QTL associated with bone response to mechanical loading 2. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (117360795)
QTL associated with bone response to mechanical loading 3. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (126594840)
Authors:
Kesavan C, Mohan S, Srivastava AK, Kapoor S, Wergedal JE, Yu H, Baylink DJ
QTL associated with wound healing/regeneration 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (105240821)
Authors:
Heber-Katz E, Leferovich JM, Bedelbaeva K, Gourevitch D
QTL associated with heterogeneity in eye lens protein photooxidation kinetics. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (129076217)
Authors:
Wisser KC, Schauerte JA, Burke DT, Galecki A, Chen S, Miller RA, Gafni A
QTL associated with mean platelet volume locus 2. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (105240821)
QTL associated with novelty/stress induced locomotor activation 7. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (119052549)
QTL associated with susceptibility to lung cancer 9. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (118625692)
QTL associated with tibia bone quality traits 2. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (129578831)
Authors:
Jiao Y, Chiu H, Fan Z, Jiao F, Eckstein EC, Beamer WG, Gu W
QTL associated with vertebral morphology and mechanical traits 9. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (129076217)
Authors:
Reeves GM, McCreadie BR, Chen S, Galecki AT, Burke DT, Miller RA, Goldstein SA
Alcohol use disorder (AUD) is a complex psychiatric disorder with strong genetic and environmental risk factors. We studied the molecular perturbations underlying risky drinking behavior by measuring transcriptome changes across the neurocircuitry of addiction in a genetic mouse model of binge drinking. Sixteen generations of selective breeding for high blood alcohol levels after a binge drinking session produced global changes in brain gene expression in alcohol-naïve High Drinking in the Dark (HDID-1) mice. Using gene expression profiles to generate circuit-level hypotheses, we developed a systems approach that integrated regulation of gene coexpression networks across multiple brain regions, neuron-specific transcriptional signatures, and knowledgebase analytics. Whole-cell, voltage-clamp recordings from nucleus accumbens shell neurons projecting to the ventral tegmental area showed differential ethanol-induced plasticity in HDID-1 and control mice and provided support for one of the hypotheses. There were similarities in gene networks between HDID-1 mouse brains and postmortem brains of human alcoholics, suggesting that some gene expression patterns associated with high alcohol consumption are conserved across species. This study demonstrated the value of gene networks for data integration across biological modalities and species to study mechanisms of disease.
Authors:
Laura B Ferguson, Lingling Zhang, Daniel Kircher, Shi Wang, R Dayne Mayfield, John C Crabbe, Richard A Morrisett, R Adron Harris, Igor Ponomarev
Alcohol use disorder (AUD) is a complex psychiatric disorder with strong genetic and environmental risk factors. We studied the molecular perturbations underlying risky drinking behavior by measuring transcriptome changes across the neurocircuitry of addiction in a genetic mouse model of binge drinking. Sixteen generations of selective breeding for high blood alcohol levels after a binge drinking session produced global changes in brain gene expression in alcohol-naïve High Drinking in the Dark (HDID-1) mice. Using gene expression profiles to generate circuit-level hypotheses, we developed a systems approach that integrated regulation of gene coexpression networks across multiple brain regions, neuron-specific transcriptional signatures, and knowledgebase analytics. Whole-cell, voltage-clamp recordings from nucleus accumbens shell neurons projecting to the ventral tegmental area showed differential ethanol-induced plasticity in HDID-1 and control mice and provided support for one of the hypotheses. There were similarities in gene networks between HDID-1 mouse brains and postmortem brains of human alcoholics, suggesting that some gene expression patterns associated with high alcohol consumption are conserved across species. This study demonstrated the value of gene networks for data integration across biological modalities and species to study mechanisms of disease.
Authors:
Laura B Ferguson, Lingling Zhang, Daniel Kircher, Shi Wang, R Dayne Mayfield, John C Crabbe, Richard A Morrisett, R Adron Harris, Igor Ponomarev
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