D. Cosgrove, R. Kalluri, J.-H. Miner, Y. Segal, D.-B. Borza 

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Choosing a mouse model to study the molecular pathobiology of Alport glomerulonephritis  D. Cosgrove, R. Kalluri, J.-H. Miner, Y. Segal, D.-B. Borza  Kidney International  Volume 71, Issue 7, Pages 615-618 (April 2007) DOI: 10.1038/sj.ki.5002115 Copyright © 2007 International Society of Nephrology Terms and Conditions

Figure 1 Schematic diagram summarizing strain-dependent differences in type IV collagen isoform switches in ARAS. Normal embryonic GBM contains only α1α2(IV) collagen networks (red). At the capillary loop stage of development in mice, a developmental switch activates expression of the COL4A3, COL4A4, and COL4A5 genes, resulting in the assembly of a subepithelial collagen network of α3α4α5(IV) chains (green), with a persistence of a subendothelial network of α1α2(IV) chains (red). In the COL4A3−/− mouse on the C57BL/6 background, an alternative isoform switch results in robust expression of α5α6(IV) networks in the GBM (blue). One report suggests very weak expression of the α5α6(IV) network in the COL4A3−/− mouse on the 129 background (dashed line).12 Kidney International 2007 71, 615-618DOI: (10.1038/sj.ki.5002115) Copyright © 2007 International Society of Nephrology Terms and Conditions