Steroid hormone estrogen elicits various physiological functions, many of which are mediated through two structurally and functionally distinct estrogen receptors, ERα and ERβ. The functional role of zinc finger protein 131 (ZNF131) is poorly understood, but it is assumed to possess transcriptional regulation activity due to the presence of a DNA binding motif. A few recent reports, including ours, revealed that ZNF131 acts as a negative regulator of ERα and that SUMO modification potentiates the negative effect of ZNF131 on estrogen signaling. However, its molecular mechanism for ERα inhibition has not been elucidated in detail. Here, we demonstrate that ZNF131 directly interacts with ERα, which consequently inhibits ERα-mediated trans-activation by suppressing its homo-dimerization. Moreover, we show that the C-terminal region of ZNF131 containing the SUMOylation site is necessary for its inhibition of estrogen signaling. Taken together, these data suggest that ZNF131 inhibits estrogen signaling by acting as an ERα-co-repressor.
|Number of pages||6|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - 2013 Jan 4|
Bibliographical noteFunding Information:
This work was supported by the National Research Foundation of Korea (NRF) Grant ( 2012R1A1A2021749 to K.C.C.) funded by the Ministry of Education, Science and Technology (MEST) and by Basic Science Research Program through NRF ( 2012-0000810 to K.C.C.), Republic of Korea. This study was also supported from the Brain Research Center of the 21st Century Frontier Research Program Technology ( 2009K-001251 to K.C.C.) funded by MEST. This work was also partially supported by a Grant of the Korea Healthcare technology R&D Project, Ministry for Health, Welfare & Family Affairs, Republic of Korea ( A092004 and A111653 to K.C.C.).
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology