Yoshimura T, Kobayashi T, Shinnoh N, Goto I
Department of Neurology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Neurochem Res. 1990 Oct;15(10):963-7. doi: 10.1007/BF00965740.
In attempts to elucidate mechanisms of demyelination in the twitcher mouse (Twi), phosphorylation and methylation of myelin basic protein (MBP) were examined in the brainstem and spinal cord of this species. Phosphorylation of MBP in isolated myelin by an endogenous kinase and an exogenous [32P]ATP was not impaired and protein kinase C activity in the brain cytosol was not reduced. When the methylation of an arginine residue of MBP was examined in slices of the brainstem and spinal cord, using [3H]methionine as a donor of the methyl groups, no difference was found between Twi and the controls. Radioactivity of the [3H] methionine residue of MBP of Twi was also similar to that of the controls. Thus, accumulation of psychosine in Twi does not interfere with the activity of endogenous kinase, methylation of MBP, and the synthesis and transport of MBP into myelin membrane.
为了阐明颤抖小鼠（Twi）脱髓鞘的机制，对该物种脑干和脊髓中髓鞘碱性蛋白（MBP）的磷酸化和甲基化进行了研究。内源性激酶和外源性[32P]ATP对分离出的髓鞘中MBP的磷酸化没有损害，并且脑细胞质中的蛋白激酶C活性也没有降低。当使用[3H]甲硫氨酸作为甲基供体，在脑干和脊髓切片中检测MBP精氨酸残基的甲基化时，未发现Twi与对照之间存在差异。Twi的MBP的[3H]甲硫氨酸残基的放射性也与对照相似。因此，半乳糖神经酰胺单己糖苷在Twi中的积累不会干扰内源性激酶的活性、MBP的甲基化以及MBP向髓鞘膜的合成和转运。
