BAX-DEFICIENT MICE WITH LYMPHOID HYPERPLASIA AND MALE GERM-CELL DEATH
BAX-DEFICIENT MICE WITH LYMPHOID HYPERPLASIA AND MALE GERM-CELL DEATH
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DOI：
10.1126/science.270.5233.96
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发表时间：
1995-10-06
期刊：
影响因子：
56.9
通讯作者：
KORSMEYER, SJ
中科院分区：
文献类型：
--
作者：
KNUDSON, CM;TUNG, KSK;KORSMEYER, SJ
BAX是BCL 2的异源二聚体伴侣，在功能获得性实验中对抗BCL 2并促进细胞凋亡。产生了Bax敲除小鼠，证明其存活，但在细胞死亡中显示谱系特异性畸变，该小鼠中的胸腺细胞和B细胞显示增生，并且Bax缺陷的卵巢包含具有过量颗粒细胞的不寻常的闭锁卵泡。与此相反，缺乏精子的男性不育的结果是曲细精管紊乱与非典型的减数分裂前生殖细胞的积累，但没有成熟的单倍体精子，多核巨细胞和发育不良的细胞伴随着大量的细胞死亡。因此，Bax的缺失导致增生或发育不全，这取决于细胞环境。
BAX, a heterodimeric partner of BCL2, counters BCL2 and promotes apoptosis in gain-of-function experiments, A Bax knockout mouse was generated that proved viable but displayed lineage-specific aberrations in cell death, Thymocytes and B cells in this mouse displayed hyperplasia, and Bax-deficient ovaries contained unusual atretic follicles with excess granulosa cells. In contrast, Bax-deficient males were infertile as a result of disordered seminiferous tubules with an accumulation of atypical premeiotic germ cells, but no mature haploid sperm, Multinucleated giant cells and dysplastic cells accompanied massive cell death. Thus, the loss of Bax results in hyperplasia or hypoplasia, depending on the cellular context.