Article citationsMore>>
Z. Wang, X. Zhang, P. Shen, B. W. Loggie, Y. Chang and T. F. Deuel, “Identification, Cloning, and Expression of Human Estrogen Receptor-Alpha36, a Novel Variant of Human Estrogen Receptor-Alpha66,” Biochemical and Biophysical Research Communications, Vol. 336, No. 4, 2005, pp. 1023-1027. doi:10.1016/j.bbrc.2005.08.226
has been cited by the following article:
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TITLE:
Estrogen Receptor Alpha 36 Gene Knockdown Promote the Expression of NF-κB in PC12 Cells
AUTHORS:
Ping Zou, Chao Qu, Yihui Xu, Hongyan Li, Dannv Han, Dan Shi, Wei Zou
KEYWORDS:
NF-κB; Estrogen Receptor Alpha 36; PC12 Cells
JOURNAL NAME:
Open Journal of Endocrine and Metabolic Diseases,
Vol.3 No.4B,
August
6,
2013
ABSTRACT: The nuclear
transcription factors κB (NF-κB) is widely existing in various kinds of cell
types in the nervous system and plays an
important role in neuron apoptosis and neurodegenerative diseases. Estrogen
receptor alpha 36 (ER-α36), is a novel
variant of ERα (as known ER-α66) which can transduce both estrogenand
antiestrogen-dependent activation of MAPK signal pathway and stimulate cell
growth. Here, we aimed to detect the
effect of ER-α36 gene silencing on
the expression of NF-κB in normal cultured PC12 cells and to provide an experimental
foundation for understanding the function of ER-α36 innerve
cells. PC12 cells with ER-α36
expression knocked down by the shRNA method. Then Western blot and immunocytochemical
staining were performed to detect the expression and
translocation of NF-κB after transfection. The results showed that NF-κB
expression was significantly higher comparing with the control group after
transfection (P 0.01). Also, NF-κB subunit entered nuclear after
transfection; Immunofluorescence staining and immunocytochemical staining of
PC12 cells demonstrated that ER-α36
was expressed mainly on the plasma membrane and on the cell nucleus membrane.
These data indicate that ER-α36 gene
silencing can increase the expression of NF-κB and promote its nuclear
translocation in PC12 cells.