These authors contributed equally to this work.
Expression of pituitary tumor–transforming gene 1 (PTTG1)/securin in hepatitis B virus (HBV)-associated liver diseases: Evidence for an HBV X protein–mediated inhibition of PTTG1 ubiquitination and degradation†
Version of Record online: 30 NOV 2009
Copyright © 2009 American Association for the Study of Liver Diseases
Volume 51, Issue 3, pages 777–787, March 2010
How to Cite
Molina-Jiménez, F., Benedicto, I., Murata, M., Martín-Vílchez, S., Seki, T., Antonio Pintor-Toro, J., Tortolero, M., Moreno-Otero, R., Okazaki, K., Koike, K., Barbero, J. L., Matsuzaki, K., Majano, P. L. and López-Cabrera, M. (2010), Expression of pituitary tumor–transforming gene 1 (PTTG1)/securin in hepatitis B virus (HBV)-associated liver diseases: Evidence for an HBV X protein–mediated inhibition of PTTG1 ubiquitination and degradation. Hepatology, 51: 777–787. doi: 10.1002/hep.23468
Potential conflict of interest: Nothing to report.
- Issue online: 2 MAR 2010
- Version of Record online: 30 NOV 2009
- Accepted manuscript online: 30 NOV 2009 12:00AM EST
- Manuscript Accepted: 28 OCT 2009
- Manuscript Received: 12 MAR 2009
- CIBERehd (funded by ISCIII)
- Ministerio de Educación y Ciencia. Grant Number: SAF2007-61201
- Ministerio de Educación y Ciencia. Grant Numbers: CP03/0020 from ISCIII, SAF2007-60677
- Fundación para la Investigación Biomédica del Hospital Universitario de la Princesa
Additional Supporting Information may be found in the online version of this article.
|HEP_23468_sm_Suppfig1.tif||598K||Supplementary figure S1. HCC sections of HBx transgenic mouse livers were stained for immunofluorescence to simultaneously detect PTTG1 (red) and HBx (green). Yellow color indicates overlap of proteins. Bar, 50 μm.|
|HEP_23468_sm_Suppfig2.tif||183K||Supplementary figure S2. (A) Chang liver, p34X, AML12 4p and 4pX cells were cultured with or without Dox for 24 h, and HBx and PTTG1 protein levels were analyzed by Western blot. Tubulin expression was assessed to ensure equal protein loading of all samples. (B) Flow cytometry analysis of cell cycle progression of p34X and 4pX cells 24 h after induction of HBx expression. Values represent the mean ± SD of three independent experiments performed at least in duplicate. (*p≤0,05 vs HBx non-expressing cells, Mann-Whitney U test).|
|HEP_23468_sm_Suppfig3.tif||25K||Supplementary figure S3. PTTG1 mRNA levels in 4pX cells in response to HBx expression were measured by quantitative RT-PCR. The results were normalized with histone H3 and represented as fold induction over control. Results are presented as the mean ± SD of three independent experiments.|
|HEP_23468_sm_Suppfig4.tif||278K||Supplementary figure S4. (A) Chang liver cells were treated with okadaic acid (OA) (1 μM), MG132 (10 μM) or both for 2 h after 48 h of doxycycline treatment. Lysates were subsequently analyzed by Western blot for the detection of PTTG1. Tubulin expression was assessed to ensure equal protein loading. (B) Hela cells were co-transfected with pCGN-HA-ubiquitin, pcDNA-PTTG1 and either pSV-HBx or pSV-hygro plasmids and treated for 4 h with MG132 (10 μM). Cell lysates were immunoprecipitated with anti-PTTG1 mAb and immunoblotted with anti-PTTG1 (bottom) and anti-HA (top) Abs. Representative results of at least two independent experiments are shown.|
|HEP_23468_sm_Suppfig5.tif||135K||Supplementary figure S5. Chang liver cells were treated for 2 h with okadaic acid (OA; 1μM) and/or MG132 (10μM) after 48 h of transfection with control or Cul1 siRNA. Lysates were subsequently analyzed by Western blot for the detection of PTTG1 and Cul1. Tubulin expression was assessed to ensure equal protein loading.|
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