Evi27 encodes a novel membrane protein with homology to the IL17 receptor
Evi27 encodes a novel membrane protein with homology to the IL17 receptor
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DOI：
10.1038/sj.onc.1203577
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发表时间：
2000-04-20
期刊：
影响因子：
8
通讯作者：
Shaughnessy, JD
中科院分区：
文献类型：
--
作者：
Tian, EM;Sawyer, JR;Shaughnessy, JD
Evi 27是BXH 2小鼠髓性白血病中逆转录病毒整合的常见位点。在这里，我表明，在Evi 27整合发生在一个CpG岛类似于6 kb上游的一个新的基因（命名为Evi 27）与IL 17受体（IL 17 r）的同源性，并在前病毒的整合结果在细胞表面上的Evi 27蛋白的表达增加。人Evi 27同源基因也被克隆并定位于染色体3 p21。在人和小鼠中均检测到Evi 27的多种异构体，表明Evi 27的表达是复杂的。一些同种型显示可能代表通过内含子掺入或通过蛋白水解切割产生的蛋白质的分泌可溶形式。在小鼠中，最高的Evi 27表达发生在肝脏和睾丸中，而在肾脏和肺中表达较低。在人类中，Evi 27在肾脏中以高水平表达，在肝脏、脑和睾丸中以中等水平表达。在造血细胞内，Evi 27的表达受到限制。北方和Western分析显示Evi 27在选定的T细胞、B细胞和骨髓细胞系中表达。这些结果表明，Evi 27表达在造血分化过程中受到严格调控。总的来说，这些研究鉴定了细胞因子受体家族的nea成员，其增加的和不协调的表达可能通过改变Evi 27控制造血细胞生长和/或分化的正常能力而导致骨髓性白血病。
Evi27 is a common site of retroviral integration in BXH2 murine myeloid leukemias. Here me show that integration at Evi27 occurs in a CpG island similar to 6 kb upstream from a novel gene (designated Evi27) with homology to the IL17 receptor (Il17r) and that proviral integrations result in increased expression of the Evi27 protein on the cell surface. The human EVI27 homology was also cloned and mapped to chromosome 3p21, Multiple Evi27 isoforms were detected at the RNA and protein level in both human and mouse, indicating that Evi27 expression is complex. Some of the isoforms are shown to likely represent secreted soluble forms of the protein produced by intron incorporation or by proteolytic cleavage. In the mouse, highest Evi27 expression occurs in liver and testes with lower expression in kidney and lung, In humans, EVI27 is expressed at high levels in the kidney, with moderate levels in the liver, brain, and testes. Within hematopoietic cells, Evi27 expression is restricted. Northern and Western analysis showed that Evi27 is expressed in selected T-cell B-cell and myeloid cell lines. These results suggest that Evi27 expression is tightly regulated during hematopoietic differentiation. Collectively, these studies identify a nea member of the cytokine receptor family whose increased and uncoordinated expression may lead to myeloid leukemia by altering Evi27's normal ability to control the growth and/or differentiation of hematopoietic cells.