TARGETED DISRUPTION OF THE FLK2/FLT3 GENE LEADS TO DEFICIENCIES IN PRIMITIVE HEMATOPOIETIC PROGENITORS

被引：475

作者：

MACKAREHTSCHIAN, K ^{[1
]}

HARDIN, JD ^{[1
]}

MOORE, KA ^{[1
]}

BOAST, S ^{[1
]}

GOFF, SP ^{[1
]}

LEMISCHKA, IR ^{[1
]}

机构：

[1] COLUMBIA UNIV,COLL PHYS & SURG,DEPT BIOCHEM & MOLEC BIOPHYS,NEW YORK,NY 10032

来源：

IMMUNITY | 1995年 / 3卷 / 01期

关键词：

D O I：

10.1016/1074-7613(95)90167-1

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：147 / 161

页数：15

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