Whole Brain Gene Expression Correlates for LM_BASELINE measured in BXD RI Males obtained using INIA Brain mRNA M430 (Jun06) RMA. The LM_BASELINE measures Baseline activity in fear conditioning apparatus under the domain Basal Behavior. The correlates were thresholded at a p-value of less than 0.001.
Authors:
Philip VM, Duvvuru S, Gomero B, Ansah TA, Blaha CD, Cook MN, Hamre KM, Lariviere WR, Matthews DB, Mittleman G, Goldowitz D, Chesler EJ
GSE27786_LSK_VS_ERYTHROBLAST_DN
Genes down-regulated in comparison of LSK versus erythroblasts.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE17721_PAM3CSK4_VS_CPG_12H_BMDM_UP
Genes up-regulated in comparison of dendritic cells (DC) stimulated with Pam3Csk4 (TLR1/2 agonist) at 12 h versus DC cells stimulated with CpG DNA (TLR9 agonist) at 12 h.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE17721_CPG_VS_GARDIQUIMOD_12H_BMDM_DN
Genes down-regulated in comparison of dendritic cells (DC) stimulated with CpG DNA (TLR9 agonist) at 12 h versus DC cells stimulated with Gardiquimod (TLR7 agonist) at 12 h.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE27786_LIN_NEG_VS_ERYTHROBLAST_DN
Genes down-regulated in comparison of lineage negative versus erythroblasts.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE32423_CTRL_VS_IL7_MEMORY_CD8_TCELL_UP
Genes up-regulated in comparison of memory CD8 T cells versus those treated with IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a>.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that act as ligand-activated transcription factors. Although prescribed for dyslipidemia and type-II diabetes, PPAR agonists also possess anti-addictive characteristics. PPAR agonists decrease ethanol consumption and reduce withdrawal severity and susceptibility to stress-induced relapse in rodents. However, the cellular and molecular mechanisms facilitating these properties have yet to be investigated. We tested three PPAR agonists in a continuous access two-bottle choice (2BC) drinking paradigm and found that tesaglitazar (PPARα/γ; 1.5 mg/kg) and fenofibrate (PPARα; 150 mg/kg) decreased ethanol consumption in male C57BL/6J mice while bezafibrate (PPARα/γ/β; 75 mg/kg) did not. We hypothesized that changes in brain gene expression following fenofibrate and tesaglitazar treatment lead to reduced ethanol drinking. We studied unbiased genomic profiles in areas of the brain known to be important for ethanol dependence, the prefrontal cortex (PFC) and amygdala, and also profiled gene expression in liver. Genomic profiles from the non-effective bezafibrate treatment were used to filter out genes not associated with ethanol consumption. Because PPAR agonists are anti-inflammatory, they would be expected to target microglia and astrocytes. Surprisingly, PPAR agonists produced a strong neuronal signature in mouse brain, and fenofibrate and tesaglitazar (but not bezafibrate) targeted a subset of GABAergic interneurons in the amygdala. Weighted gene co-expression network analysis (WGCNA) revealed co-expression of treatment-significant genes. Functional annotation of these gene networks suggested that PPAR agonists might act via neuropeptide and dopaminergic signaling pathways in the amygdala. Our results reveal gene targets through which PPAR agonists can affect alcohol consumption behavior.
Authors:
Laura B Ferguson, Dana Most, Yuri A Blednov, R Adron Harris
Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that act as ligand-activated transcription factors. Although prescribed for dyslipidemia and type-II diabetes, PPAR agonists also possess anti-addictive characteristics. PPAR agonists decrease ethanol consumption and reduce withdrawal severity and susceptibility to stress-induced relapse in rodents. However, the cellular and molecular mechanisms facilitating these properties have yet to be investigated. We tested three PPAR agonists in a continuous access two-bottle choice (2BC) drinking paradigm and found that tesaglitazar (PPARα/γ; 1.5 mg/kg) and fenofibrate (PPARα; 150 mg/kg) decreased ethanol consumption in male C57BL/6J mice while bezafibrate (PPARα/γ/β; 75 mg/kg) did not. We hypothesized that changes in brain gene expression following fenofibrate and tesaglitazar treatment lead to reduced ethanol drinking. We studied unbiased genomic profiles in areas of the brain known to be important for ethanol dependence, the prefrontal cortex (PFC) and amygdala, and also profiled gene expression in liver. Genomic profiles from the non-effective bezafibrate treatment were used to filter out genes not associated with ethanol consumption. Because PPAR agonists are anti-inflammatory, they would be expected to target microglia and astrocytes. Surprisingly, PPAR agonists produced a strong neuronal signature in mouse brain, and fenofibrate and tesaglitazar (but not bezafibrate) targeted a subset of GABAergic interneurons in the amygdala. Weighted gene co-expression network analysis (WGCNA) revealed co-expression of treatment-significant genes. Functional annotation of these gene networks suggested that PPAR agonists might act via neuropeptide and dopaminergic signaling pathways in the amygdala. Our results reveal gene targets through which PPAR agonists can affect alcohol consumption behavior.
Authors:
Laura B Ferguson, Dana Most, Yuri A Blednov, R Adron Harris
Genes with particular expression in the Anterior olfactory nucleus, dorsal part. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Orbital area, lateral part, layer 1. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Orbital area, ventrolateral part, layer 1. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Granular lamina of the cochlear nuclei. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Koelliker-Fuse subnucleus. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Anterior olfactory nucleus, external part. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Anterior olfactory nucleus, lateral part. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Parabigeminal nucleus. Data represent fold expression difference in structure versus grey matter average expression.
QTL associated with loss of righting induced by ethanol 8. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (154849280)
Authors:
Radcliffe RA, Bohl ML, Lowe MV, Cycowski CS, Wehner JM
QTL associated with non-insulin-dependent diabetes mellitus 6. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (154748774)
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