Project description:Schnurri-2 (Shn-2), an NF-kappa B site-binding protein, tightly binds to the enhancers of major histocompatibility complex (MHC) class I genes and inflammatory cytokines, which have been shown to harbor common variant single nucleotide polymorphisms associated with schizophrenia. Shn-2 knockout mice show behavioral abnormalities that strongly resemble those of schizophrenics. We performed gene expression microarray analysis of dentate gyri from Shn-2 knockout and wild-type control mice. Dentate gyrus RNA isolated from six Shn-2 knockout and six control wild-type mice were compared.
Project description:Schnurri-2 (Shn-2), an NF-kappa B site-binding protein, tightly binds to the enhancers of major histocompatibility complex (MHC) class I genes and inflammatory cytokines, which have been shown to harbor common variant single nucleotide polymorphisms associated with schizophrenia. Shn-2 knockout mice show behavioral abnormalities that strongly resemble those of schizophrenics. We performed gene expression microarray analysis of prefrontal cortices from Shn-2 knockout and wild-type control mice. Prefrontal cortex RNA isolated from six Shn-2 knockout and six control wild-type mice were compared.
Project description:Schnurri-2 (Shn-2), an NF-kappa B site-binding protein, tightly binds to the enhancers of major histocompatibility complex (MHC) class I genes and inflammatory cytokines, which have been shown to harbor common variant single nucleotide polymorphisms associated with schizophrenia. Shn-2 knockout mice show behavioral abnormalities that strongly resemble those of schizophrenics. We performed gene expression microarray analysis of dentate gyri from Shn-2 knockout and wild-type control mice.
Project description:Schnurri-2 (Shn-2), an NF-kappa B site-binding protein, tightly binds to the enhancers of major histocompatibility complex (MHC) class I genes and inflammatory cytokines, which have been shown to harbor common variant single nucleotide polymorphisms associated with schizophrenia. Shn-2 knockout mice show behavioral abnormalities that strongly resemble those of schizophrenics. We performed gene expression microarray analysis of prefrontal cortices from Shn-2 knockout and wild-type control mice.
Project description:Gene expression was measured from the dentate gyrus and entorhinal cortex harvested from human postmortem samples. We harvested the dentate gyrus DG from healthy human brains ranging from 33 to 88 years of age. Additionally, from each brain we harvested the entorhinal cortex (EC) as a within-brain control. Using Affymetrix microarray chips we generated gene-expression profiles of each individual tissue samples. DG expression levels were first normalized against the EC, and the normalized DG transcripts were then correlated against age.
Project description:This study examined the proteome profile in the hippocampus, medial prefrontal cortex, and striatum of APPswe/PS1dE9 transgenic mice (APP/PS1) model of Alzheimer’s disease compared to wild-type mice. The effect of tocotrienol-rich fraction (TRF), a mixture of vitamin E analogs derived from palm oil supplementation on the proteome profile of APP/PS1 mice hippocampus, medial prefrontal cortex, and striatum was also investigated. The analysis was performed using ultrahigh-performance liquid chromatography coupled with Q Exactive HF Orbitrap mass spectrometry. This study was in hoped to understand the mechanisms of Alzheimer’s disease at proteome level, and pre-emptive activity of TRF to combat the disease.
Project description:To identify genes responsible for stem and progenitor cells maintenance, we sought here to find genes underlying premature neural aging, and whose deregulated expression could be rescued by running. Through RNA sequencing we analyzed the transcriptomic profiles of the dentate gyrus isolated from Btg1 wild-type or Btg1 knockout adult (two-month-old) mice submitted to physical exercise or sedentary. In Btg1 knockout mice, 545 genes were deregulated, relative to wild-type, while 2081 genes were deregulated by running. We identified 42 genes whose expression was not only down-regulated in the dentate gyrus of Btg1 knockout, but was also counter-regulated to control levels by running in Btg1 knockout mice, vs. sedentary.
