These authors contributed equally to this work.
Evidence that TMEM67 causes polycystic kidney disease through activation of JNK/ERK-dependent pathways
Article first published online: 16 APR 2013
© 2013 International Federation for Cell Biology
Cell Biology International
Volume 37, Issue 7, pages 694–702, July 2013
How to Cite
Du, E., Li, H., Jin, S., Hu, X., Qiu, M. and Han, R. (2013), Evidence that TMEM67 causes polycystic kidney disease through activation of JNK/ERK-dependent pathways. Cell Biology International, 37: 694–702. doi: 10.1002/cbin.10081
- Issue published online: 4 JUN 2013
- Article first published online: 16 APR 2013
- Accepted manuscript online: 2 MAR 2013 08:30AM EST
- Manuscript Accepted: 13 FEB 2013
- Manuscript Received: 13 NOV 2012
Additional supporting information can be found in the online version of this article:
|cbin10081-sm-0001-SupFig-S1.jpg||512K||Figure S1. Canonical Wnt signalling was not activated by overexpression of TMEM67. HEK 293 cells were transfected with control vector (−) or Flag-tagged-TMEM67 vector (+) for 48. (A) Cells were analysed by Western blotting with antibodies against p-GSK3β (Ser 9) and GSK. β-Actin was visualised as a loading control. (B) Western blots were statistically analysed following the normalisation by using Image J densitometry. The bar graphs represent the level of phosphorylation of GSK3β (n = 3).|
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