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Journal of Virology, November 2009, p. 11983-11988, Vol. 83, No. 22
0022-538X/09/$08.00+0     doi:10.1128/JVI.00034-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

FAT10: a Novel Mediator of Vpr-Induced Apoptosis in Human Immunodeficiency Virus-Associated Nephropathy{triangledown}

Alexandra Snyder,1 Zygimantas Alsauskas,1 Pengfei Gong,1 Paul E. Rosenstiel,1 Mary E. Klotman,2 Paul E. Klotman,1 and Michael J. Ross1*

Mount Sinai School of Medicine, Division of Nephrology, Box 1243, 1 Gustave L Levy Place, New York, New York 10029,1 Mount Sinai School of Medicine, Division of Infectious Diseases, Box 1090, 1 Gustave L Levy Place, New York, New York 100292

Received 7 January 2009/ Accepted 5 August 2009

Human immunodeficiency virus (HIV)-associated nephropathy is a significant cause of morbidity and mortality in HIV-infected persons. Vpr-induced cell cycle dysregulation and apoptosis of renal tubular epithelial cells are important components of the pathogenesis of HIV-associated nephropathy (HIVAN). FAT10 is a ubiquitin-like protein that is upregulated in renal tubular epithelial cells in HIVAN. In these studies, we report that Vpr induces increased expression of FAT10 in tubular cells and that inhibition of FAT10 expression prevents Vpr-induced apoptosis in human and murine tubular cells. Moreover, we found that Vpr interacts with FAT10 and that these proteins colocalize at mitochondria. These studies establish FAT10 as a novel mediator of Vpr-induced cell death.

* Corresponding author. Mailing address: Mount Sinai Division of Nephrology, Box 1243, 1 Gustave L Levy Place, New York, NY 10029. Phone: (212) 241-0131. Fax: (212) 987-0389. E-mail: michael.ross{at}mssm.edu

{triangledown} Published ahead of print on 2 September 2009.

Journal of Virology, November 2009, p. 11983-11988, Vol. 83, No. 22
0022-538X/09/$08.00+0     doi:10.1128/JVI.00034-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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