| Literature DB >> 30373551 |
Uwe Schirmer1, Heidi Fiegl2, Marco Pfeifer1, Alain G Zeimet2, Elisabeth Müller-Holzner2, Peter K Bode3, Verena Tischler3, Peter Altevogt4.
Abstract
Following publication of the original article [1], we have been alerted to errors in Figs. 2 and 8. In Fig. 2B, the GAPDH loading control for Hec1A cells is shown twice in error (in Fig. 2B and Fig. 2C). In Fig. 8, in testis case 1 (first column) the MAGE-A4 staining panel was repeated and also appears as the NY-ESO-1 staining panel in error. The corrected versions of Fig. 2 and Fig. 8 are shown below. We apologize for this inconvenience.Entities:
Year: 2018 PMID: 30373551 PMCID: PMC6205797 DOI: 10.1186/s12885-018-4928-y
Source DB: PubMed Journal: BMC Cancer ISSN: 1471-2407 Impact factor: 4.430
Fig. 2Regulation of L1CAM expression by epigenetic mechanisms. (a) RT-PCR analysis of cells treated for 5 days with the indicated concentration of 5-AzaC, TSA or both compounds. DMSO was used as a mock control. Cells were lysed and mRNA was isolated and transcribed into cDNA. β-actin served as internal standard. (b) Cells were treated as described above and cell lysates were prepared for Western blot analysis. MAb L1-11A was used as a primary antibody followed by peroxidase conjugated Goat anti mouse IgG and ECL detection. (c) TSA and VA up-regulate L1CAM expression. Cells were treated and analyzed as described in (b)
Fig. 8IHC analysis of testis and EC tissues. Expression of NY-ESO-1 and MAGE-A4 but absence of L1CAM in normal human testis tissue. Conversely, L1CAM is expressed in type II EC but NY-ESO-1 and MAGE-A4 are undetectable. Note that a representative case of n = 5 is shown. Sequential tissue sections were analysed by IHC