ETS家族成员Tel拮抗造血细胞中的Fli-1表型。

The ETS family member Tel antagonizes the Fli-1 phenotype in hematopoietic cells.

作者信息

Kwiatkowski B A, Zielinska-Kwiatkowska A G, Bauer T R, Hickstein D D

机构信息

Medical Research Service, VA Puget Sound Health Care System, Seattle, Washington 98108, USA.

出版信息

Blood Cells Mol Dis. 2000 Feb;26(1):84-90. doi: 10.1006/bcmd.2000.0282.

DOI:10.1006/bcmd.2000.0282

PMID:10772879

Abstract

The ETS family member Tel is rearranged in human leukemia of both myeloid and lymphoid origin while the ETS member Fli-1 is insertionally activated in Friend erythroleukemia in mice and is translocated to the EWS locus in Ewing's sarcoma. In previous studies we demonstrated that Tel binds to Fli-1 and blocks transactivation of megakaryocytic promoters by Fli-1. In this study we demonstrate that expression of Fli-1 in the leukemia cell line K562 induces a megakaryocytic phenotype and the expression of the platelet markers GPIX, GP1balpha, and GPIIb. Introduction of Tel blocked the megakaryocytic phenotype induced by Fli-1, suggesting a biological correlation to the biochemical interaction of Tel and Fli-1 reported previously.

摘要

ETS家族成员Tel在髓系和淋巴系起源的人类白血病中发生重排，而ETS成员Fli-1在小鼠的Friend红白血病中被插入激活，并在尤因肉瘤中转位至EWS基因座。在先前的研究中，我们证明Tel与Fli-1结合并阻断Fli-1对巨核细胞启动子的反式激活。在本研究中，我们证明白血病细胞系K562中Fli-1的表达诱导了巨核细胞表型以及血小板标志物GPIX、GP1balpha和GPIIb的表达。引入Tel可阻断Fli-1诱导的巨核细胞表型，提示其与先前报道的Tel和Fli-1的生化相互作用存在生物学关联。