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Data suggest that Pdzrn3 (Montrer PDZRN3 Protéines) mediates endocytosis of dephosphorylated CLDN16 and represents an important component of CLDN16-trafficking machinery in renal tube epithelial cells. (Pdzrn3 (Montrer PDZRN3 Protéines) = PDZ domain containing RING finger 3 (Montrer PDZRN3 Protéines) protein; CLDN16 = claudin 16)
detected a novel mutation in CLDN16 for the first time. The clinical and genetic findings from this study will help to expand the understanding of this rare disease, FHHNC
claudin-16 gene (CLDN16) mutations result in amelogenesis imperfect.
CLDN16 mutations are associated with familial hypomagnesaemia with hypercalciuria and nephrocalcinosis.
1,25(OH)2 VitD transcriptionally inhibits renal claudin-16 expression by a mechanism sensitive to CaSR (Montrer CASR Protéines) and Mg(2 (Montrer MUC7 Protéines)+).
A novel CLDN16 mutation has been identified in a large consanguineous family with familial hypomagnesaemia with hypercalciuria and nephrocalcinosis.
These results suggest that STX8 (Montrer STX8 Protéines) mediates the recycling of CLDN16 and constitutes an important component of the CLDN16 trafficking machinery in the kidney.
Six different mutations of CLDN16 were detected (five missense and one nonsense); three of the missense mutations were previously unknown (p.Cys80Tyr, p.Lys183Glu, and p.Gly233Arg).
A novel mutation of CLDN16 gene is responsible for familial hypomagnesaemia in Turkish children.
Claudin-16 plays a role beyond that of an initial metastasis repressor in breast cancer.
Claudin-16 sequences were not usually amplified from a small number of sperm cells (< or =10 cells) but claudin-16 DNA sequences were occasionally detected when a large number of sperm cells (> or =50 cells) were present.
Renal lesions in Japanese Black cattle are not necessarily associated with homozygous deletion of the CL-16 gene.
1,25(OH)2 VitD transcriptionally inhibits renal claudin-16 expression by a mechanism sensitive to CaSR (Montrer CASR Protéines) and Mg(2 (Montrer MCOLN1 Protéines)+).
Mg(2 (Montrer MCOLN1 Protéines)+)-loaded animals displayed hypermagnesemia with increasing urine Mg(2 (Montrer MCOLN1 Protéines)+)/Ca(2 (Montrer CA2 Protéines)+) levels paralleled by a decrease in claudin-16 protein and mRNA in the kidney.
data suggest that claudin-16 forms a non-selective paracellular cation channel (Montrer TRPV1 Protéines), rather than a selective Mg(2 (Montrer MCOLN1 Protéines)+)/Ca(2 (Montrer CA2 Protéines)+) channel as previously proposed
Perturbation in salt and acid-base metabolism in CLDN16 knockout mice has its origin in the defective cation permeability selectivity of the thick ascending limb of the nephron.
Insights into driving forces and paracellular permeability from claudin-16 knockdown mouse
Claudin-16 and claudin-19 (Montrer CLDN19 Protéines) interaction is required for their assembly into tight junctions and for renal reabsorption of magnesium.
Tight junctions represent one mode of cell-to-cell adhesion in epithelial or endothelial cell sheets, forming continuous seals around cells and serving as a physical barrier to prevent solutes and water from passing freely through the paracellular space. These junctions are comprised of sets of continuous networking strands in the outwardly facing cytoplasmic leaflet, with complementary grooves in the inwardly facing extracytoplasmic leaflet. The protein encoded by this gene, a member of the claudin family, is an integral membrane protein and a component of tight junction strands. It is found primarily in the kidneys, specifically in the thick ascending limb of Henle, where it acts as either an intercellular pore or ion concentration sensor to regulate the paracellular resorption of magnesium ions. Defects in this gene are a cause of primary hypomagnesemia, which is characterized by massive renal magnesium wasting with hypomagnesemia and hypercalciuria, resulting in nephrocalcinosis and renal failure. This gene and the CLDN1 gene are clustered on chromosome 3q28.
, hypomagnesemia 3, with hypercalciuria and nephrocalcinosis
, H59D2a protein