DNA damage-induced translocation of S100A11 into the nucleus regulates cell proliferation
1 Core Unit Chip Application (CUCA), Institute of Human Genetics and Anthropology, University Hospital Jena, 07740 Jena, Germany
2 Department of Molecular Biology, Fritz Lipmann Institut (FLI) - Leibniz Institute for Age Research, 07743 Jena, Germany
3 Current Address: Abt. Molekulare Onkologie, Universitätsmedizin Göttingen, Georg-August-Universität, 37077 Göttingen, Germany
4 Current Address: Membrane Trafficking Group; Fritz Lipmann Institut (FLI) - Leibniz Institute for Age Research, 07743 Jena, Germany
5 Current Address: Biomolecular Photonics Group, University Hospital Jena, 07740 Jena, Germany
BMC Cell Biology 2010, 11:100 doi:10.1186/1471-2121-11-100Published: 17 December 2010
Additional file 1:
Expression analysis of S100A11 protein in different human cell lines by immunoblotting. Protein extracts of U-2 OS osteosacroma cells (lane 1) and HaCaT keratinocytes (lane 2) were subjected to immunoblotting against endogenous S100A11 using a specific antibody. As a control for equal protein loading corresponding actin levels were shown by immunoblot.
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Additional file 2:
Distribution of GFP in DNA damaged U-2 OS cells. U-2 OS cells were transfected with a GFP construct, treated with bleomycin (BLM; 12.5 IU/ml) for 30 min and analyzed by two-color immunostaining followed by laser scanning microscopy for GFP (green) and for γH2AX (red) 30 min after BLM treatment.
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Additional file 3:
Translocation of S100A11 into the nucleus of human A431 cells after stress stimulation. Fixed cells treated with bleomycin (BLM) for 30 min were immunostained with anti-S100A11 antibody and anti-γH2AX antibody. In BLM treated cells increased staining of S100A11 in the nucleus can be observed.
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