Role of ubiquitin-like protein FAT10 in epithelial apoptosis in renal disease.

نویسندگان

  • Michael J Ross
  • Matthew S Wosnitzer
  • Michael D Ross
  • Benedetta Granelli
  • G Luca Gusella
  • Mohammad Husain
  • Lewis Kaufman
  • Matthew Vasievich
  • Vivette D D'Agati
  • Patricia D Wilson
  • Mary E Klotman
  • Paul E Klotman
چکیده

Dysregulated apoptosis of renal tubular epithelial cells (RTEC) is an important component of the pathogenesis of several renal diseases, including HIV-associated nephropathy (HIVAN), the most common cause of chronic kidney failure in HIV-infected patients. In HIVAN, RTEC become infected by HIV-1 in a focal distribution, and HIV-1 infection has been shown to induce apoptosis in vitro. In microarray studies that used a novel renal tubular epithelial cell line from a patient with HIVAN, it was found that the ubiquitin-like protein FAT10 is one of the most upregulated genes in HIV-infected cells. Previously, FAT10 was shown to induce apoptosis in murine fibroblasts. The expression of FAT10 in HIVAN and the ability of FAT10 to induce apoptosis in human RTEC therefore were studied. This study revealed that FAT10 expression is induced after infection of RTEC by HIV-1 and that expression of FAT10 induces apoptosis in RTEC in vitro. Moreover, it was found that inhibition of endogenous FAT10 expression abrogated HIV-induced apoptosis of RTEC. Immunohistochemical studies demonstrated increased FAT10 expression in a murine model of HIVAN, in HIVAN biopsy samples, and in autosomal dominant polycystic kidney disease, another renal disease that is characterized by cystic tubular enlargement and epithelial apoptosis. These results suggest a novel role for FAT10 in epithelial apoptosis, which is an important component of the pathogenesis of many renal diseases.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

The Ubiquitin-Like Protein FAT10 Mediates NF- B Activation

NFB is a central mediator of innate immunity and contributes to the pathogenesis of several renal diseases. FAT10 is a TNF–inducible ubiquitin-like protein with a putative role in immune response, but whether FAT10 participates in TNF–induced NFB activation is unknown. Here, using renal tubular epithelial cells (RTECs) derived from FAT10 / and FAT10 / mice, we observed that FAT10 deficiency abr...

متن کامل

The ubiquitin-like protein FAT10 forms covalent conjugates and induces apoptosis.

FAT10 is a ubiquitin-like protein that is encoded in the major histocompatibility complex class I locus and is synergistically inducible with interferon-gamma and tumor necrosis factor alpha. The molecule consists of two ubiquitin-like domains in tandem arrangement and bears a conserved diglycine motif at its carboxyl terminus commonly used in ubiquitin-like proteins for isopeptide linkage to c...

متن کامل

Disruption of FAT10-MAD2 binding inhibits tumor progression.

FAT10 (HLA-F-adjacent transcript 10) is a ubiquitin-like modifier that is commonly overexpressed in various tumors. It was found to play a role in mitotic regulation through its interaction with mitotic arrest-deficient 2 (MAD2). Overexpression of FAT10 promotes tumor growth and malignancy. Here, we identified the MAD2-binding interface of FAT10 to be located on its first ubiquitin-like domain ...

متن کامل

FAT10 is a proteasomal degradation signal that is itself regulated by ubiquitination

FAT10 is a ubiquitin-like protein modifier that is induced in vertebrates following certain inflammatory stimuli. Its functions and the repertoire of its target substrates have remained elusive. In contrast to ubiquitin, its cellular abundance is tightly controlled by both transcriptional and posttranslational regulation, and it was reported to be rapidly degraded by the proteasome. Here we pro...

متن کامل

Conjugation of the Ubiquitin Activating Enzyme UBE1 with the Ubiquitin-Like Modifier FAT10 Targets It for Proteasomal Degradation

The ubiquitin-like modifier HLA-F adjacent transcript 10 (FAT10) directly targets its substrates for proteasomal degradation by becoming covalently attached via its C-terminal diglycine motif to internal lysine residues of its substrate proteins. The conjugation machinery consists of the bispecific E1 activating enzyme Ubiquitin-like modifier activating enzyme 6 (UBA6), the likewise bispecific ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Journal of the American Society of Nephrology : JASN

دوره 17 4  شماره 

صفحات  -

تاریخ انتشار 2006