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The Habc domain of syntaxin 3 is a ubiquitin binding domain. Sci Rep. 2020 ;10(1):21350. .
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Casein kinase 1ε and 1α as novel players in polycystic kidney disease and mechanistic targets for (R)-roscovitine and (S)-CR8. Am J Physiol Renal Physiol. 2018 ;315:F57–F73. .
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Emerging targeted strategies for the treatment of autosomal dominant polycystic kidney disease. Clinical Kidney Journal. 2018 ;11(suppl_1):i27–i38. .
Tracking Endocytosis and Intracellular Trafficking of Epitope-tagged Syntaxin 3 by Antibody Feeding in Live, Polarized MDCK Cells. Bio-Protocol. 2018 ;8(3):e2453. .
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Regulation of Polycystin-1 Function by Calmodulin Binding. PLoS One. 2016 ;11(8):e0161525. .
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. .
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Regulation of STATs by polycystin-1 and their role in polycystic kidney disease. JAK-STAT. 2013 ;2:0–1. .
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. .
Folate-conjugated rapamycin slows progression of polycystic kidney disease. Journal of the American Society of Nephrology. 2012 ;23:1674. .
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Regulation of mTOR by polycystin-1: is polycystic kidney disease a case of futile repair?. Cell Cycle. 2006 ;5:2425–2429. .
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. 2006 ;103:5466–5471. .
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