FAT10: A novel mediator of Vpr-induced apoptosis in human immunodeficiency virus-associated nephropathy

Alexandra Snyder, Zygimantas Alsauskas, Pengfei Gong, Paul E. Rosenstiel, Mary E. Klotman, Paul E. Klotman, Michael J. Ross

Research output: Contribution to journalArticle

39 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)11983-11988
Number of pages6
JournalJournal of virology
Volume83
Issue number22
DOIs
StatePublished - Nov 1 2009
Externally publishedYes

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

Fingerprint Dive into the research topics of 'FAT10: A novel mediator of Vpr-induced apoptosis in human immunodeficiency virus-associated nephropathy'. Together they form a unique fingerprint.

  • Cite this

    Snyder, A., Alsauskas, Z., Gong, P., Rosenstiel, P. E., Klotman, M. E., Klotman, P. E., & Ross, M. J. (2009). FAT10: A novel mediator of Vpr-induced apoptosis in human immunodeficiency virus-associated nephropathy. Journal of virology, 83(22), 11983-11988. https://doi.org/10.1128/JVI.00034-09