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Cellular proliferation and telomerase activity in CHRF-288-11 cells.

机译:CHRF-288-11细胞中的细胞增殖和端粒酶活性。

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Telomerase activity is detected in many immortalized cell lines. Recent studies suggest that terminal differentiation of some of these cell lines is associated with a reduction in telomerase activity. However, the question remains whether the reduction in telomerase activity results from terminal differentiation or from cessation of cellular proliferation. This was explored in the megakaryocytic cell line CHRF-288-11. Cells were treated with phorbol 12-myristate 13-acetate (PMA), which induces terminal differentiation of CHRF-288-11 cells, EGTA, serum depletion, and okadaic acid. All treatments resulted in cessation of proliferation. Except for okadaic acid, these treatments also induced inhibition of telomerase within 7 days. Restoring the original growth conditions of cells treated with PMA, EGTA and serum depletion resulted in the reversal of telomerase inhibition and an acceleration of proliferation. Apparent inhibition of telomerase was observed to follow the cessation of proliferation, whereas enhanced telomerase activity was noted to precede acceleration in proliferation. Thus, telomerase activity usually reflects the proliferative status rather than the differentiated status of CHRF-288-11 cells.
机译:在许多永生细胞系中检测到端粒酶活性。最近的研究表明,其中一些细胞系的终末分化与端粒酶活性的降低有关。然而,问题仍然在于端粒酶活性的降低是由于终末分化还是由于细胞增殖的停止。在巨核细胞系CHRF-288-11中对此进行了研究。用佛波醇12-肉豆蔻酸酯13-乙酸酯(PMA)处理细胞,该物质可诱导CHRF-288-11细胞,EGTA,血清耗竭和冈田酸的终末分化。所有治疗均导致增殖停止。除冈田酸外,这些处理方法还可以在7天内抑制端粒酶。恢复用PMA,EGTA处理的细胞的原始生长条件和血清耗竭可导致端粒酶抑制作用的逆转和增殖的加速。观察到端粒酶的明显抑制是在增殖停止后发生的,而端粒酶活性的增强被认为是在增殖加速之前。因此,端粒酶活性通常反映CHRF-288-11细胞的增殖状态而不是分化状态。

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