Genetic models: Clues for understanding the pathogenesis of idiopathic nephrotic syndrome

Journal of Clinical Investigation

Volumn 109, Issue 4, 2002, Pages 447-449

  Antignac, Corinne ^a  

^a HÔPITAL NECKER ENFANTS MALADES   (France)

Author keywords

[No Author keywords available]

Indexed keywords

ACTIN BINDING PROTEIN; ALPHA ACTININ; CD2 ASSOCIATED PROTEIN; NEPHRIN; PODOCIN; UNCLASSIFIED DRUG;

ALLELE; ANIMAL MODEL; AUTOSOMAL RECESSIVE DISORDER; BASEMENT MEMBRANE; CHROMOSOME 13; DISEASE SEVERITY; DNA MICROARRAY; GENE LOCUS; GENE MUTATION; GENE OVEREXPRESSION; GENETIC ANALYSIS; GENETIC LINKAGE; GENETIC MODEL; GLOMERULOSCLEROSIS; GLOMERULUS FILTRATION; HETEROZYGOSITY; IMMUNOPATHOLOGY; KIDNEY DISEASE; KNOCKOUT MOUSE; MOLECULAR INTERACTION; MOUSE STRAIN; NEPHRITIS; NOTE; PATHOGENESIS; PODOCYTE; PRIORITY JOURNAL; RETINITIS PIGMENTOSA; THYMECTOMY; THYMOMA;

EID: 0036175951     PISSN: 00219738     EISSN: None     Source Type: Journal    
DOI: 10.1172/JCI0215094     Document Type: Note

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5. Mutations in ACTN4, encoding alpha-actinin-4, cause familial focal segmental glomerulosclerosis
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7. NPHS2, encoding the glomerular protein podocin, is mutated in autosomal recessive steroid-resistant nephrotic syndrome
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10. CD2AP localizes to the slit diaphragm and binds to nephrin via a novel C-terminal domain
11. Podocin, a raft-associated component of the glomerular slit diaphragm, interacts with CD2AP and nephrin
12. Podocin localizes in the kidney to the slit diaphragm area
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14. Nephritogenic mAb 5-1-6 is directed at the extracellular domain of rat nephrin
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