Guo G G, Gu M, Etlinger J D
Department of Cell Biology and Anatomy, New York Medical College, Valhalla 10595.
J Biol Chem. 1994 Apr 29;269(17):12399-402.
The 240-kDa proteasome inhibitor has been reported to be an ATP-stabilized component (CF-2) of the 26 S proteasome complex. We now report that this inhibitory factor is indistinguishable from delta-aminolevulinic acid dehydratase (ALAD), the second enzyme in the pathway of heme synthesis, based upon the following observations: 1) common sequence of the first 14 N-terminal amino acids; 2) identical migration on native and SDS-polyacrylamide gel electrophoresis; 3) identical isoelectric points of pH 7.1; 4) cross-reactivity of specific polyclonal antibodies; 5) similar dehydratase and proteasome inhibitor specific activities in both proteins; and 6) the presence of both activities in recombinant ALAD. The dual role of this protein as CF-2 in the ATP/ubiquitin-dependent pathway and in heme synthesis may be an example of "gene sharing" and explains the unexpected abundance of ALAD noted in earlier studies.
据报道,240 kDa的蛋白酶体抑制剂是26S蛋白酶体复合物的一种ATP稳定成分(CF-2)。基于以下观察结果,我们现在报告该抑制因子与血红素合成途径中的第二种酶δ-氨基乙酰丙酸脱水酶(ALAD)无法区分:1)前14个N端氨基酸的共同序列;2)在天然和SDS聚丙烯酰胺凝胶电泳上的相同迁移;3)相同的pH 7.1等电点;4)特异性多克隆抗体的交叉反应性;5)两种蛋白质中相似的脱水酶和蛋白酶体抑制剂比活性;以及6)重组ALAD中两种活性的存在。这种蛋白质在ATP/泛素依赖性途径和血红素合成中作为CF-2的双重作用可能是“基因共享”的一个例子,并解释了早期研究中注意到的ALAD意外丰富的现象。