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首页> 外文期刊>International Journal of Neuroscience >Inclusion formation by ataxins -1, -2, -3, and -7.
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Inclusion formation by ataxins -1, -2, -3, and -7.

机译:由紫杉醇-1,-2,-3和-7形成​​包涵体。

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摘要

The authors studied inclusion formation in vitro using transiently transfected PC12 cells, with epitope-tagged and untagged full-length and truncated wild-type and expanded ataxins -1, -2, -3, and -7. At 72 hours, no inclusions were seen with wild-type full-length or truncated ataxins -2, -3, or -7, and only one with ataxin-1. Truncation abolished nuclear localization of ataxins -1 and -7, and allowed nuclear entry of ataxin-2. Of the expanded ataxins, only -1 and -2 formed inclusions, and those of ataxin-2 were rare and exclusively cytoplasmic. Truncation resulted in inclusion formation by ataxins -3 and -7, increased ataxin-1 inclusions, and enabled formation of nuclear ataxin-2 inclusions. There was no recruitment of wild-type ataxin-1 to expanded ataxin-1 inclusions.
机译:作者研究了使用瞬时转染的PC12细胞在体外形成包涵体的过程,其中带有表位标记和未标记的全长和截短的野生型以及扩展的紫杉醇-1,-2,-3和-7。在72小时时,野生型全长或截短的紫杉醇-2,-3或-7没有发现夹杂物,而紫杉醇-1则只有一个。截短消除了紫杉素-1和-7的核定位,并允许紫杉素-2的核进入。在扩展的紫杉醇中,只有-1和-2形成了内含物,而紫杉醇-2的则很少,而且仅是胞质的。截短导致由共生紫杉醇-3和-7形成​​包涵体,增加了共生紫杉醇-1的包涵体,并使得形成了核生紫杉醇-2夹杂物。没有募集野生型紫杉醇-1以扩大紫杉醇-1包涵体。

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