RETINOIC ACID-INDUCED GRANULOCYTIC DIFFERENTIATION OF HL-60 MYELOID-LEUKEMIA CELLS IS MEDIATED DIRECTLY THROUGH THE RETINOIC ACID RECEPTOR (RAR-ALPHA)
RETINOIC ACID-INDUCED GRANULOCYTIC DIFFERENTIATION OF HL-60 MYELOID-LEUKEMIA CELLS IS MEDIATED DIRECTLY THROUGH THE RETINOIC ACID RECEPTOR (RAR-ALPHA)
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DOI：
10.1128/mcb.10.5.2154
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发表时间：
1990-05-01
影响因子：
5.3
通讯作者：
MUELLER, L
中科院分区：
文献类型：
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作者：
COLLINS, SJ;ROBERTSON, KA;MUELLER, L
维甲酸（RA）诱导HL-60早幼粒细胞白血病细胞系以及某些其他人类髓性白血病的终末粒细胞分化。特异性RA受体是核转录因子的类固醇甲状腺激素超家族的成员，最近已被确定。我们开发了一个相对抵抗ra诱导分化的HL-60亚克隆。与RA敏感亲本HL-60细胞的核RA受体相比，该抗RA亚克隆的特异性核RA受体对RA的亲和力降低，分子量降低。逆转录病毒载体介导将RA受体（RAR- α）的一个拷贝转导到抗RA的HL-60亚克隆中，恢复了这些细胞对RA的敏感性。这些观察结果表明RAR-。在介导ra诱导的HL-60白血病细胞终末分化中起关键和核心作用。
Retinoic acid (RA) induces terminal granulocytic differentiation of the HL-60 promyelocytic leukemia cell line as well as certain other human myeloid leukemias. Specific RA receptors that are members of the steroid-thyroid hormone superfamily of nuclear transcription factors have recently been identified. We developed an HL-60 subclone that was relatively resistant to RA-induced differentiation. Specific nuclear RA receptors in this RA-resistant subclone had a decreased affinity for RA and exhibited a lower molecular weight compared with nuclear RA receptors from the RA-sensitive parental HL-60 cells. Retroviral vector-mediated Transduction of a single copy of the RA receptor (RAR-.alpha.) into this RA-resistant HL-60 subclone restored the sensitivity of these cells to RA. These observations indicate that RAR-.alpha. plays a critical and central role in mediating RA-induced terminal differentiation of HL-60 leukemia cells.