto-oncogene c-fos can be induced in cells to high transcript levels by numerous exogenous stimuli. We show here by S1 nuclease protection assay that mere mechanical disaggregation and incubation at 37 degrees C induces high levels of c-fos hnRNA and subsequently of mature mRNA in neonatal mouse cerebellar tissue. This specific increase of c-fos steady-state levels is dependent on the incubation time with a maximal level of induction (over 40-fold) after approximately 1 h. The accumulation of c-fos transcripts is suppressed by alpha-amanitin while cycloheximide intensifies induction only moderately. Excessive elevation of c-fos mRNA levels is age-dependent and occurs only in early postnatal but not in adult cerebellar tissue. We conclude that the steady-state level of c-fos transcripts is inducible in a development-dependent manner, and thus may be involved in normal neurogenesis of the mammalian cerebellum.

摘要

原癌基因c-fos可被多种外源性刺激诱导在细胞中达到高转录水平。我们在此通过S1核酸酶保护试验表明,单纯的机械分散和37℃孵育可在新生小鼠小脑组织中诱导高水平的c-fos核不均一RNA(hnRNA),随后诱导成熟mRNA的产生。c-fos稳态水平的这种特异性增加取决于孵育时间,大约1小时后诱导水平达到最大值(超过40倍)。c-fos转录本的积累受到α-鹅膏蕈碱的抑制,而环己酰亚胺仅适度增强诱导作用。c-fos mRNA水平的过度升高具有年龄依赖性,仅发生在出生后早期的小脑组织中,而在成年小脑组织中则不发生。我们得出结论,c-fos转录本的稳态水平可通过发育依赖性方式诱导,因此可能参与哺乳动物小脑的正常神经发生。

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Proto-oncogene c-fos is highly induced by disruption of neonatal but not of mature brain tissue.原癌基因c-fos在新生脑组织而非成熟脑组织被破坏时会被高度诱导。
Brain Res. 1987 Apr;388(1):51-6. doi: 10.1016/0169-328x(87)90020-9.
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Removal of an mRNA destabilizing element correlates with the increased oncogenicity of proto-oncogene fos.去除一种mRNA不稳定元件与原癌基因fos致癌性增加相关。
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An animal model of hypoxia-induced perinatal seizures.缺氧诱导围产期癫痫的动物模型。
Ital J Neurol Sci. 1995 Feb-Mar;16(1-2):59-68. doi: 10.1007/BF02229075.
2
Analysis of cDNA clones that code for the transmembrane forms of the mouse neural cell adhesion molecule (NCAM) and are generated by alternative RNA splicing.
Nucleic Acids Res. 1987 Nov 11;15(21):8621-41. doi: 10.1093/nar/15.21.8621.
3
Developmental changes of neuron-specific enolase and neurofilament proteins in primary neural culture.
Histochemistry. 1988;89(3):295-9. doi: 10.1007/BF00493155.
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NCAM-180, the large isoform of the neural cell adhesion molecule of the mouse, is encoded by an alternatively spliced transcript.NCAM-180是小鼠神经细胞黏附分子的大型异构体,由一个可变剪接转录本编码。
Nucleic Acids Res. 1988 May 25;16(10):4217-25. doi: 10.1093/nar/16.10.4217.
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Fos-jun and the primary genomic response in the nervous system. Possible physiological role and pathophysiological significance.Fos-jun与神经系统中的初级基因组反应。可能的生理作用和病理生理意义。
Mol Neurobiol. 1990 Spring-Summer;4(1-2):27-55. doi: 10.1007/BF02935584.
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c-fos protein like immunoreactivity in non-neuronal cells of rat peripheral nerve after transection.大鼠外周神经横断后非神经元细胞中类c-fos蛋白免疫反应性
Acta Neuropathol. 1991;82(1):66-71. doi: 10.1007/BF00310925.