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Katharine Smith, PhD

Assistant Professor

Contact Information:

University of Colorado Denver
Department of Pharmacology
Mail Stop 8303, RC1-North
12800 East 19th Ave
Aurora CO 80045

Phone: (303) 724-0267
Fax: (303) 724-3663
Office: RC1-North, P18-6117

Affiliated Programs


Selected publications:

  1. Katharine R. Smith, Katherine J. Kopeikina, Jessica Fawcett-Patel, Katherine Leaderbrand, Ruoqi Gao, Britta Schürmann, Kristoffer Myczek, Jelena Radulovic, Geoffrey T. Swanson and Peter Penzes (2014). Psychiatric risk factorANK3/Ankyrin-G nanodomains regulate the structure and function of glutamatergic synapses, Neuron, PMID:25374361.  
  2. Katharine R. Smith, Elizabeth C. Davenport, Jing Wei, Xiangning Li, Manavendra Pathania, Victoria Vaccaro, Zhen Yanand Josef T. Kittler (2014). GIT1 and bPIX are essential for GABAA receptor synaptic stability and inhibitory neurotransmission, Cell Reports, PMID:25284783.
  3. Katharine R. Smith, James Muir, Yijian Rao, Marietta Browarski, Marielle Gruenig, David F. Sheehan, Volker Haucke, Josef T Kittler (2012), Stabilisation of GABAA receptors at endocytic zones is mediated by an AP2 binding motif within the GABAA receptor β3 subunit, Journal of Neuroscience, PMID: 22396422.
  4. James Muir, I Lorena Arancibia-Carcamo*, Andrew F MacAskill*, Katharine R. Smith*, Lewis Griffin, Josef T Kittler (2010), NMDA receptors regulate GABAA receptor lateral mobility and clustering at inhibitory synapses through serine 327 on theγ2 subunit, Proc Natl Acad Sci U S A, PMID: 20823221, *equal contribution to the work. 
  5. Katharine R. Smith and Josef T Kittler (2010), The cell biology of synaptic inhibition in health and disease, Current Opinion in Neurobiology, PMID: 20650630. 
  6. Katharine R. Smith*, Kristina McAinsh*, G Chen, I Lorena Arancibia-Carcamo, Volker Haucke, Zhen Yan, Stephen J Moss, Josef T Kittler (2008), Regulation of inhibitory synaptic transmission by a conserved atypical interaction of GABAAreceptor β- and γ-subunits with the clathrin AP2 adaptor, Neuropharmacology, PMID: 18662706.*equal contribution to the work.​