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

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Snyder, A; Alsauskas, Z; Gong, P; Rosenstiel, PE; Klotman, ME; Klotman, PE; Ross, MJ

Published Date

  • November 2009

Published In

Volume / Issue

  • 83 / 22

Start / End Page

  • 11983 - 11988

PubMed ID

  • 19726511

Pubmed Central ID

  • PMC2772664

Electronic International Standard Serial Number (EISSN)

  • 1098-5514

Digital Object Identifier (DOI)

  • 10.1128/JVI.00034-09


  • eng

Conference Location

  • United States