Hisamatsu H, Shimbara N, Saito Y, Kristensen P, Hendil K B, Fujiwara T, Takahashi E, Tanahashi N, Tamura T, Ichihara A, Tanaka K
Institute for Enzyme Research, University of Tokushima, Japan.
J Exp Med. 1996 Apr 1;183(4):1807-16. doi: 10.1084/jem.183.4.1807.
Interferon (IFN) gamma induces replacements of the proteasomal subunits X and Y by LMP7 and LMP2, respectively, resulting in an alteration of the proteolytic specificity. We found a third pair of proteasome subunits expressed reciprocally in response to IFN-gamma. Molecular cloning of a cDNA encoding one subunit designated as Z, downregulated by IFN-gamma, showed that it is a novel proteasomal subunit with high homology to MECL1, which is markedly induced by IFN-gamma. Thus, IFN-gamma induces subunit replacements of not only X and Y by LMP7 and LMP2, respectively, but also of Z by MECL1, producing proteasomes responsible for immunological processing of endogenous antigens. When processed from their precursors, three pairs of the 10 homologous, but distinct, beta-type subunits of eukaryotic proteasomes, that is, X/LMP7, Y/LMP2, and Z/MECL1, have an NH2-terminal threonine residue, assumed to be part of a catalytic center. These findings suggest that the altered molecular organization of the proteasome induced by IFN-gamma may be responsible for acquisition of its functional change.
干扰素(IFN)γ分别诱导蛋白酶体亚基X和Y被LMP7和LMP2取代,导致蛋白水解特异性改变。我们发现了第三对蛋白酶体亚基,它们在对IFN-γ的反应中相互表达。编码一个被命名为Z的亚基的cDNA的分子克隆显示,它是一个与MECL1高度同源的新型蛋白酶体亚基,而MECL1被IFN-γ显著诱导。因此,IFN-γ不仅分别诱导X和Y被LMP7和LMP2取代,还诱导Z被MECL1取代,产生负责内源性抗原免疫处理的蛋白酶体。当真核生物蛋白酶体的10个同源但不同的β型亚基的三对从其前体加工而来时,即X/LMP7、Y/LMP2和Z/MECL1,都有一个假定为催化中心一部分的NH2末端苏氨酸残基。这些发现表明,IFN-γ诱导的蛋白酶体分子组织改变可能是其功能变化的原因。