Down-regulation of β1-adrenoceptors gene expression by short interfering RNA impairs the memory retrieval in the basolateral amygdala of rats

2007 ◽  
Vol 428 (2-3) ◽  
pp. 77-81 ◽  
Author(s):  
Ai Ling Fu ◽  
Xue Bin Yan ◽  
Li Sui
2010 ◽  
Vol 6 ◽  
pp. 1744-8069-6-2 ◽  
Author(s):  
Liu Si Lan ◽  
Yang Jian Ping ◽  
Wang Li Na ◽  
Jiang Miao ◽  
Qiu Qiao Cheng ◽  
...  

Endocrinology ◽  
2008 ◽  
Vol 149 (9) ◽  
pp. 4702-4709 ◽  
Author(s):  
Erik R. Nelson ◽  
Hamid R. Habibi

Thyroid hormones are important mediators of growth and development in vertebrates and act by binding to a specific family of thyroid receptors (TRs). The TRs belong to the nuclear receptor superfamily, with two conserved regions, a DNA binding domain and a ligand binding domain (LBD). We recently demonstrated the presence of four TR subtypes in goldfish, two with complete DNA binding domains and LBDs (TRα-1 and TRβ) and two novel forms including a transcript resembling TRα with variation in the LBD as well as a TRα-truncated (TRα-t) form lacking a LBD. To study the functional significance of TR subtypes, we first investigated the regulation of hepatic goldfish deiodinase type 3 (D3) by T3 and validated a bioassay in which D3 gene expression is up-regulated significantly in vivo and in vitro. Using short interfering RNA, TRα-1, TRβ, or TRα-t was specifically knocked down and thyroid hormone-induced D3 gene expression was measured. short interfering RNA against TRα-1 or TRβ reduced the T3 induction of deiodinase gene expression to 50% or less than 25% of control (T3 treated) cells, respectively. Knocking down TRα-t alone, however, increased D3 expression 500-fold supporting the hypothesis that TRα-t plays a modulatory role in thyroid hormone-induced gene expression. Our results provide important insight into thyroid receptor biology in goldfish and a framework for the better understanding of thyroid receptor function in all vertebrates.


2005 ◽  
Vol 280 (23) ◽  
pp. 22437-22444 ◽  
Author(s):  
Hong Chen ◽  
Szu-wei Tu ◽  
Jer-Tsong Hsieh

Human DAB2IP (hDAB2IP), a novel GTPase-activating protein modulating the Ras-mediated signaling and tumor necrosis factor-mediated apoptosis, is a potent growth inhibitor in human prostate cancer (PCa). Loss of hDAB2IP expression in PCa is due to altered epigenetic regulation (i.e. DNA methylation and histone modification) of its promoter region. The elevated polycomb Ezh2, a histone methyltransferase, has been associated with PCa progression. In this study, we have demonstrated that an increased Ezh2 expression in normal prostatic epithelial cells can suppress hDAB2IP gene expression. In contrast, knocking down the endogenous Ezh2 levels in PCa by a specific small interfering RNA can increase hDAB2IP expression. The association of Ezh2 complex (including Eed and Suz12) with hDAB2IP gene promoter is also detected in PCa cells but not in normal prostatic epithelial cells. Increased Ezh2 expression in normal prostatic epithelial cells by cDNA transfection facilitates the recruitment of other components of Ezh2 complex to the hDAB2IP promoter region accompanied with the increased levels of methyl histone H3 (H3) and histone deacetylase (HDAC1). Consistently, data from PCa cells transfected with Ezh2 small interfering RNA demonstrated that reduced Ezh2 levels resulted in the dissociation of Ezh2 complex accompanied with decreased levels of both methyl H3 and HDAC1 from hDAB2IP gene promoter. We further unveiled that the methylation status of Lys-27 but not Lys-9 of H3 in hDAB2IP promoter region is consistent with the hDAB2IP levels in both normal prostatic epithelial cells and PCa cells. Together, we conclude that hDAB2IP gene is a target gene of Ezh2 in prostatic epithelium, which provides an underlying mechanism of the down-regulation of hDAB2IP gene in PCa.


2021 ◽  
Author(s):  
Mitsuhiro Kinoshita ◽  
Atsushi Yamada ◽  
Kiyohito Sasa ◽  
Kaori Ikezaki ◽  
Tatsuo Shirota ◽  
...  

Abstract Nephronectin (Npnt) is an extracellular matrix protein and ligand of integrin α8β1 known to promote differentiation of osteoblasts. A search for factors that regulate Npnt gene expression in osteoblasts revealed that phorbol 12-myristate 13-acetate (PMA), which activates protein kinase C (PKC), had a strong effect to suppress that expression. Research was then conducted to elucidate the signaling pathway responsible for regulation of Npnt gene expression by PMA in osteoblasts. Treatment of MC3T3-E1 cells with PMA suppressed cell differentiation and Npnt gene expression. Effects were noted at a low concentration of PMA, and were time- and dose-dependent. Furthermore, treatment with the PKC signal inhibitor Gö6983 inhibited down-regulation of Npnt expression, while transfection with small interfering RNA (siRNA) of PKCα, c-Jun, and c-Fos suppressed that down-regulation. The present results suggest regulation of Npnt gene expression via the PKCα and c-Jun/c-Fos pathway.


PLoS ONE ◽  
2017 ◽  
Vol 12 (4) ◽  
pp. e0175784 ◽  
Author(s):  
Valentina Perri ◽  
Marsha Pellegrino ◽  
Francesca Ceccacci ◽  
Anita Scipioni ◽  
Stefania Petrini ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mitsuhiro Kinoshita ◽  
Atsushi Yamada ◽  
Kiyohito Sasa ◽  
Kaori Ikezaki ◽  
Tatsuo Shirota ◽  
...  

AbstractNephronectin (Npnt) is an extracellular matrix protein and ligand of integrin α8β1 known to promote differentiation of osteoblasts. A search for factors that regulate Npnt gene expression in osteoblasts revealed that phorbol 12-myristate 13-acetate (PMA), which activates protein kinase C (PKC), had a strong effect to suppress that expression. Research was then conducted to elucidate the signaling pathway responsible for regulation of Npnt gene expression by PMA in osteoblasts. Treatment of MC3T3-E1 cells with PMA suppressed cell differentiation and Npnt gene expression. Effects were noted at a low concentration of PMA, and were time- and dose-dependent. Furthermore, treatment with the PKC signal inhibitor Gö6983 inhibited down-regulation of Npnt expression, while transfection with small interfering RNA (siRNA) of PKCα, c-Jun, and c-Fos suppressed that down-regulation. The present results suggest regulation of Npnt gene expression via the PKCα and c-Jun/c-Fos pathway.


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