Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair

Deborah J. Veis, Christine M. Sorenson, John R. Shutter, Stanley J. Korsmeyer

Research output: Contribution to journalArticlepeer-review

1424 Scopus citations

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.

Original languageEnglish
Pages (from-to)229-240
Number of pages12
JournalCell
Volume75
Issue number2
DOIs
StatePublished - Oct 22 1993

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