QTL for high-dose ethanol actions on Chr14 at D14Mit1 (5.65 Mbp , Build 37)
Description:
high-dose ethanol actions spans 0.00 - 30.65 Mbp (NCBI Build 37) on Chr14. 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 chewing on Chr14 at D14Mit54 (23.48 Mbp , Build 37)
Description:
METH responses for chewing spans 0.00 - 48.48 Mbp (NCBI Build 37) on Chr14. 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 behavioral response to methamphetamines 9. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (36137026)
QTL associated with dystrophic cardiac calcinosis 4. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (30304100)
QTL associated with insulin dependent diabetes susceptibility 12. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (35170432)
QTL associated with insulin dependent diabetes susceptibility 8. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (21656627)
QTL associated with modifier of ocular retardation 2. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (25745310)
QTL associated with resistance to thymic deletion 3. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (13403047)
Authors:
Liston A, Lesage S, Gray DH, O\'Reilly LA, Strasser A, Fahrer AM, Boyd RL, Wilson J, Baxter AG, Gallo EM, Crabtree GR, Peng K, Wilson SR, Goodnow CC
QTL associated with susceptibility to lung cancer 13. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (36918833)
QTL associated with Theiler's murine encephalomyelitis virus induced demyelinating disease susceptibility 3. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (36137026)
Authors:
Bureau JF, Drescher KM, Pease LR, Vikoren T, Delcroix M, Zoecklein L, Brahic M, Rodriguez M
QTL associated with white blood cell quantitative locus 6. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (17356225)
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Bipolar disorder. The EFO term bipolar disorder was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
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
Alcohol transcriptome changes in mice microglia total homogenate 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
Data from GEO GSE194368 and analyzed using GEO2R, only top gene shown. Authors identified transcriptional adaptations of GR signaling in the amygdala of humans with OUD. Thus, GRs, their coregulators and downstream systems may represent viable therapeutic targets to treat the “stress side” of OUD.
Authors:
Stephanie A Carmack, Janaina C M Vendruscolo, M Adrienne McGinn, Jorge Miranda-Barrientos, Vez Repunte-Canonigo, Gabriel D Bosse, Daniele Mercatelli, Federico M Giorgi, Yu Fu, Anthony J Hinrich, Francine M Jodelka, Karen Ling, Robert O Messing, Randall T Peterson, Frank Rigo, Scott Edwards, Pietro P Sanna, Marisela Morales, Michelle L Hastings, George F Koob, Leandro F Vendruscolo
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