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α‐Actinin4 nuclear translocation mediates gonadotropin‐releasing hormone stimulation of follicle‐stimulating hormone β‐subunit gene transcription in LβT2 cells
Author(s) -
Yu Han,
Li Zhengjun,
Ghosh Dipanjana,
Lim Teck Kwang,
He Yuehui,
Lin Qingsong
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.03.067
Subject(s) - stimulation , follicle stimulating hormone , chemistry , hormone , endocrinology , chromosomal translocation , medicine , gonadotropin , protein subunit , gene , transcription (linguistics) , microbiology and biotechnology , biology , luteinizing hormone , biochemistry , linguistics , philosophy
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.