Evidence map›Paper›PMID 19959714›Full record

ArticleJournal of the American Society of Nephrology : JASN2010

The ubiquitin-like protein FAT10 mediates NF-kappaB activation.

Pengfei Gong, Allon Canaan, Bin Wang, Jeremy Leventhal, Alexandra Snyder, Viji Nair, Clemens D Cohen, Matthias Kretzler, Vivette D'Agati, Sherman Weissman and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 92 citations in OpenAlex.

  1. Trial
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  13. The Functional Roles of ISG15/ISGylation in Cancer.Molecules (Basel, Switzerland) · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 2 countries.

Pengfei GongDivision of Nephrology, Department of Medicine, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
Allon Canaan
Bin Wang
Jeremy Leventhal
Alexandra Snyder
Viji Nair
Clemens D Cohen
Matthias Kretzler
Vivette D'Agati
Sherman Weissman
Michael J Ross
University of Michigan–Ann Arbor · USYale University · USColumbia University · USIcahn School of Medicine at Mount Sinai · USUniversity Hospital of Zurich · CH

Funding

University of Michigan O'Brien Kidney Translational Core CenterP30DK081943 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PENNATHUR, SUBRAMANIAM · 2008 to 2022
$12.9M
The role of FAT10 in the pathogenesis of HIV-associated nephropathyR01DK078510 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ROSS, MICHAEL J · 2007 to 2011
$1.8M
NIDDK NIH HHS P30 DK081943NIDDK NIH HHS P30 DK081943-01NIDDK NIH HHS R01 DK078510
6 · The paper itself

Abstract

NF-kappaB is a central mediator of innate immunity and contributes to the pathogenesis of several renal diseases. FAT10 is a TNF-alpha-inducible ubiquitin-like protein with a putative role in immune response, but whether FAT10 participates in TNF-alpha-induced NF-kappaB activation is unknown. Here, using renal tubular epithelial cells (RTECs) derived from FAT10(-/-) and FAT10(+/+) mice, we observed that FAT10 deficiency abrogated TNF-alpha-induced NF-kappaB activation and reduced the induction of NF-kappaB-regulated genes. Despite normal IkBalpha degradation and polyubiquitination, FAT10 deficiency impaired TNF-alpha-induced IkBalpha degradation and nuclear translocation of p65 in RTECs, suggesting defective proteasomal degradation of polyubiquitinated IkBalpha. In addition, FAT10 deficiency reduced the expression of the proteasomal subunit low molecular mass polypeptide 2 (LMP2). Transduction of FAT10(-/-) RTECs with FAT10 restored LMP2 expression, TNF-alpha-induced IkBalpha degradation, p65 nuclear translocation, and NF-kappaB activation. Furthermore, LMP2 transfection restored IkBalpha degradation in FAT10(-/-) RTECs. In humans, common types of chronic kidney disease associated with tubulointerstitial upregulation of FAT10. These data suggest that FAT10 mediates NF-kappaB activation and may promote tubulointerstitial inflammation in chronic kidney diseases.

Indexed as

AnimalsBiopsyCell LineChemokine CCL2Chemokine CXCL2Cysteine EndopeptidaseseIF-2 KinaseEpithelial CellsHumansI-kappa B ProteinsKidney TubulesLiverMiceMice, Inbred C57BLMice, KnockoutModels, AnimalCcl2 protein, mouseChemokine CCL2Chemokine CXCL2Cxcl2 protein, mouseCysteine EndopeptidaseseIF-2 KinaseFAT10 protein, mouseI-kappa B ProteinsLMP-2 proteinNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanNfkbia protein, mouseTumor Necrosis Factor-alphaUbiquitins

Identifiers

PMID19959714
PMCPMC2834541
OpenAlexW2158524682

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.