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 in the Weimbs Laboratory is centered around two related areas of investigation:
- 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.
- 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.
Soo-Hoo L, Banna CD, Radeke CM, Sharma N, Albertolle ME, Low SH, Weimbs T, Vandenberg CA. The SNARE Protein Syntaxin 3 Confers Specificity for Polarized Axonal Trafficking in Neurons. PLoS One. 2016 ;11(9):e0163671.
Doerr N, Wang Y, Kipp KR, Liu G, Benza JJ, Pletnev V, Pavlov TS, Staruschenko A, Mohieldin AM, Takahashi M, Nauli SM, Weimbs T. Regulation of Polycystin-1 Function by Calmodulin Binding. PLoS One. 2016 ;11(8):e0161525.
Kipp KR, Rezaei M, Lin L, Dewey EC, Weimbs T. A mild reduction of food intake slows disease progression in an orthologous mouse model of polycystic kidney disease. Am J Physiol Renal Physiol. 2016 ;310: F726 –F731.
Rothé B, Leal-Esteban L, Bernet F, Urfer S, Doerr N, Weimbs T, Iwaszkiewicz J, Constam DB. Bicc1 polymerization regulates the localization and silencing of bound mRNA. Mol Cell Biol. 2015 ;35:3339-3353.
Olsan EE, Matsushita T, Rezaei M, Weimbs T. Exploitation of the Polymeric Immunoglobulin Receptor for Antibody Targeting to Renal Cyst Lumens in Polycystic Kidney Disease. J Biol Chem. 2015 ;290:15679–15686.
Talbot JJ, Song X, Wang X, Rinschen MM, Doerr N, LaRiviere WB, Schermer B, Pei YP, Torres VE, Weimbs T. The cleaved cytoplasmic tail of polycystin-1 regulates Src-dependent STAT3 activation. J Am Soc Nephrol. 2014 ;25(8):1737-48.
Weimbs T, Talbot JJ. STAT3 signaling in polycystic kidney disease. Drug Discovery Today: Disease Mechanisms. 2013 ;10(3-4):e113-e118.
Weimbs T, Olsan EE, Talbot JJ. Regulation of STATs by polycystin-1 and their role in polycystic kidney disease. JAK-STAT. 2013 ;2:0–1.
Stayner C, Shields J, Slobbe L, Shillingford JM, Weimbs T, Eccles MR. Rapamycin-mediated suppression of renal cyst expansion in del34 Pkd1-/- mutant mouse embryos: An investigation of the feasibility of renal cyst prevention in the foetus. Nephrology. 2012 ;17:739–747.
Shillingford JM, Leamon CP, Vlahov IR, Weimbs T. Folate-conjugated rapamycin slows progression of polycystic kidney disease. Journal of the American Society of Nephrology. 2012 ;23:1674.