Ng S Y, Erba H, Latter G, Kedes L, Leavitt J
Armand Hammer Cancer Research Center, Linus Pauling Institute of Science and Medicine, Palo Alto, California 94306.
Mol Cell Biol. 1988 Apr;8(4):1790-4. doi: 10.1128/mcb.8.4.1790-1794.1988.
HuT-14T is a highly tumorigenic fibroblast cell line which exhibits a reduced steady-state level of beta-actin due to coding mutations in one of two beta-actin alleles. The normal rate of total actin synthesis could be restored in some clones of cells following transfection of the functional beta-actin gene but not following transfection of the functional gamma-actin gene. In gamma-actin gene-transfected substrains that have increased rates of gamma-actin synthesis, beta-actin synthesis is further reduced in a manner consistent with an autoregulatory mechanism, resulting in abnormal ratios of actin isoforms. Thus, both beta- and gamma-actin proteins can apparently regulate the synthesis of their coexpressed isoforms. In addition, decreased synthesis of normal beta-actin seems to correlate with a concomitant down-regulation of tropomyosin isoforms.
HuT-14T是一种具有高度致瘤性的成纤维细胞系,由于两个β-肌动蛋白等位基因之一发生编码突变,其β-肌动蛋白的稳态水平降低。在转染功能性β-肌动蛋白基因后,一些细胞克隆中总肌动蛋白的正常合成速率可以恢复,但转染功能性γ-肌动蛋白基因后则不能。在γ-肌动蛋白合成速率增加的γ-肌动蛋白基因转染亚系中,β-肌动蛋白合成以与自调节机制一致的方式进一步降低,导致肌动蛋白异构体比例异常。因此,β-肌动蛋白和γ-肌动蛋白蛋白显然都可以调节其共表达异构体的合成。此外,正常β-肌动蛋白合成的减少似乎与原肌球蛋白异构体的下调同时发生。