Department of Neuroscience, Cell Biology, & Anatomy
Medical Research Building, Room 2.143D (O)/ 2.100 (L)
Route: 1069 | Tel: (409) 266-1659 | firstname.lastname@example.org
Education and Training
Postdoctoral Fellow: Johns Hopkins University School of Medicine and The Scripps Research Institute
Ph.D.: University of Texas Graduate School of Biomedical Science
Living cells constantly sense and respond to mechanical stimuli arising from the outer world, neighboring cells and surrounding extracellular matrix by converting them into biochemical signals that trigger specific cellular responses. This process is
termed mechanotransduction and is fundamental to hearing, touch, nociception, respiration, and proprioception. However, the molecules that mediate/regulate mechanotransduction are poorly defined. Thus, identifying molecules underlying mechanotransduction
in mechanosensory cells, uncovering their modulating mechanisms, and describing their roles in varies diseases/symptoms are the primary foci of sensory biology studies, which hold the promise to understand sensory processing and uncover novel strategies
for mechanosensory disorders.
My long-term research goals involve the development of a comprehensive understanding of the molecular mechanisms of sensory perception and related disorders in order to develop new methods for treatment. In the near
future, I will identify molecules underlying/modulating mechanotransduction in sensory neurons and define the mechanisms underlying the plasticity of mechanotransduction in varies diseases/symptoms, including deafness and mechanical pain.
Wu Z*, Li L, Li G, Xu G, and Yang Q*. Decreasing neuronal excitability by targeting KCNQ channels improves neurobehavioral function after spinal cord injury. J Pharmacol Exp Ther., 2020; 373: 72-80 * Co-corresponding author
Cunningham C, Qiu X, Wu Z, Zhao B, Peng G, Kim YH, Lauer A, and Müller U. TMIE defines pore and gating properties of the mechanotransduction channel of mammalian cochlear hair cells. Neuron, 2020; 107: 126-143
Cunningham C, Wu Z, Jafari A, Zhao B, Schrode K, Harkins-Perry S, Lauer A, Mueller U. The murine catecholamine methyltransferase mTOMT is essential for mechanotransduction by cochlear hair cells. Elife, 2017; e24318
Wu Z, Grillet N, Zhao B, Cunningham C, Harkins-Perry S, Coste B, Ranade S, Zebarjadi N, Beurg M, Fettiplace R, Patapoutian A, Müller U. Mechanosensory hair cells express two molecularly distinct mechanotransduction channels. Nat.
Neurosci., 2017; 20: 24-33
Zhao B, Wu Z, Müller U. Murine Fam65b forms ring-like structures at the base of stereocilia critical for mechanosensory hair cell function. Elife, 2016; 5: e14222. PMCID: PMC4898930
Zhao B, Wu Z, Grillet N, Yan L, Xiong W, Harkins-Perry S, Müller U. TMIE is an essential component of the mechanotransduction machinery of cochlear hair cells. Neuron. 2014; 84: 954-967. PMCID: PMC4258123
Yang Q, Wu Z, Hadden JK, Odem MA, Zuo Y, Crook RJ, Frost JA, Walters ET. Persistent pain after spinal cord injury is maintained by primary afferent activity. J. Neurosci. 2014; 34: 10765-10769. PMCID: PMC4122805Wu Z
Yang Q, Crook RJ, O'Neil RG, Walters ET. TRPV1 channels make major contributions to behavioral hypersensitivity and spontaneous activity in nociceptors after spinal cord injury. Pain. 2013; 154: 2130-2141.