Role of Ubiquitin-Like Protein FAT10 in Epithelial Apoptosis in Renal Disease

Ross, Michael J.; Wosnitzer, Matthew S.; Ross, Michael D.; Granelli, Benedetta; Gusella, G. Luca; Husain, Mohammad; Kaufman, Lewis; Vasievich, Matthew P.; D’Agati, Vivette D.; Wilson, Patricia D.; Klotman, Mary E.; Klotman, Paul E.

doi:10.1681/asn.2005070692

Cited by 78 publications

(83 citation statements)

References 47 publications

(53 reference statements)

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“…A recent publication showed, that a high induction of FAT10 expression is also achieved by a synergistic treatment of HepG2 cells with TNF-␣ in combination with IL-6 (Choi et al, 2014). Upregulation of FAT10 expression induced caspase-dependent apoptosis in HeLa cells, renal tubular epithelial cells as well as mouse fibroblasts (Liu et al, 1999;Raasi et al, 2001;Ross et al, 2006). However, the role of FAT10 in apoptosis is contradictory because other publications showed a pro-survival role of FAT10 (Canaan et al, 2006).…”

Section: Fat10 In Adaptive and Innate Immunitymentioning

confidence: 99%

“…Spinnenhirn and colleagues (Spinnenhirn et al, 2014) showed that the presence of FAT10 resulted in a prolonged life span of S. Typhimurium-infected mice, pointing to a protective role of FAT10. It is assumed that FAT10 plays additional roles in innate immunity since an up-regulation of FAT10 expression was described in HIV-infected renal tubular epithelial cells (RTECs) (Ross et al, 2006;Snyder et al, 2009) and during Kaposi sarcomaassociated herpesvirus infection (Hong et al, 2004). Moreover, the group of J.-Y.…”

Section: Fat10 In Adaptive and Innate Immunitymentioning

confidence: 99%

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The ubiquitin-like modifier FAT10 in cancer development

Aichem

Groettrup

2016

The International Journal of Biochemistry & Cell Biology

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a b s t r a c tDuring the last years it has emerged that the ubiquitin-like modifier FAT10 is directly involved in cancer development. FAT10 expression is highly up-regulated by pro-inflammatory cytokines IFN-␥ and TNF-␣ in all cell types and tissues and it was also found to be up-regulated in many cancer types such as glioma, colorectal, liver or gastric cancer. While pro-inflammatory cytokines within the tumor microenvironment probably contribute to FAT10 overexpression, an increasing body of evidence argues that pro-malignant capacities of FAT10 itself largely underlie its broad and intense overexpression in tumor tissues. FAT10 thereby regulates pathways involved in cancer development such as the NF-B-or Wnt-signaling. Moreover, FAT10 directly interacts with and influences downstream targets such as MAD2, p53 or ␤-catenin, leading to enhanced survival, proliferation, invasion and metastasis formation of cancer cells but also of non-malignant cells. In this review we will provide an overview of the regulation of FAT10 expression as well as its function in carcinogenesis.

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Section: Fat10 In Adaptive and Innate Immunitymentioning

confidence: 99%

Section: Fat10 In Adaptive and Innate Immunitymentioning

confidence: 99%

The ubiquitin-like modifier FAT10 in cancer development

Aichem

Groettrup

2016

The International Journal of Biochemistry & Cell Biology

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“…FAT10 consists of two ubiquitin-like domains in tandem array and bears a free diglycine motif at its C terminus, which is required for the covalent conjugation to as yet unidentifi ed target proteins 6,14 . Th e biological function of FAT10 remains poorly understood, but it has been shown that overexpression of FAT10 leads to caspase-dependent apoptosis in a mouse fi broblast cell line 13 and renal tubular epithelial cells 15 . In addition, FAT10 has been shown to serve as a signal for proteasomal degradation independently of the ubiquitylation system 16,17 .…”

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confidence: 99%

USE1 is a bispecific conjugating enzyme for ubiquitin and FAT10, which FAT10ylates itself in cis

et al. 2010

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The ubiquitin-like modifi er FAT10 targets proteins for degradation by the proteasome and is activated by the E1 enzyme UBA6. In this study, we identify the UBA6-specifi c E2 enzyme (USE1) as an interaction partner of FAT10. Activated FAT10 can be transferred from UBA6 onto USE1 in vitro , and endogenous USE1 and FAT10 can be coimmunoprecipitated from intact cells. Small interfering RNA-mediated downregulation of USE1 mRNA resulted in a strong reduction of FAT10 conjugate formation under endogenous conditions, suggesting that USE1 is a major E2 enzyme in the FAT10 conjugation cascade. Interestingly, USE1 is not only the fi rst E2 enzyme but also the fi rst known substrate of FAT10 conjugation, as it was effi ciently auto-FAT10ylated in cis but not in trans .

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“…[22][23][24] We previously reported that FAT10 is upregulated in HIVinfected renal tubular epithelial cells (RTECs) in vitro and in kidney specimens from patients with HIV-associated nephropathy and autosomal polycystic kidney disease and that increased expression of FAT10 induces apoptosis in RTECs. 25 Knockout of FAT10 causes minimal phenotypic changes in unstressed mice; however, these mice exhibit increased sensitivity to death after LPS injection. 26 FAT10 is constitutively expressed in mature dendritic cells and B cells 27,28 and is also inducible by the proinflammatory cytokines IFN-␥ and TNF-␣ in cells of various tissue origins 29,30 ; however, the role of FAT10 in the regulation of immune response has not been studied.…”

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confidence: 99%