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Alpha1-chimaerin, a Rac1 GTPase-activating protein, is expressed at reduced mRNA levels in the brain of Alzheimer's disease patients.


ABSTRACT: Alpha1-chimaerin is a GTPase-activating protein (GAP) for Rac1, a member of the Rho small GTPase family, whose action leads to the inactivation of Rac1. Rac1 activity is upregulated in Alzheimer's disease, but little is known about the role of ?1-chimaerin. In this study, we investigated the expression and localization of ?1-chimaerin mRNA in postmortem human brains from patients with Alzheimer's disease and control subjects. In situ hybridization studies demonstrated that ?1-chimaerin was expressed by neurons in the neo-cortex of the temporal lobe and the hippocampus of both controls and Alzheimer's disease cases, with the signal intensity dramatically decreased in patients with Alzheimer's disease. Real-time PCR analysis confirmed a significant reduction of ?1-chimaerin mRNA expression in the temporal cortex of Alzheimer's disease cases. In contrast, ?2-chimaerin mRNA levels showed no significant difference between the groups. The present study showed reduced ?1-chimaerin expression in the brain of Alzheimer's disease cases, suggesting a role in the upregulation of Rac1 activity during the disease process.

SUBMITTER: Kato T 

PROVIDER: S-EPMC4382517 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature

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Alpha1-chimaerin, a Rac1 GTPase-activating protein, is expressed at reduced mRNA levels in the brain of Alzheimer's disease patients.

Kato Tomoko T   Konishi Yoshihiro Y   Shimohama Shun S   Beach Thomas G TG   Akatsu Hiroyasu H   Tooyama Ikuo I  

Neuroscience letters 20150209


Alpha1-chimaerin is a GTPase-activating protein (GAP) for Rac1, a member of the Rho small GTPase family, whose action leads to the inactivation of Rac1. Rac1 activity is upregulated in Alzheimer's disease, but little is known about the role of α1-chimaerin. In this study, we investigated the expression and localization of α1-chimaerin mRNA in postmortem human brains from patients with Alzheimer's disease and control subjects. In situ hybridization studies demonstrated that α1-chimaerin was expre  ...[more]

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