TY - JOUR
T1 - Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair
AU - Veis, Deborah J.
AU - Sorenson, Christine M.
AU - Shutter, John R.
AU - Korsmeyer, Stanley J.
N1 - Funding Information:
We thank Dr. John Kissane for expert analysis of the renal pathology. We thank Karen Haag for expert animal care and technical assistance. Authors D. J. V., C. M. S., and J. R. S. all made substantial contributions to this paper. D. J. V. was supported by National Institutes of Health (NIH) training grant 5T32 EY 07108-04. This work was supported in part by NIH program project number 49712-05.
PY - 1993/10/22
Y1 - 1993/10/22
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0027427492&partnerID=8YFLogxK
U2 - 10.1016/0092-8674(93)80065-M
DO - 10.1016/0092-8674(93)80065-M
M3 - Article
C2 - 8402909
AN - SCOPUS:0027427492
SN - 0092-8674
VL - 75
SP - 229
EP - 240
JO - Cell
JF - Cell
IS - 2
ER -