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Travis Salisbury

Associate Professor
Department of Biomedical Sciences
Marshall University
United States of America

Biography

I have 12 years of experience in studies on regulation of gene expression in response to signaling. My work on regulated gene expression started during my postdoctoral training. My research identified that gonadotropin releasing hormone (GnRH), which signals through a G protein coupled receptor (GPCR), regulates gene expression by activating the transcriptional coactivator β-catenin. Finding that GPCR signaling regulated β- catenin activity was novel, because β-catenin had historically been associated with the developmental Wnt signaling pathway. Currently, I supervise an active laboratory, teach medical and graduate students and I was promoted to associate professor with tenure in 2015. My work remains focused on signal-regulated gene expression. Our recent studies have identified that the aryl hydrocarbon receptor (AHR), which is a ligandactivated transcription factor, responds to and mediates signaling pathways in breast cancer cells including insulin like growth factor 2 (IGF2), tumor necrosis factor (TNF) and adipokines. Evidence that IGF2, TNF, and adipokines signal through AHR is an important shift in its role, considering that AHR is best known for mediating the toxic and gene expression effects of the environmental toxicant TCDD

Research Interest

Dioxins, signaling cross-talk

Publications

  • Welcoming beta-catenin to the gonadotropin-releasing hormone transcriptional network in gonadotropes.

  • Maximal activity of the luteinizing hormone beta-subunit gene requires beta-catenin.

  • In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin and 2,3,4,7,8-pentachlorodibenzofuran reduces growth and disrupts reproductive parameters in female rats.

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