Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.febslet.2012.03.067
Title: α-Actinin4 nuclear translocation mediates gonadotropin-releasing hormone stimulation of follicle-stimulating hormone β-subunit gene transcription in LβT2 cells
Authors: Yu, H.
Li, Z. 
Ghosh, D.
Lim, T.K. 
He, Y. 
Lin, Q. 
Keywords: ACTN4
Calmodulin-like domain
Fshβ
GnRH
Nuclear translocation
Issue Date: 21-May-2012
Citation: Yu, H., Li, Z., Ghosh, D., Lim, T.K., He, Y., Lin, Q. (2012-05-21). α-Actinin4 nuclear translocation mediates gonadotropin-releasing hormone stimulation of follicle-stimulating hormone β-subunit gene transcription in LβT2 cells. FEBS Letters 586 (10) : 1466-1471. ScholarBank@NUS Repository. https://doi.org/10.1016/j.febslet.2012.03.067
Abstract: Gonadotropin-releasing hormone (GnRH) regulates the synthesis and secretion of follicle-stimulating hormone (FSH) by stimulating the transcription of Fshβ gene. Our iTRAQ quantitative proteomics result showed that the abundance of α-actinin4 (ACTN4) increased in the nuclei of LβT2 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 Fshβ gene (mFshβ) 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 mFshβ gene transcription. © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Source Title: FEBS Letters
URI: http://scholarbank.nus.edu.sg/handle/10635/115360
ISSN: 00145793
DOI: 10.1016/j.febslet.2012.03.067
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.

SCOPUSTM   
Citations

3
checked on Sep 18, 2023

WEB OF SCIENCETM
Citations

2
checked on Sep 18, 2023

Page view(s)

309
checked on Sep 21, 2023

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.