To compare "for cause" renal biopsies (bx) from adult recipients of pediatric-donor kidneys (PDK) versus adult-donor kidneys (ADKs), we reviewed 103 graft bx from 50 PDK recipients and 85 bx from 49 ADK recipients. PDK bx displayed more frequent glomerular pathology with immune complex-mediated glomerulonephritis present in 11/103 PDK versus 1/85 ADK (p < 0.05). In 15/103 PDK bx and 1/85 ADK (p = 0.001), the association of glomerular sclerosis, expanded mesangium, and halo of prominent podocytes by light microscopy, and ultrastructural glomerular basement membrane lamellation, configured a characteristic glomerulopathy.
The function of the relatively well-studied DNA replication origins in the yeast Saccharomyces cerevisiae is dependent upon interactions between origin replication complex (ORC) proteins and several defined origin sequence elements, including the 11 bp ARS consensus sequence (ACS). Although the ORC proteins, as well as numerous other protein components required for DNA replication initiation, are largely conserved between yeast and mammals, DNA sequences within mammalian replication origins are highly variable and sequences homologous to the yeast ACS elements are generally not present. We have previously identified several replication initiation sites within the nontranscribed spacer region of the human ribosomal RNA gene, and found that two highly utilized sites each contain a homologue of the yeast ACS embedded within a DNA unwinding element and a matrix attachment region. Here we examine protein binding within these initiation sites, and demonstrate that these ACS homologues specifically bind the alternate splicing factor SF2/ASF as well as GAPDH in vitro, and present evidence that the SF2/ASF interaction also occurs within the nuclei of intact cells. As the moderate upregulation of SF2/ASF has been linked to oncogenesis through the promotion of alternatively spliced forms of several regulatory proteins, our results suggest an additional mechanism by which SF2/ASF may influence the transformed cell phenotype.
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