ArticleThe American journal of pathology2007
Development of immunoglobulin A nephropathy- like disease in beta-1,4-galactosyltransferase-I-deficient mice.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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.
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
41 citing papers in PubMed, 69 citations in OpenAlex.
- Novel urinary glycan profiling by lectin array serves as the biomarkers for predicting renal prognosis in patients with IgA nephropathy.Scientific reports · 2021Trial
- Review
- Recent advances in pathogenetic concepts and disease modeling of IgA nephropathy.Clinical kidney journal · 2025Review
- Lactobacillus casei Cell Wall Extract and Production of Galactose-Deficient IgA1 in a Humanized IGHA1 Mouse Model.Journal of the American Society of Nephrology : JASN · 2025Article
- Lessons from IgA Nephropathy Models.International journal of molecular sciences · 2024Review
- Intestinal epithelium dysfunctions cause IgA deposition in the kidney glomeruli of intestine-specific Ap1m2-deficient mice.EBioMedicine · 2024Article
- Oral bacteria induce IgA autoantibodies against a mesangial protein in IgA nephropathy model mice.Life science alliance · 2024Article
- N-glycosylation, a leading role in viral infection and immunity development.Molecular biology reports · 2022Review
- N-Glycosylation and Inflammation; the Not-So-Sweet Relation.Frontiers in immunology · 2022Review
- Are there animal models of IgA nephropathy?Seminars in immunopathology · 2021Review
- History of IgA Nephropathy Mouse Models.Journal of clinical medicine · 2021Review
- The glyco-redox interplay: Principles and consequences on the role of reactive oxygen species during protein glycosylation.Redox biology · 2021Review
- Various biological functions of carbohydrate chains learned from glycosyltransferase-deficient mice.Experimental animals · 2020Article
- B4GALT1-congenital disorders of glycosylation: Expansion of the phenotypic and molecular spectrum and review of the literature.Clinical genetics · 2020Article
- TLR9 activation induces aberrant IgA glycosylation via APRIL- and IL-6-mediated pathways in IgA nephropathy.Kidney international · 2020Article
- Roles for Golgi Glycans in Oogenesis and Spermatogenesis.Frontiers in cell and developmental biology · 2019Review
- Glycopatterns of Urinary Protein as New Potential Diagnosis Indicators for Diabetic Nephropathy.Journal of diabetes research · 2017Article
- The Origin and Activities of IgA1-Containing Immune Complexes in IgA Nephropathy.Frontiers in immunology · 2016Review
- O-linked glycosylation determines the nephritogenic potential of IgA rheumatoid factor.Journal of the American Society of Nephrology : JASN · 2014Article
- Uncoupling of glomerular IgA deposition and disease progression in alymphoplasia mice with IgA nephropathy.PloS one · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beta4 galactosylation of glycoproteins plays important roles in protein conformation, stability, transport, and clearance from the circulation. Recent studies have revealed that aberrant glycosylation causes various human diseases. Here we report that mice lacking beta-1,4-galactosyltransferase (beta4GalT)-I, which transfers galactose to the terminal N-acetylglucosamine of N- and O-linked glycans in a beta-1,4 linkage, spontaneously developed human immunoglobulin A nephropathy (IgAN)-like glomerular lesions with IgA deposition and expanded mesangial matrix. beta4GalT-I-deficient mice also showed high serum IgA levels with increased polymeric forms as in human IgAN. IgAN is the most common form of glomerulonephritis, and a significant proportion of patients progress to renal failure. However, pathological molecular mechanisms of IgAN are poorly understood. In humans, abnormal character of serum IgA, especially serum IgA1 with aberrant galactosylation and sialylation of O-glycans in its hinge region is thought to contribute to the pathogenesis of IgAN. Mouse IgA has N-glycans but not O-glycans, and beta4-galactosylation and sialylation of the N-glycans on the serum IgA from beta4GalT-I-deficient mice was completely absent. This is the first report demonstrating that genetic remodeling of protein glycosylation causes IgAN. We propose that carbohydrates of serum IgA are involved in the development of IgAN, whether the carbohydrates are O-glycans or N-glycans.
Indexed as
Identifiers
What OpenQuestion holds
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.