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Abstract
bcl-2-/-mice complete embryonic development, but display growth retardation and early
mortality postnatally. Hematopoiesis including lymphocyte differentiation is initially
normal, but thymus and spleen undergo massive apoptotic involution. Thymocytes require
an apoptotic signal to manifest accelerated cell death. Renal failure results from
severe polycystic kidney disease characterized by dilated proximal and distal tubular
segments and hyperproliferation of epithelium and interstitium. bcl-2-/-mice turn
gray with the second hair follicle cycle, implicating a defect in redox-regulated
melanin synthesis. The abnormalities in these loss of function mice argue that Bcl-2
is a death repressor molecule functioning in an antioxidant pathway.