ArticlePediatric nephrology (Berlin, Germany)2010
A tubulointerstitial nephritis antigen gene defect causes childhood-onset chronic renal failure.
Article in Pediatric nephrology (Berlin, Germany), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Patterns of gene expression characterize T1 and T3 clear cell renal cell carcinoma subtypes.PloS one · 2019Article
- Tubulointerstitial nephritis: diagnosis, treatment, and monitoring.Pediatric nephrology (Berlin, Germany) · 2017Review
- Nonfunction of the ECT2 gene may cause renal tubulointerstitial injury leading to focal segmental glomerulosclerosis.Clinical and experimental nephrology · 2012Article
- Acute tubulointerstitial nephritis.Pediatric nephrology (Berlin, Germany) · 2012Review
- Role of extracellular matrix renal tubulo-interstitial nephritis antigen (TINag) in cell survival utilizing integrin (alpha)vbeta3/focal adhesion kinase (FAK)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B-serine/threonine kinase (AKT) signaling pathway.The Journal of biological chemistry · 2011Article
- Transcriptional profiling identifies TNS4 function in epithelial tubulogenesis.Current biology : CB · 2011Article
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Authors and funding
9 authors at 1 institution in 1 country.
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Abstract
Tubulointerstitial nephritis antigen (TIN-ag), which has been localized to the renal tubular basement membrane, is a target antigen in some forms of TIN. Physiologically, TIN-ag is thought to be important in maintaining the structure of renal tubular basement membrane. Here we describe a child with chronic renal failure showing a human TIN-ag gene (hTIN-ag) deletion. Immunohistochemical examination using an antihuman TIN-ag monoclonal antibody showed attenuation or lack of TIN-ag staining along the renal tubular basement membrane, whereas nephrocystin staining was normal in renal tubules. Polymerase chain reaction detected no amplification band corresponding to hTIN-ag in this patient. Testing for a deletion in this gene showed nearly complete deletion. By using array-comparative genomic hybridization method, large deletion of a gene mapped on chromosome 6p11-6p12 was demonstrated, corresponding to the locus where hTIN-ag is located. Therefore, an hTIN-ag defect may be a potent cause of end-stage renal failure in childhood.
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