Barra Y, Tanaka K, Isselbacher K J, Khoury G, Jay G
Mol Cell Biol. 1985 Jun;5(6):1295-300. doi: 10.1128/mcb.5.6.1295-1300.1985.
The identification of a unique major histocompatibility complex class I gene, designated Q10, which encodes a secreted rather than a cell surface antigen has led to questions regarding its potential role in regulating immunological functions. Since the Q10 gene is specifically activated only in the liver, we sought to define the molecular mechanisms which control its expression in a tissue-specific fashion. Results obtained by transfection of the cloned Q10 gene, either in the absence or presence of a heterologous transcriptional enhancer, into a variety of cell types of different tissue derivations are consistent with the Q10 gene being regulated at two levels. The first is by a cis-dependent mechanism which appears to involve site-specific DNA methylation. The second is by a trans-acting mechanism which would include the possibility of an enhancer binding factor. The ability to efficiently express the Q10 gene in certain transfected cell lines offers an opportunity to obtain this secreted class I antigen in quantities sufficient for functional studies; this should also make it possible to define regulatory sequences which may be responsible for the tissue-specific expression of Q10.
一种独特的主要组织相容性复合体I类基因(命名为Q10)被鉴定出来,它编码的是一种分泌型而非细胞表面抗原,这引发了关于其在调节免疫功能中潜在作用的问题。由于Q10基因仅在肝脏中被特异性激活,我们试图确定以组织特异性方式控制其表达的分子机制。通过将克隆的Q10基因转染到各种不同组织来源的细胞类型中,无论有无异源转录增强子,所获得的结果都与Q10基因在两个水平上受到调控一致。第一个水平是通过顺式依赖机制,这似乎涉及位点特异性DNA甲基化。第二个水平是通过反式作用机制,这可能包括增强子结合因子的可能性。在某些转染细胞系中高效表达Q10基因的能力为获得足够数量用于功能研究的这种分泌型I类抗原提供了机会;这也应该能够确定可能负责Q10组织特异性表达的调控序列。