Oncotarget

Research Papers:

Actin-binding protein alpha-actinin 4 (ACTN4) is a transcriptional co-activator of RelA/p65 sub-unit of NF-kB.

Vasilisa Aksenova, Lidia Turoverova, Mikhail Khotin, Karl-Eric Magnusson, Eugene Tulchinsky, Gerry Melino, George P Pinaev, Nikolai Barlev, Dmitri Tentler _

PDF  |  HTML  |  Order a Reprint  |  This article has been corrected. Oncotarget. 2018; 9:34450.

Oncotarget. 2012; 4:362-373. https://doi.org/10.18632/oncotarget.901

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Abstract

Vasilisa Aksenova1,2, Lidia Turoverova1, Mikhail Khotin1, Karl-Eric Magnusson3, Eugene Tulchinsky4, Gerry Melino2,5, George P. Pinaev1, Nickolai Barlev1,2,6, and Dmitri Tentler1,2

1 Institute of Cytology, Russian Academy of Sciences, Tikhoretsky av., 4, St. Petersburg, Russia

2 Laboratory of Molecular Pharmacology, Saint-Petersburg Technological Institute, 26 Moskovsky Prospect, St. Petersburg, Russia

3 Division of Medical Microbiology, Department of Clinical and Experimental Medicine, Linköping University, SE-581 85 Linköping, Sweden

4 Department of Cancer Studies and Molecular Medicine, University of Leicester, RKCSB, LRI, Leicester, UK

5 MRC Toxicology Unit, Leicester, UK

6 Department of Biochemistry, University of Leicester, Lancaster Road, Leicester, UK

Correspondence:

Vasilisa Aksenova, email:

Dmitri Tentler, email:

Keywords: ACTN4, RelA/p65, transcription regulation, MMP

Received: February 22, 2013 Accepted: February 26, 2013 Published: February 28, 2013

Abstract

ACTN4 is an actin-binding protein that participates in cytoskeleton organisation. It resides both in the cytoplasm and nucleus and physically associates with various transcription factors. Here, we describe an effect of ACTN4 expression on transcriptional activity of the RelA/p65 subunit of NF-kB. We demonstrate that ACTN4 enhances RelA/p65-dependant expression of c-fos, MMP-3 and MMP-1 genes, but it does not affect TNC, ICAM1 and FN1 expression. Importantly, actin-binding domains of ACTN4 are not critical for the nuclear translocation and co-activation of RelA/p65-dependent transcription. Collectively, our data suggest that in the nucleus, ACTN4 functions as a selective transcriptional co-activator of RelA/p65.


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