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Department of Physiology [K. S., P. A. F.] and Institute of Human Virology and Division of Infectious Disease, Department of Medicine [M. L., U. B-P., A. L., A. H., B. L., P. A. F.], University of Maryland Medical School, Baltimore, Maryland 21201; Howard Hughes Medical Institute and Division of Molecular Oncology, Departments of Medicine and Pathology, Washington University School of Medicine, St. Louis, Missouri 63110 [C. M. K., S. J. K.]; Forschungszentrum Karlsruhe, Institut fuer Genetik, Postfach 3640, 76021 Karlsruhe, Germany [R. J.]; and Institut fuer Diabetesforschung, Koelner Platz 1, 80804 Munich, Germany [H. W.]
The impact of gain of Bcl-2 function on mammary epithelial cell survival was compared with loss of Bax function during the two stages of mammary gland involution. Bcl-2 gain of function reduced apoptosis 50% during the first stage and increased cell survival 70% during the second stage. Complete loss of Bax reduced apoptosis by 20% during the first stage without second stage effect. Partial loss of Bax was ineffective but increased cell survival 2.4-fold when combined with Bcl-2 gain. Gain of Bcl-2 function is more potent than loss of Bax function in regulating mammary epithelial cell survival in vivo.
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