BCL-2-DEFICIENT MICE DEMONSTRATE FULMINANT LYMPHOID APOPTOSIS, POLYCYSTIC KIDNEYS, AND HYPOPIGMENTED HAIR

被引：1420

作者：

VEIS, DJ ^{[1
]}

SORENSON, CM ^{[1
]}

SHUTTER, JR ^{[1
]}

KORSMEYER, SJ ^{[1
]}

机构：

[1] WASHINGTON UNIV, SCH MED, HOWARD HUGHES MED INST, DEPT PATHOL, ST LOUIS, MO 63110 USA

来源：

CELL | 1993年 / 75卷 / 02期

关键词：

D O I：

10.1016/0092-8674(93)80065-M

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：229 / 240

页数：12

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