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Molecular and Cellular Biology, December 2006, p. 9484-9496, Vol. 26, No. 24
0270-7306/06/$08.00+0     doi:10.1128/MCB.01030-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

The DEK Nuclear Autoantigen Is a Secreted Chemotactic Factor{triangledown}

Nirit Mor-Vaknin,1 Antonello Punturieri,2,6,8 Kajal Sitwala,1,7 Neil Faulkner,1,7 Maureen Legendre,1 Michael S. Khodadoust,1,6 Ferdinand Kappes,1 Jeffrey H. Ruth,3 Alisa Koch,3,6 David Glass,9 Lilli Petruzzelli,4,6 Barbara S. Adams,5 and David M. Markovitz1,6,7*

Department of Internal Medicine, Division of Infectious Diseases,1 Department of Internal Medicine, Division of Pulmonary Medicine,2 Department of Internal Medicine, Division of Rheumatology,3 Department of Internal Medicine, Division of Hematology and Oncology,4 Department of Pediatrics, Division of Rheumatology,5 Program in Immunology,6 Cellular and Molecular Biology Program, University of Michigan Medical Center, Ann Arbor, Michigan 48109,7 Division of Lung Diseases, NHLBI, Bethesda, Maryland,8 Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 452299

Received 8 June 2006/ Returned for modification 13 July 2006/ Accepted 15 September 2006

The nuclear DNA-binding protein DEK is an autoantigen that has been implicated in the regulation of transcription, chromatin architecture, and mRNA processing. We demonstrate here that DEK is actively secreted by macrophages and is also found in synovial fluid samples from patients with juvenile arthritis. Secretion of DEK is modulated by casein kinase 2, stimulated by interleukin-8, and inhibited by dexamethasone and cyclosporine A, consistent with a role as a proinflammatory molecule. DEK is secreted in both a free form and in exosomes, vesicular structures in which transcription-modulating factors such as DEK have not previously been found. Furthermore, DEK functions as a chemotactic factor, attracting neutrophils, CD8+ T lymphocytes, and natural killer cells. Therefore, the DEK autoantigen, previously described as a strictly nuclear protein, is secreted and can act as an extracellular chemoattractant, suggesting a direct role for DEK in inflammation.

* Corresponding author. Mailing address: University of Michigan, 5220 MSRB III, 1150 West Medical Center Drive, Ann Arbor, MI 48109-0640. Phone: (734) 647-1786. Fax: (734) 764-0101. E-mail: dmarkov{at}umich.edu.

{triangledown} Published ahead of print on 9 October 2006.

Molecular and Cellular Biology, December 2006, p. 9484-9496, Vol. 26, No. 24
0270-7306/06/$08.00+0     doi:10.1128/MCB.01030-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Khodadoust, M. S., Verhaegen, M., Kappes, F., Riveiro-Falkenbach, E., Cigudosa, J. C., Kim, D. S.L., Chinnaiyan, A. M., Markovitz, D. M., Soengas, M. S. (2009). Melanoma Proliferation and Chemoresistance Controlled by the DEK Oncogene. Cancer Res. 69: 6405-6413 [Abstract] [Full Text]  
  • Kappes, F., Fahrer, J., Khodadoust, M. S., Tabbert, A., Strasser, C., Mor-Vaknin, N., Moreno-Villanueva, M., Burkle, A., Markovitz, D. M., Ferrando-May, E. (2008). DEK Is a Poly(ADP-Ribose) Acceptor in Apoptosis and Mediates Resistance to Genotoxic Stress. Mol. Cell. Biol. 28: 3245-3257 [Abstract] [Full Text]  


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