Bucher P, Corthésy P, Imbert J, Nabholz M
Swiss Institute for Experimental Cancer Research (ISREC), Epalinges, Switzerland.
Immunobiology. 1997 Dec;198(1-3):136-43. doi: 10.1016/s0171-2985(97)80034-4.
IL-2 stimulates expression of the alpha subunit of the high affinity IL-2 receptor (IL-2R alpha) in antigen-activated T lymphocytes, by increasing IL-2R alpha gene transcription. This response is mediated by a 52 nt IL-2 responsive enhancer (IL-2rE) that is conserved between mouse and man. The mouse enhancer is 1.3 kb upstream of the transcription start site and co-localizes with an inducible DNasel hypersensitive site, whereas the human homologue maps to -4 kb. The human IL-2rE is functional in rodent cells. Both enhancers contain two potential STAT binding sites and an Ets consensus motif. One of the STAT motifs overlaps with a binding site for GATA factors. Functional analysis of the mouse and human enhancers indicates that IL-2-activated STAT5 and the constitutively active Ets protein Elf-1 play a predominant role in controlling IL-2rE activity.
白细胞介素-2(IL-2)通过增加IL-2Rα基因转录,刺激抗原激活的T淋巴细胞中高亲和力IL-2受体(IL-2Rα)α亚基的表达。这种反应由一个52个核苷酸的IL-2反应增强子(IL-2rE)介导,该增强子在小鼠和人类之间保守。小鼠增强子位于转录起始位点上游1.3 kb处,并与一个可诱导的DNase超敏位点共定位,而人类同源物定位于-4 kb处。人类IL-2rE在啮齿动物细胞中具有功能。两种增强子都包含两个潜在的信号转导和转录激活因子(STAT)结合位点和一个Ets共有基序。其中一个STAT基序与GATA因子的结合位点重叠。对小鼠和人类增强子的功能分析表明,IL-2激活的STAT5和组成型活性Ets蛋白Elf-1在控制IL-2rE活性中起主要作用。