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Dr. Kathryn Medler

Associate Professor
Cooke 619
phone: (716) 645-4947
email: kmedler@buffalo.edu

Further research info

Dr. Medler details her research on
National Public Radio's Academic Minute

 

Research Summary

My lab studies the physiology of signal transduction pathways and the regulation of these pathways in neuronal systems. We focus on peripheral sensory systems, primarily the taste system. The long term goal of the lab is to understand how signaling mechanisms are regulated within taste cells and how this regulation impacts the generation of the stimulus signal to the brain. We use molecular and physiological techniques, including patch clamp analysis and calcium imaging to investigate how signaling mechanisms function in taste cells.

Selected Publications

  • Gao, Y. , Toska, E. , Denmon, D., Roberts, S.G.E., and Medler, K.F. (2014) WT1 regulates the development of the posterior taste field. Development In press.
  • Medler, K.F. (2014) Taste cells and calcium signaling. Invited chapter in “Calcium: Chemistry, Analysis, Function, and Effects” for Food and Nutritional Components in Focus. Editor: Professor Victor R Preedy. Published by Royal Society of Chemistry
  • Maliphol, A.B., Garth, D.J. and Medler, K.F., (2013) Diet-induced obesity reduces the responsiveness of the peripheral taste system. PLoS ONE 8(11):e79403.
  • Toska, E., Shandilya, J., Medler, K.F., Goodfellow, S.J., and Roberts, S.G.E. (2013) Prohibitin is required for transcriptional repression by the WT1-BASP1 complex. Oncogene 10.1038/onc.2013.447.
  • Rebello, M.R., Maliphol, A.B., and Medler, K.F. (2013). Ryanodine receptors selectively interact with L type calcium channels in mouse taste cells. PLoS ONE 8(6):e68174
  • Toska, E., Campbell, H.A., Shandilya, J., Goodfellow, S.J., Shore, P., Medler, K.F., and Roberts, S.G.E. (2012) Repression of transcription by WT1-BASP1 requires the myristoylation of BASP1 and the PIP2-dependent recruitment of Histone Deacetylase. Cell Reports 2(3):462-9.
  • Goodfellow, S.J., Rebello, M.R., Toska, E., Zeef,L., Rudd, S., Medler, K.F., and Roberts, S.G.E. (2011) WT1 and its transcriptional cofactor BASP1 redirect the differentiation pathway of an established blood cell line. Biochemical Journal 435(1):113-25.
  • Rebello, M. R., Aktas, A and Medler, K.F. (2011) Expression of calcium binding proteins in mouse taste receptor cells. J. Histo & Cyto. 59(5): 530-539.
  • Medler, K.F. (2011) Multiple roles for TRPs in the taste system: Not your typical TRPs. Invited chapter in “The Transient receptor potential channels” for the Advances in Experimental Medicine and Biology 704:831-46. Editor: Dr. Md. Shahidul Islam. Published by Springer, Inc.
  • Starostik, M.R, Rebello, M.R., Cotter, K.A. , Kulik, A. and Medler, K.F. (2010) Expression of GABAergic receptors in mouse taste receptor cells. PLoS ONE 5(10): e13639.
  • Rebello, M. R. and Medler, K.F. (2010) Ryanodine receptors selectively contribute to taste evoked responses in mouse taste receptor cells. Eur. J. Neurosci. 32(11): 1825-1835.
  • Medler, K.F. (2010) Calcium signaling in taste cells: Regulation Required. Invited referred review for Chemical Senses. 35(9):753-65
  • Szebenyi, S.A., Laskowski, A.I., and Medler, K.F. (2010) Sodium/calcium exchangers selectively regulate calcium signaling in mouse taste receptor cells. J. Neurophys. 104: 529-538.
  • Laskowski, A.I. and Medler, K.F.(2009) Sodium/calcium exchangers contribute to the regulation of cytosolic calcium levels in mouse taste cells. J. Physiol. 587(16): 4077-4089.selected for Faculty of 1000 Biology
  • Hacker, K. and Medler, K.F. (2008) Mitochondrial calcium buffering contributes to the maintenance of basal calcium levels in mouse taste cells. J. Neurophys.100(4):2177-91
  • Medler, K.F. (2008) Signaling mechanisms controlling taste cell function. CREGE, 18 (2): 125-137.
  • Clapp, T.R., Medler, K.F., Damak, S., Margolskee R.F., and Kinnamon, S.C. (2006) Mouse taste cells with G protein-coupled taste receptors lack voltage-gated calcium channels and SNAP-25. BMC Biology 4(1):7 *highly accessed designation.
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