The data from embryonic NBs suggest that Pros can directly bind to the ase region and regulates its expression. In the absence of this regulation, GMCs maintain the stem cell fate and continue to grow into malignant tumors. Our data are of particular relevance in light of the recently postulated role of stem cells in the formation of malignant tumors. Failure to limit self-renewal capacity in stem cells or defects in progenitor cell differentiation can both lead to the formation of cells that continue to proliferate and ultimately form tumors. While genes acting in stem cells are thought to promote self-renewal, genes required in differentiating cells are thought to promote differentiation and limit proliferation and are therefore candidate tumor suppressors. Our data challenge this view and show that the path to differentiation is initiated in the stem cell and therefore even genes specific to stem cells can act as tumor suppressors. It will be interesting to determine whether a similar mechanism acts in mammalian neural stem cells as well. If it does, the expression pattern of a gene can no longer be used as a main criterium for whether it promotes or inhibits self-renewal in stem cell lineages. Acute interstitial nephritis is a general cause of acute LY 78335 kidney injury. Patients with AIN can either completely recover or progress to chronic kidney disease or end-stage renal disease. Although several LY 2087101 antifibrotic strategies have been proposed, there are no effective treatments for kidney fibrosis. Kidney fibrosis is generally considered to result from tissue inflammation and the tissue repair/wound healing responses. Wound healing is a complex process involving several signal transduction systems, and ultimately can result in scar formation. The first phase begins with tissue damage caused by antiinflammatory cytokines. The next phase is defined by deposition of granulation tissue and new extracellular matrix proteins. Acute inflammatory reactions are considered to be a part of early wound healing and play a key role in triggering fibrosis. Since prevention of the initial fibrotic process in AIN may lead to retention of kidney function, we investigated what kinds of signaling systems mediate kidney fibrosis associated with AIN. There are two major WNT signaling pathways, the canonical and the non-canonical pathways.WNT is a family of highly conserved glycoproteins, and 19WNT members have been identified so far in humans. The WNT/Frizzled signal transduction system is a highly complex cascade that is fundamental for a wide variety of physiological processes, as well as pathological states. Some WNT proteins were previously investigated in kidney interstitial fibrosis, but the relation between WNT10A and kidney fibrosis has not been determined. We asked whether WNT10A promotes kidney fibrosis. We previously reported that WNT10A is expressed in dermal fibroblasts, and that a-SMApositive cells are involved in wound healing. Myofibroblasts, or activated fibroblasts with a-SMA expression, differentiate from diverse sources including local interstitial fibroblasts, vascular pericytes, and endothelial cells.