A Mutation in the TRPC6 Cation Channel Causes Familial Focal Segmental Glomerulosclerosis

By M. Winn, P. Conlon, K. Lynn, M. Farrington, T. Creazzo, April F. Hawkins, N. Daskalakis, S. Y. Kwan, S. Ebersviller, J. Burchette and 4 more. Science, 2005

1,108 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Nephrology

View Paper: https://www.semanticscholar.org/paper/3d11a56618b1121b0d4ce72aa942ae76336bf1ec

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. Raghu Kalluri

In Molecular Biology

1. Raghu Kalluri
2. H. Sugimoto
3. D. Clapham
4. M. Nieto
5. Youhua Liu
6. Jeremy S. Duffield
7. R. Weinberg
8. D. Hanahan

In Nephrology

1. M. Nieto
2. Jeremy S. Duffield

Citations in the corpus

• TRP Channels (2012, neutral): “from it possible role in heart failure discussed above , there are also indications linking TRPC7 to a mild form autosomal dominant polycystic kidney disease (ADPKD) glutamic acid residue 697.”
• The actin cytoskeleton of kidney podocytes is a direct target of the antiproteinuric effect of cyclosporine A (2008, background): “, increased TRPC6-mediated calcium influx may cause FSG”
• TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function (2005, background): “Winn and colleagues identified a family with autosomal dominant focal segmental glomerulosclerosis (FSGS) that segregated with a point mutation in the gene TRPC6 on chromosome 11q (ref”