The expression of Oct-4 is only seen before cells become specialized, leading to speculation that it might participate in controlling this process. These results, obtained in cultured stem cells, match observations on subtle differences in Oct-4 levels in different cell types in the early mouse embryo. They also have broader implications for stem cell research. It is caused by defects in the glomerulus, the kidney's filtration apparatus. This disorder is rarely seen on its own, but it is a frequent complication in common chronic illnesses such as diabetes, lupus and multiple myeloma.
Patients often suffer renal failure and require dialysis or a kidney transplant.
Geneticists have focused on identifying the genes responsible for the rarer familial forms of the disease by gene hunting in affected families. The gene encodes a protein which the scientists named podocin, because it is present almost exclusively in specialized cells in the glomerulus called podocytes. As the human genome project nears completion, much ado has been made about how much we will learn about the 100,000 or so genes that reside within the nucleus of a human cell. These parasites are generally harmless, but they can occasionally disrupt the function of a gene by inserting within it. Such a mechanism can create new copies of genes by converting their expressed RNA into DNA, which then insert into new genomic sites.