TARGETED DISRUPTION OF THE FLK2/FLT3 GENE LEADS TO DEFICIENCIES IN PRIMITIVE HEMATOPOIETIC PROGENITORS
TARGETED DISRUPTION OF THE FLK2/FLT3 GENE LEADS TO DEFICIENCIES IN PRIMITIVE HEMATOPOIETIC PROGENITORS
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DOI：
10.1016/1074-7613(95)90167-1
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发表时间：
1995-07-01
期刊：
影响因子：
32.4
通讯作者：
LEMISCHKA, IR
中科院分区：
文献类型：
--
作者：
MACKAREHTSCHIAN, K;HARDIN, JD;LEMISCHKA, IR
flk 2受体酪氨酸激酶与造血发育有关。产生flk 2缺陷的小鼠。突变体发育成具有正常成熟造血群体的健康成年人。然而，它们具有原始B淋巴祖细胞的特异性缺陷，骨髓移植实验揭示了突变干细胞在T细胞和骨髓重建方面的进一步缺陷。缺乏c-kit和flk 2的小鼠表现出更严重的表型，其特征是造血细胞数量总体大幅减少，淋巴祖细胞相对频率进一步降低，以及出生后致死。总之，这些数据表明flk 2在多能干细胞和淋巴样分化中发挥作用。
The flk2 receptor tyrosine kinase has been implicated in hematopoietic development. Mice deficient in flk2 were generated. Mutants developed into healthy adults with normal mature hematopoietic populations. However, they possessed specific deficiencies in primitive B lymphoid progenitors, Bone marrow transplantation experiments revealed a further deficiency in T cell and myeloid reconstitution by mutant stem cells. Mice deficient for both c-kit and flk2 exhibited a more severe phenotype characterized by large overall decreases in hematopoietic cell numbers, further reductions in the relative frequencies of lymphoid progenitors, and a postnatal lethality. Taken together, the data suggest that flk2 plays a role both in multipotent stem cells and in lymphoid differentiation.