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Thomas Weimbs

Associate Professor

Contact Information

Phone: (805) 893-4144
Email: weimbs@lifesci.ucsb.edu
Office: 2113 LSB
Website: Weimbs Lab

Address

Molecular, Cellular, and Developmental Biology
University of California, Santa Barbara
Santa Barbara, CA 93106-9625

Bio

Dr. Weimbs received his doctoral degree from the Department of Biochemistry of the University of Cologne, Germany, in 1993. He conducted postdoctoral research at the Department of Anatomy, University of California at San Francisco until 1999. In the same year, he joined the Department of Cell Biology in the Lerner Research Institute of the Cleveland Clinic as an Assistant Professor where he established his research laboratory focusing on investigating membrane trafficking and epithelial cell polarity as well as molecular mechanisms underlying polycystic kidney disease. In 2005, Dr. Weimbs was recruited to the Department of Molecular, Cellular, and Developmental Biology and moved his laboratory to UCSB. Dr. Weimbs is currently an Associate Professor in MCDB and in the Neuroscience Research Institute.

Research

Research in the Weimbs Laboratory is centered around two related areas of investigation:

  1. Autosomal-dominant polycystic kidney disease (ADPKD) is considered the most common life-threatening, monogenic inherited disease. ADPKD affects over 600,000 people in the US alone, is a leading cause of kidney failure, and also leads to significant cardiovascular complications. Currently, no treatment exists for this disease, and most patients require renal transplantation or life-long dialysis for survival. Research in the Weimbs Laboratory is aimed at understanding the molecular mechanisms that lead to renal cyst growth and disease progression, and to identify and test new strategies for therapy.
  2. SNAREs and epithelial cell polarity: Most human cell types are "polarized", i.e. they exhibit asymmetry, which is essential to their function. This includes epithelial cells that make up most major human organs such as the kidney, liver, lungs, GI tract, exocrine glands etc. Carcinogenesis is accompanied by the progressive loss of epithelial cell polarity. Current research in the Weimbs lab is aimed at investigating novel signaling functions of so-called SNARE proteins which are essential for the establishment and maintenance of cell polarity.

Selected Publications

  • Jonathan M. Shillingford, Christopher P. Leamon, Iontcho R. Vlahov, and Thomas Weimbs (2012) Folate-Conjugated Rapamycin Slows Progression of Polycystic Kidney Disease J Am Soc Nephrol 23: Published online before print August 2, 2012
  • Erin E. Olsan, Sambuddho Mukherjee, Beatrix Wulkersdorfer, Jonathan M. Shillingford, Adrian J. Giovannone, Gueorgui Todorov, Xuewen Song, York Pei, and Thomas Weimbs (2011) Signal transducer and activator of transcription-6 (STAT6) inhibition suppresses renal cyst growth in polycystic kidney disease. Proceedings of the National Academy of Sciences of the USA 108, 18067-18072
  • Elena Reales, Nikunj Sharma, Seng Hui Low, Heike Fölsch, Thomas Weimbs (2011) Basolateral Sorting of Syntaxin 4 Is Dependent on Its N-terminal Domain and the AP1B Clathrin Adaptor, and Required for the Epithelial Cell Polarity. PLoS ONE 6(6): e21181
  • Talbot, J, J Shillingford, S Vasanth, N Doerr, S Mukherjee, M Kinter, T Watnick, and T Weimbs (2011) Polycystin-1 Regulates STAT Activity by a Dual Mechanism. Proceedings of the National Academy of Sciences of the USA 108, 7985-7990
  • Weimbs T (2011) Third-Hit Signaling in Renal Cyst Formation. J. Am. Soc. Nephrol. 22, 793-795
  • Shillingford, JM, Piontek, KB, Germino, GG and Weimbs, T (2010) Rapamycin Ameliorates PKD Resulting from Conditional Inactivation of Pkd1. J Am Soc Nephrol, 21, 489-97
  • Weimbs T. (2007) Polycystic kidney disease and renal injury repair: common pathways, fluid flow and the function of polycystin-1. Am J Physiol Renal Physiol. 293, F1423–F1432
  • Sharma N, Low SH, Misra S, Pallavi B, Weimbs T (2006) Apical targeting of syntaxin 3 is essential for epithelial cell polarity The Journal of Cell Biology 173, 937–948
  • Shillingford JM, Murcia NS, Larson CH, Low SH, Hedgepeth R, Brown N, Flask CA, Novick AC, Goldfarb DA, Kramer-Zucker A, Walz G, Piontek KB, Germino GG, Weimbs T (2006) The mTOR pathway is regulated by polycystin-1 and its inhibition reverses renal cystogenesis in polycystic kidney disease. Proceedings of the National Academy of Sciences of the USA 103, 5466-5471
  • Low SH, Vasanji A, Nanduri J, He M, Sharma N, Koo M, Drazba J, Weimbs T. (2006) Syntaxins 3 and 4 Are Concentrated in Separate Clusters on the Plasma Membrane prior to the Establishment of Cell Polarity. Molecular Biology of the Cell 17, 977-989
  • Low SH, Vasanth S, Larson CH, Mukherjee S, Sharma N, Kinter MT, Kane ME, Obara T, and Weimbs T (2006) Polycystin-1, STAT6 and P100 function in a novel pathway that transduces ciliary mechanosensation to gene expression and is activated in polycystic kidney disease. Developmental Cell 10, 57-69