Associated Papers
Genetic screening in kidney transplant candidates.
Le Moal P et al.
Clinical Kidney Journal, 2026
Sequence and Structure-Based Analyses of Human Ankyrin Repeats.
Chakrabarty B et al.
Molecules (basel, Switzerland), 2022
Early presentation of cystic kidneys in a family with a homozygous INVS mutation.
Oud MM et al.
American Journal of Medical Genetics. Part A, 2014
Inversin, Wnt signaling and primary cilia.
Lienkamp S et al.
Differentiation; Research in Biological Diversity, 2012
A homozygous mutation in INVS causing juvenile nephronophthisis with abnormal reactivity of the Wnt/beta-catenin pathway.
Bellavia S et al.
Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association, 2010
Mutations of NPHP2 and NPHP3 in infantile nephronophthisis.
Tory K et al.
Kidney International, 2009
Genome-wide analysis to predict protein sequence variations that change phosphorylation sites or their corresponding kinases.
Ryu GM et al.
Nucleic Acids Research, 2009
19139070 (PubMed )
Supplement: gkn1008_nar-01723-s-2008-File009.xls › TypeI_
Inversin, the gene product mutated in nephronophthisis type II, functions as a molecular switch between Wnt signaling pathways.
Simons M et al.
Nature Genetics, 2005
Mutations in INVS encoding inversin cause nephronophthisis type 2, linking renal cystic disease to the function of primary cilia and left-right axis determination.
Otto EA et al.
Nature Genetics, 2003
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