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The detection of noxious or damaging stimuli is an ancient process that alerts living organisms to environmental dangers. Harmful stimuli activate receptors on specific sensory neurons called nociceptors, which mediate information transfer via the spinal cord to higher order processing centers resulting in protective behaviors and awareness of pain. Pain disorders are associated with many human diseases and constitute a burden in human societies. In a recent study on CIP (Congenital Insensitivity to Pain), several mutations have been identified in a novel candidate disease-causing gene, PRDM12. Prdm12 encodes an evolutionarily conserved zinc finger transcription factor that is strongly expressed in the developing and adult nervous system, including in the dorsal root ganglia that contain the cell bodies of the sensory neurons. A recent work of the laboratory has shown that Prdm12 is required for sensory neurogenesis in the frog. We are currently studying in mammals its role and mecanism of action in nociceptor genenesis and in pain perception in the adult, using genetic approaches in the mouse and the identification of its in vivo targets (using RNA-seq and ChIP-seq). Emerging evidences link epigenetic mechanisms to chronic and neuropathic pain. Therefore, our studies on Prdm12 could contribute to the development of novel therapeutic options for pain relief.
• F.R.S.-FNRS et Fonds associés (hors FRIA)
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