Role of JunB in erythroid differentiation

被引:28
作者
Jacobs-Helber, SM
Abutin, RM
Tian, C
Bondurant, M
Wickrema, A
Sawyer, ST
机构
[1] Virginia Commonwealth Univ, Med Coll Virginia, Dept Pharmacol Toxicol, MVC Stn, Richmond, VA 23298 USA
[2] Dept Vet Affairs Med Ctr, Nashville, TN 37232 USA
[3] Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN 37232 USA
[4] Univ Illinois, Hematol Oncol Sect, Chicago, IL 60607 USA
关键词
D O I
10.1074/jbc.M107243200
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
The role of junB as a regulator of erythroid cell survival, proliferation, and differentiation was tested by controlled expression of Jun Bin the erythropoietin (EPO)-dependent erythroleukemia cell line HCD57. JunB induced erythroid differentiation as evidenced by increased expression of the erythroid-specific proteins beta-globin, spectrin-alpha, and TER-119. Expression of JunB for at least 48 h was required for the differentiated phenotype to emerge. Differentiation was accompanied by a slower rate of proliferation and an increase in the expression of the cell cycle inhibitory protein p27. p27 protein expression increased due to reduced turnover without changes in transcription, indicating global changes in cell physiology following JunB induction. JunB expression was also studied in mouse and human primary erythroid cells. JunB expression increased immediately in both primary mouse cells and HCD57 cells treated with EPO and quickly returned to base-line levels, followed by a secondary rise in JunB in primary erythroid cells, but not in HCD57 cells, 36-48 h later. This result suggested that the initial EPO-dependent JunB induction was not sufficient to induce differentiation, but that the late EPO-independent JunB expression in primary erythroid cells was necessary for differentiation. This study suggests that JunB is an important regulator of erythroid differentiation.
引用
收藏
页码:4859 / 4866
页数:8
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