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亨廷顿蛋白包涵体不会下调R6/2型亨廷顿舞蹈症小鼠中的特定基因。

Huntingtin inclusions do not down-regulate specific genes in the R6/2 Huntington's disease mouse.

作者信息

Sadri-Vakili G, Menon A S, Farrell L A, Keller-McGandy C E, Cantuti-Castelvetri I, Standaert D G, Augood S J, Yohrling G J, Cha J-H J

机构信息

Massachusetts General Hospital, MassGeneral Institute for Neurodegenerative Disease, 114 16th Street/B114- 2001, Charlestown, MA 02129-4404, USA.

出版信息

Eur J Neurosci. 2006 Jun;23(12):3171-5. doi: 10.1111/j.1460-9568.2006.04871.x.

Abstract

Transcriptional dysregulation is a central pathogenic mechanism in Huntington's disease (HD); HD and transgenic mouse models of HD demonstrate down-regulation of specific genes at the level of mRNA expression. Furthermore, neuronal intranuclear inclusions (NIIs) have been identified in the brains of R6/2 mice and HD patients. One possibility is that NIIs contribute to transcriptional dysregulation by sequestering transcription factors. We therefore assessed the relationship between NIIs and transcriptional dysregulation in the R6/2 mouse, using double-label in situ hybridization combined with immunohistochemistry, and laser capture microdissection combined with quantitative real-time PCR. There was no difference in transcript levels of specific genes between NII-positive and NII-negative neurons. These results demonstrate that NIIs do not cause decreases in D2, PPE and PSS mRNA levels in R6/2 striatum and therefore are not involved in the down-regulation of these specific genes in this HD model. In addition, these observations argue against the notion that NIIs protect against transcriptional dysregulation in HD.

摘要

转录失调是亨廷顿舞蹈病(HD)的核心致病机制;HD及HD转基因小鼠模型在mRNA表达水平上显示出特定基因的下调。此外,在R6/2小鼠和HD患者的大脑中已发现神经元核内包涵体(NIIs)。一种可能性是,NIIs通过隔离转录因子导致转录失调。因此,我们采用双标记原位杂交结合免疫组化,以及激光捕获显微切割结合定量实时PCR的方法,评估了R6/2小鼠中NIIs与转录失调之间的关系。NII阳性神经元和NII阴性神经元之间特定基因的转录水平没有差异。这些结果表明,NIIs不会导致R6/2纹状体中D2、PPE和PSS mRNA水平降低,因此在该HD模型中不参与这些特定基因的下调。此外,这些观察结果反驳了NIIs可防止HD转录失调的观点。

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