ArticleFEBS letters2008
Uteroglobin interacts with the heparin-binding site of fibronectin and prevents fibronectin-IgA complex formation found in IgA-nephropathy.
Article in FEBS letters, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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.
Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Identification and validation of epithelial‑mesenchymal transition‑related genes for diabetic nephropathy by WGCNA and machine learning.Molecular medicine reports · 2025Article
- Screening of the Key Genes and Signalling Pathways for Diabetic Nephropathy Using Bioinformatics Analysis.Frontiers in endocrinology · 2022Article
- Comprehensive analysis of diabetic nephropathy expression profile based on weighted gene co-expression network analysis algorithm.BMC nephrology · 2021Article
- CD45 exclusion- and cross-linking-based receptor signaling together broaden FcεRI reactivity.Science signaling · 2018Article
- Genetics and immunopathogenesis of IgA nephropathy.Clinical reviews in allergy & immunology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Immunoglobulin A (IgA)-nephropathy (IgAN) is the most common primary renal glomerular disease in the world that has no effective treatment. High levels of circulating IgA-fibronectin (Fn) complexes, characteristically found in IgAN patients, are suggested to cause abnormal deposition of IgA and Fn in the renal glomeruli of these patients causing renal failure. We previously reported that binding of Fn to uteroglobin (UG), a multifunctional anti-inflammatory protein, inhibits Fn-IgA heteromerization. However, the specific site of Fn-UG interaction until now remained unidentified. We report here that UG interacts with the heparin-binding site of Fn and propose that small molecules competing for interaction with this site may reduce the level of circulating Fn-IgA complexes in IgAN.
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Registered trials
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.