We found that the inactivation of REST resulted in an increased abundance of K v7.4 channels at the transcript, protein, and functional levels. Null inactivation of full-length REST did not affect the development of normal HCs and SGNs but manifested as progressive hearing loss in adult mice. We performed conditional null deletion of Rest (cKO), mainly restricted to murine hair cells (HCs) and auditory neurons (aka spiral ganglion neurons ). The identity of REST target genes and molecular details of how REST regulates them are emerging. Repressor element 1-silencing transcription factor (REST) is a transcriptional repressor that recognizes neuron-restrictive silencer elements in the mammalian genomes in a tissue- and cell-specific manner. The Hebei Collaboration Innovation Center for Mechanism, Diagnosis and Treatment of Neurological and Psychiatric Disease, Hebei Medical University, China.Department of Physiology and Cell Biology, School of Medicine, University of Nevada, United States.Faculty of Biological Sciences, University of Leeds, United Kingdom.Kavli Institute for Nanoscience Discovery, University of Oxford, United Kingdom.Department of Psychiatry, University of Oxford, United Kingdom.Lab of Pathology, Hebei Medical University, China.The Key Laboratory of Neural and Vascular Biology, Ministry of Education, Hebei Medical University, China.
Center for Innovative Drug Research and Evaluation, Institute of Medical Science and Health, Hebei Medical University, China.Department of Pharmacology, The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, China.
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