Copyright
©2008 The WJG Press and Baishideng.
World J Gastroenterol. Jun 28, 2008; 14(24): 3819-3828
Published online Jun 28, 2008. doi: 10.3748/wjg.14.3819
Published online Jun 28, 2008. doi: 10.3748/wjg.14.3819
Figure 1 A: Characterisation of the p53 status and analysis of parvoviral proteins in different human tumor cells by Western blot.
Cells were cultured for 2 d and lysed with RIPA buffer, and 50 µg of total protein was subjected to SDS-PAGE. For p53 protein detection, blots were incubated with the monoclonal DO-7 antibody; B: Production of parvoviral proteins in H-1 PV-infected p53 different tumor cells. Hep3B4P and HepG2 cells were H-1 PV-infected (MOI = 20 pfu/cell) and grown for 1 to 3 d. After lysis with RIPA buffer, 50 &mgr;g of total proteins were equally diluted and separated on SDS-PAGE. For parvoviral protein detection, blots were incubated with the NS1-specific antibody[37].
- Citation: Sieben M, Herzer K, Zeidler M, Heinrichs V, Leuchs B, Schuler M, Cornelis JJ, Galle PR, Rommelaere J, Moehler M. Killing of p53-deficient hepatoma cells by parvovirus H-1 and chemotherapeutics requires promyelocytic leukemia protein. World J Gastroenterol 2008; 14(24): 3819-3828
- URL: https://www.wjgnet.com/1007-9327/full/v14/i24/3819.htm
- DOI: https://dx.doi.org/10.3748/wjg.14.3819