QTL for METH responses for home cage activity on Chr3 at Evi1 (30.85 Mbp , Build 37)
Description:
METH responses for home cage activity spans 5.85 - 55.85 Mbp (NCBI Build 37) on Chr3. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
QTL for high-dose ethanol actions on Chr3 at D3Mit21 (39.41 Mbp , Build 37)
Description:
high-dose ethanol actions spans 14.41 - 64.41 Mbp (NCBI Build 37) on Chr3. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
Authors:
Erwin VG, Markel PD, Johnson TE, Gehle VM, Jones BC
QTL for METH responses for home cage activity on Chr3 at Il2 (39.85 Mbp , Build 37)
Description:
METH responses for home cage activity spans 14.85 - 64.85 Mbp (NCBI Build 37) on Chr3. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
QTL associated with experimental allergic encephalomyelitis susceptibility 20. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (28475226)
QTL associated with HIV-associated nephropathy 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (24235798)
QTL associated with thymocyte proliferative response 3. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (21370177)
Authors:
Hsu HC, Mountz JD, Williams RW, Shelton BJ, Yang PA, Matsuki Y, Xu X, Dodd CH, Li L, Geiger H, Zhang HG, Van Zant G
Kyoto Encyclopedia of Genes and Genomes (KEGG) Geneset. This geneset contains genes that participate in the "Osteoclast differentiation" pathway. This set was automatically constructed using the KEGG API and enumerating all mouse pathways.
gene2kegg v. 0.1.1
Last updated 2015.09.10
Differentially expressed genes and fold change (FDR-adjusted P-value < 0.05) between BCG-challenged and Control mice within cell type and supporting literature review.
Alcohol transcriptome changes in mice microglia p-value
Description:
Microglia are fundamentally important immune cells within the central nervous system (CNS) that respond to environmental challenges to maintain normal physiological processes. Alterations in steady-state cellular function and over-activation of microglia can facilitate the initiation and progression of neuropathological conditions such as Alzheimer’s disease, Multiple Sclerosis, and Major Depressive Disorder. Alcohol consumption disrupts signaling pathways including both innate and adaptive immune responses that are necessary for CNS homeostasis. Coordinate expression of these genes is not ascertained from an admixture of CNS cell-types, underscoring the importance of examining isolated cellular populations to reveal systematic gene expression changes arising from mature microglia. Unbiased RNA-Seq profiling was used to identify gene expression changes in isolated prefrontal cortical microglia in response to recurring bouts of voluntary alcohol drinking behavior. The voluntary ethanol paradigm utilizes long-term consumption ethanol that results in escalated alcohol intake and altered cortical plasticity that is seen in humans. Gene coexpression analysis identified a coordinately regulated group of genes, unique to microglia, that collectively are associated with alcohol consumption. Genes within this group are involved in toll-like receptor signaling and transforming growth factor beta signaling. Network connectivity of this group identified Siglech as a putative hub gene and highlighted the potential importance of proteases in the microglial response to chronic ethanol. In conclusion, we identified a distinctive microglial gene expression signature for neuroimmune responses related to alcohol consumption that provides valuable insight into microglia-specific changes underlying the development of substance abuse, and possibly other CNS disorders.
Authors:
Gizelle M McCarthy, Sean P Farris, Yuri A Blednov, R Adron Harris, R Dayne Mayfield
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