ArticleScientific reports2016
COL4A6 is dispensable for autosomal recessive Alport syndrome.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- A panel of Diversity Outbred mouse embryonic stem cells: enabling the functional characterization of natural genetic variationbioRxiv : the preprint server for biology · 2026Article
- The Protective Role of KANK1 in Podocyte Injury.International journal of molecular sciences · 2024Article
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- Case report: Unilateral panuveitis as a manifestation of Alport syndrome in a Chinese pediatric patient.Frontiers in genetics · 2022Article
- Creation of X-linked Alport syndrome rat model with Col4a5 deficiency.Scientific reports · 2021Article
- Podocyte-specific Crb2 knockout mice develop focal segmental glomerulosclerosis.Scientific reports · 2021Article
- TF-RBP-AS Triplet Analysis Reveals the Mechanisms of Aberrant Alternative Splicing Events in Kidney Cancer: Implications for Their Possible Clinical Use as Prognostic and Therapeutic Biomarkers.International journal of molecular sciences · 2021Article
- Article
- A Novel Prognostic Model of Endometrial Carcinoma Based on Clinical Variables and Oncogenomic Gene Signature.Frontiers in molecular biosciences · 2020Article
- Modification of an aggressive model of Alport Syndrome reveals early differences in disease pathogenesis due to genetic background.Scientific reports · 2019Article
- Basement membrane collagens and disease mechanisms.Essays in biochemistry · 2019Review
- Type IV collagen α6 chain is a regulator of keratin 10 in keratinization of oral mucosal epithelium.Scientific reports · 2018Article
- Long-term follow-up of an Alport syndrome patient with a novel mutation ofInternational journal of clinical and experimental pathology · 2017Article
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alport syndrome is caused by mutations in the genes encoding α3, α4, or α5 (IV) chains. Unlike X-linked Alport mice, α5 and α6 (IV) chains are detected in the glomerular basement membrane of autosomal recessive Alport mice, however, the significance of this finding remains to be investigated. We therefore generated mice lacking both α3 and α6 (IV) chains and compared their renal function and survival with Col4a3 knockout mice of 129 × 1/Sv background. No significant difference was observed in the renal function or survival of the two groups, or when the mice were backcrossed once to C57BL/6 background. However, the survival of backcrossed double knockout mice was significantly longer than that of the mice of 129 × 1/Sv background, which suggests that other modifier genes were involved in this phenomenon. In further studies we identified two Alport patients who had a homozygous mutation in intron 46 of COL4A4. The α5 and α6 (IV) chains were focally detected in the glomerular basement membrane of these patients. These findings indicate that although α5 and α6 (IV) chains are induced in the glomerular basement membrane in autosomal recessive Alport syndrome, their induction does not seem to play a major compensatory role.
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