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NF-κB contributes to transcription of placenta growth factor and interacts with metal responsive transcription factor-1 in hypoxic human cells

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Biol. Chem., Vol. 387, pp. 113, January 2006• Copyright  by Walter de Gruyter • Berlin • New York. DOI 10.1515/BC.2006.015

2006/2111051

Article in press - uncorrected proof

Erratum

NF-kB contributes to transcription of placenta growth factor

and interacts with metal responsive transcription factor-1 in

hypoxic human cells

Mirjam Cramer1, Ivana Nagy1, Brian J. Murphy2, Max Gassmann3, Michael O. Hottiger4, Oleg

Georgiev1and Walter Schaffner1,*

1Institut fu¨r Molekularbiologie, Universita¨t Zu¨rich, Winterthurerstrasse 190, CH-8057 Zu¨rich, Switzerland 2Biosciences Division, SRI International, Menlo Park, CA 94025, USA

3Institute for Veterinary Physiology, Vetsuisse Faculty and Zurich Center for Integrative Human Physiology (ZIHP),

University of Zurich, Winterthurerstrasse 260, CH-8057 Zurich, Switzerland

4Institut fu¨r Veterina¨rbiochemie und Molekularbiologie, Universita¨t Zu¨rich, Winterthurerstrasse 190, CH-8057 Zu¨rich,

Switzerland

* Corresponding author

e-mail: walter.schaffner@molbio.unizh.ch

Biol. Chem. 386, pp. 865–872.

Due to a printing error Figure 4 was not shown in color, but in grayscale. Shown below is the colored version of this Figure. We apologize for any inconvenience that might have been caused by this error.

Figure 4 Hypoxia induces nuclear translocation of MTF-1 and NF-kB p65.

Immunofluorescence experiments showing subcellular distribution of NF-kB p65 and MTF-1. pC-hMTF-VSV and, to obtain similar fluorescence signal intensities, pC-NF-kB p65 were transfected into HEK293 cells. Cells were serum-starved for 24 h and either left untreated, exposed to hypoxia (4 h), or treated with 200mMZnCl2(2 h) or 20 ng/ml TNF-a (30 min). MTF-1 is shown in green

(left panel), NF-kB p65 is shown in red (second left panel). DNA was stained with 49,69-diamino-2-phenylindole (DAPI, right panel, blue).

Figure

Figure 4 Hypoxia induces nuclear translocation of MTF-1 and NF-kB p65.

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