首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Immunocytochemical study on the distribution of c-myb in the central nervous system of the transgenic mice expressing a human copper/zinc superoxide dismutase mutation.
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Immunocytochemical study on the distribution of c-myb in the central nervous system of the transgenic mice expressing a human copper/zinc superoxide dismutase mutation.

机译:免疫细胞化学研究c-myb在表达人铜/锌超氧化物歧化酶突变的转基因小鼠中枢神经系统中的分布。

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摘要

Although our previous study showed the constitutive expression of c-myb in neurons, suggesting that this gene might be involved in the normal function of these cells, there were no reports on the expression pattern of c-myb under pathological conditions. In the present study, we first investigated the changes in c-myb immunoreactivities (IRs) in the central nervous system of the transgenic mice expressing a human copper/zinc superoxide dismutase (Cu/Zn SOD) mutation. The distribution of c-myb was enhanced in the various brain regions of transgenic mice expressing a mutated human Cu/Zn SOD gene. Immunohistochemistry showed intensely stained c-myb IR glial cells with the appearance of astrocytes within the various brain regions of transgenic mice such as the gray matter of the midbrain, medulla oblongata and spinal cord. Even though the exact functions of c-myb in the normal and pathological states were not clearly revealed until now, we think that the increase in c-myb expression in the mutant mice could be due to the compensate mechanism of the astrocytes for the reduced defence against superoxide toxicity because the only known function of c-myb was its correlation with the prevention of programmed cell death, which could be deduced from the previous studies.
机译:尽管我们先前的研究显示了c-myb在神经元中的组成型表达,表明该基因可能参与了这些细胞的正常功能,但尚无有关病理条件下c-myb表达模式的报道。在本研究中,我们首先研究了表达人铜/锌超氧化物歧化酶(Cu / Zn SOD)突变的转基因小鼠中枢神经系统中c-myb免疫反应性(IR)的变化。 c-myb的分布在表达突变的人Cu / Zn SOD基因的转基因小鼠的各个大脑区域中得到增强。免疫组织化学显示,在转基因小鼠的各个大脑区域,如中脑灰质,延髓和脊髓,星形胶质细胞均出现了染色强烈的c-myb IR神经胶质细胞。尽管到目前为止,尚不清楚c-myb在正常和病理状态下的确切功能,但我们认为突变小鼠中c-myb表达的增加可能是由于星形胶质细胞对防御力降低的补偿机制所致。对抗过氧化物毒性,因为c-myb唯一已知的功能是其与程序性细胞死亡的预防相关,这可以从先前的研究中推论得出。

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