首页> 外文期刊>Molecular and Cellular Biology >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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Retinoic acid-induced granulocytic differentiation of HL-60 myeloid leukemia cells is mediated directly through the retinoic acid receptor (RAR-alpha).

机译:维甲酸诱导的HL-60髓性白血病细胞的粒细胞分化直接通过维甲酸受体(RAR-alpha)介导。

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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.
机译: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样白血病的终末粒细胞分化。最近已经确定了特定的RA受体,它们是核转录因子的类固醇-甲状腺激素超家族的成员。我们开发了相对抗RA诱导分化的HL-60亚克隆。与来自RA敏感的亲本HL-60细胞的RA核仁受体相比,该RA抗性亚克隆中的特定RA核仁受体亲和力降低,分子量降低。逆转录病毒载体介导的单拷贝的RA受体(RAR-alpha)转导到这种抗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-α在介导RA诱导的HL-60白血病细胞的终末分化中起着至关重要的作用。

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