Identification of two novel, alternatively spliced mRNA transcripts of the human follicle‐stimulating hormone receptor
Identification of two novel, alternatively spliced mRNA transcripts of the human follicle‐stimulating hormone receptor
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DOI：
10.1002/mrd.22227
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发表时间：
2013-11
影响因子：
2.5
通讯作者：
Jun Zhou;Yiting Huang;Lili Li;Liang Zhu;Dan Zhang;Suzhan Zhang;Yiding Chen
中科院分区：
文献类型：
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作者：
Jun Zhou;Yiting Huang;Lili Li;Liang Zhu;Dan Zhang;Suzhan Zhang;Yiding Chen
糖蛋白激素受体含有由多个外显子编码的大的细胞外结构域，这些外显子可以选择性剪接。使用人卵巢表面上皮，我们克隆了人卵泡刺激素受体（FSH-R）基因的两个新剪接变体，hFSH-R2和hFSH-R3。 hFSH-R2 剪接变体与全长 FSH-R mRNA 的不同之处在于删除了外显子 10 并在外显子 9 后包含了两个小外显子，而 hFSH-R3 剪接变体仅保留了全长转录物的外显子 1-6。两种变体均以低水平表达，但在 30 名不同受试者的卵泡液细胞中均检测到。将这两种变体分别转染到 KGN 细胞（一种表达野生型 FSH-R 的卵巢癌细胞系）中，可减少 FSH 介导的 ERK1/2、Akt 和 p38/MAPK 磷酸化。此外，HEK293T 细胞中 hFSH-R2 或 hFSH-R3 与全长 FSH-R 的体外共表达减少了通过全长 FSH-R 的信号转导。需要进一步的研究来充分阐明这些受体亚型的功能。摩尔。重现。开发。 80: 916–923, 2013。© 2013 Wiley periodicals, Inc.
Glycoprotein hormone receptors contain large extracellular domains encoded by multiple exons that can be alternatively spliced. Using human ovarian surface epithelium, we cloned two new splice variants of the human follicle‐stimulating hormone receptor (FSH‐R) gene, hFSH‐R2 and hFSH‐R3. The hFSH‐R2 splice variant differed from the full‐length FSH‐R mRNA by the deletion of exon 10 and inclusion of two small exons after exon 9 whereas the hFSH‐R3 splice variant retained only exons 1–6 of the full‐length transcript. Both variants were expressed at low levels, but were detected in cells from follicular fluid derived from 30 different subjects. Transfection of these two variants individually into KGN cells, an ovarian cancer cell line that expresses wild‐type FSH‐R, reduced FSH‐mediated phosphorylation of ERK1/2, Akt, and p38/MAPK. Furthermore, in vitro co‐expression of either hFSH‐R2 or hFSH‐R3 and full‐length FSH‐R in HEK293T cells reduced signal transduction through full‐length FSH‐R. Further studies are needed to fully elucidate the functions of these receptor isoforms. Mol. Reprod. Dev. 80: 916–923, 2013. © 2013 Wiley Periodicals, Inc.