Decreased expression of striatal signaling genes in a mouse model of Huntington's disease

被引：581

作者：

Luthi-Carter, R

Strand, A

Peters, NL

Solano, SM

Hollingsworth, ZR

Menon, AS

Frey, AS

Spektor, BS

Penney, EB

Schilling, G

Ross, CA

Borchelt, DR

Tapscott, SJ

Young, AB

Cha, JHJ

Olson, JM ^{[1
]}

机构：

[1] Fred Hutchinson Canc Res Ctr, Human Biol Div, Seattle, WA 98109 USA

[2] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA

[3] Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA

[4] Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA

[5] Johns Hopkins Univ, Sch Med, Dept Neuropathol, Baltimore, MD 21205 USA

来源：

HUMAN MOLECULAR GENETICS | 2000年 / 9卷 / 09期

关键词：

D O I：

10.1093/hmg/9.9.1259

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

To understand gene expression changes mediated by a polyglutamine repeat expansion in the human huntingtin protein, we used oligonucleotide DNA arrays to profile similar to 6000 striatal mRNAs in the R6/2 mouse, a transgenic Huntington's disease (HD) model. We found diminished levels of mRNAs encoding components of the neurotransmitter, calcium and retinoid signaling pathways at both early and late symptomatic time points (6 and 12 weeks of age). We observed similar changes in gene expression in another HD mouse model (N171-82Q). These results demonstrate that mutant huntingtin directly or indirectly reduces the expression of a distinct set of genes involved in signaling pathways known to be critical to striatal neuron function.

引用

页码：1259 / 1271

页数：13

共 60 条

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