The clinical and histopathologic variability of this common genetic disorder - a leading cause of renal failure - cannot be explained by inherited mutation. Instead, the disease evidently progresses by a second hit: somatic mutation superimposed on germline mutation. The source of the mutability appears to be DNA triple-helixing, as mediated by some odd genetic code, the longest polypyrimidine tract ever found in the human genome.
|Original language||English (US)|
|Number of pages||22|
|State||Published - Mar 15 1997|
ASJC Scopus subject areas