伪-Actinin4 nuclear translocation mediates gonadotropin-releasing hormone stimulation of follicle-stimulating hormone 尾-subunit gene transcription in L尾T2 cells

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• 作者：Han Yu^a ; Zhengjun Li^b ; Dipanjana Ghosh^a ; Teck Kwang Lim^a ; Yuehui He^a ; ^c ; Qingsong Lin^a ; ^{dbslinqs@nus.edu.sg}
• 关键词：GnRH ; Fsh尾 ; ACTN4 ; Calmodulin-like domain ; Nuclear translocation
• 出版年：2012
• 期刊代码：70_00145793
• 类别：bio
• 出版时间：21 May, 2012
• 卷：586
• 期：10
• 页码：1466-1471
• 文件大小：718 K

摘要

Gonadotropin-releasing hormone (GnRH) regulates the synthesis and secretion of follicle-stimulating hormone (FSH) by stimulating the transcription of Fsh尾 gene. Our iTRAQ quantitative proteomics result showed that the abundance of 伪-actinin4 (ACTN4) increased in the nuclei of L尾T2 cells upon GnRH induction. Using RNA interference, reverse transcription and real-time PCR, luciferase and transient transfection assays, we proved that ACTN4 is involved in the regulation of mouse Fsh尾 gene (mFsh尾) transcription and its C-terminal calmodulin (CaM)-like domain is crucial for this process. Our study suggests that ACTN4 nuclear translocation mediates GnRH stimulation of mFsh尾 gene transcription.