Repeated H2O2 exposure drives cell cycle progression in an in vitro model of ulcerative colitis
Article first published online: 9 OCT 2013
© 2013 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
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Journal of Cellular and Molecular Medicine
Volume 17, Issue 12, pages 1619–1631, December 2013
How to Cite
Poehlmann, A., Reissig, K., Schönfeld, P., Walluscheck, D., Schinlauer, A., Hartig, R., Lessel, W., Guenther, T., Silver, A. and Roessner, A. (2013), Repeated H2O2 exposure drives cell cycle progression in an in vitro model of ulcerative colitis. Journal of Cellular and Molecular Medicine, 17: 1619–1631. doi: 10.1111/jcmm.12150
- Issue published online: 25 DEC 2013
- Article first published online: 9 OCT 2013
- Manuscript Accepted: 4 SEP 2013
- Manuscript Received: 18 JUL 2013
|jcmm12150-sup-0001-FigS1.tif||image/tif||1335K||Figure S1 Down-regulation of p54 splicing variants of phospho-JNK (▼) and up-regulation of p46 splicing variants of phospho-JNK (●) in C-cell cultures. Lysates from C1−C10 cells and from HCEC cells were immunoblotted with anti-phospho-JNK and -β-actin antibodies. x-fold expression is relative to HCEC cells and relative to β-actin, which was estimated through densitometric analysis.|
|jcmm12150-sup-0002-FigS2.tif||image/tif||1660K||Figure S2 Expression of caspase 9, 8 and 3 in C-cell cultures. Lysates from C1−C10 cells and HCEC cells were immunoblotted with anti-caspase 9, -caspase 8, -caspase 3 and -β-actin antibodies. β-actin served as loading control, and fold expression relative to HCEC is given below the blots. Data of HCEC and of C1−C3 cells are published in .|
|jcmm12150-sup-0003-FigS3.tif||image/tif||1117K||Figure S3 C3 and C10 cells show increased Il-6 release compared with HCEC cells.|
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