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• W2048589552 abstract "Estrogen-related receptor (ERR) is a member of the nuclear receptor superfamily that has strong homology with estrogen receptor (ER) α. ERR has three subtypes (α, β, and γ) expressed in estrogen-sensitive organs, including ovary, breast, and brain. No endogenous ligands of ERRs have been identified, but these receptors share a common DNA element with ERα and control estrogen-mediated gene transcription. Recent evidence suggests a role of ERRs in estrogen-related pathophysiology, but the detailed mechanisms of ERR functions in estrogen-related tissues are unclear. Using live-cell imaging with fluorescent protein labeling, we found that only ERRβ among the ERRs exhibits a punctate intranuclear pattern overlapping with ERα following 17β-estradiol (E2)-stimulation. Fluorescence recovery after photobleaching showed significant reduction of the mobility of ligand-activated ERα with co-expression of ERRβ. Fluorescence resonance energy transfer revealed that ERRβ directly interacts with ERα. The N-terminal domain of ERRβ was identified as the region that interacts with ERα. We also found a correlation between punctate cluster formation of ERα and interaction between the receptors. Expression of ERRβ significantly repressed ERα-mediated transactivity, whereas that of other ERR subtypes had no effect on the transactivity of ERα. Consistent with this finding, E2-stimulated proliferation of MCF-7 breast carcinoma cells and bcl-2 expression was significantly inhibited by expression of ERRβ. These results provide strong evidence for a suppressive effect of ERRβ on estrogen signaling through reduction of the intranuclear mobility of ERα. The findings further suggest a unique inhibitory role for ERRβ in estrogen-dependent cellular function such as cancer cell proliferation.Background: The role of orphan nuclear receptor ERRβ in estrogen-related pathophysiology is poorly understood.Results: ERRβ repressed the transactivity of ERα and proliferation of MCF-7 breast carcinoma cells through reduction of the intranuclear mobility of ERα.Conclusion: ERRβ affects ERα dynamics and function.Significance: Regulation of ERRβ will provide a potential therapeutic approach for estrogen-related cancer. Estrogen-related receptor (ERR) is a member of the nuclear receptor superfamily that has strong homology with estrogen receptor (ER) α. ERR has three subtypes (α, β, and γ) expressed in estrogen-sensitive organs, including ovary, breast, and brain. No endogenous ligands of ERRs have been identified, but these receptors share a common DNA element with ERα and control estrogen-mediated gene transcription. Recent evidence suggests a role of ERRs in estrogen-related pathophysiology, but the detailed mechanisms of ERR functions in estrogen-related tissues are unclear. Using live-cell imaging with fluorescent protein labeling, we found that only ERRβ among the ERRs exhibits a punctate intranuclear pattern overlapping with ERα following 17β-estradiol (E2)-stimulation. Fluorescence recovery after photobleaching showed significant reduction of the mobility of ligand-activated ERα with co-expression of ERRβ. Fluorescence resonance energy transfer revealed that ERRβ directly interacts with ERα. The N-terminal domain of ERRβ was identified as the region that interacts with ERα. We also found a correlation between punctate cluster formation of ERα and interaction between the receptors. Expression of ERRβ significantly repressed ERα-mediated transactivity, whereas that of other ERR subtypes had no effect on the transactivity of ERα. Consistent with this finding, E2-stimulated proliferation of MCF-7 breast carcinoma cells and bcl-2 expression was significantly inhibited by expression of ERRβ. These results provide strong evidence for a suppressive effect of ERRβ on estrogen signaling through reduction of the intranuclear mobility of ERα. The findings further suggest a unique inhibitory role for ERRβ in estrogen-dependent cellular function such as cancer cell proliferation. Background: The role of orphan nuclear receptor ERRβ in estrogen-related pathophysiology is poorly understood. Results: ERRβ repressed the transactivity of ERα and proliferation of MCF-7 breast carcinoma cells through reduction of the intranuclear mobility of ERα. Conclusion: ERRβ affects ERα dynamics and function. Significance: Regulation of ERRβ will provide a potential therapeutic approach for estrogen-related cancer." @default.
• W2048589552 created "2016-06-24" @default.
• W2048589552 creator A5030086603 @default.
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• W2048589552 creator A5084472017 @default.
• W2048589552 date "2015-05-01" @default.
• W2048589552 modified "2023-10-13" @default.
• W2048589552 title "Estrogen-related Receptor β Reduces the Subnuclear Mobility of Estrogen Receptor α and Suppresses Estrogen-dependent Cellular Function" @default.
• W2048589552 cites W1491569850 @default.
• W2048589552 cites W1592463243 @default.
• W2048589552 cites W1599762863 @default.
• W2048589552 cites W1631244035 @default.
• W2048589552 cites W1965322994 @default.
• W2048589552 cites W1969392840 @default.
• W2048589552 cites W1969478295 @default.
• W2048589552 cites W1972531835 @default.
• W2048589552 cites W1973775511 @default.
• W2048589552 cites W1974900814 @default.
• W2048589552 cites W1976658071 @default.
• W2048589552 cites W1981159999 @default.
• W2048589552 cites W1984151469 @default.
• W2048589552 cites W1986622643 @default.
• W2048589552 cites W1990579890 @default.
• W2048589552 cites W1993904629 @default.
• W2048589552 cites W2000483250 @default.
• W2048589552 cites W2002351432 @default.
• W2048589552 cites W2006622169 @default.
• W2048589552 cites W2008066256 @default.
• W2048589552 cites W2009089542 @default.
• W2048589552 cites W2013355489 @default.
• W2048589552 cites W2014889785 @default.
• W2048589552 cites W2036067118 @default.
• W2048589552 cites W2037634249 @default.
• W2048589552 cites W2039576757 @default.
• W2048589552 cites W2041816506 @default.
• W2048589552 cites W2043633408 @default.
• W2048589552 cites W2044480687 @default.
• W2048589552 cites W2044565056 @default.
• W2048589552 cites W2049866636 @default.
• W2048589552 cites W2055570003 @default.
• W2048589552 cites W2056569159 @default.
• W2048589552 cites W2060034283 @default.
• W2048589552 cites W2066260773 @default.
• W2048589552 cites W2066286957 @default.
• W2048589552 cites W2067083629 @default.
• W2048589552 cites W2067980525 @default.
• W2048589552 cites W2071129618 @default.
• W2048589552 cites W2076192875 @default.
• W2048589552 cites W2080149353 @default.
• W2048589552 cites W2080536099 @default.
• W2048589552 cites W2090754786 @default.
• W2048589552 cites W2093535482 @default.
• W2048589552 cites W2093718545 @default.
• W2048589552 cites W2099518138 @default.
• W2048589552 cites W2101052783 @default.
• W2048589552 cites W2102827103 @default.
• W2048589552 cites W2105373189 @default.
• W2048589552 cites W2111819089 @default.
• W2048589552 cites W2112980664 @default.
• W2048589552 cites W2121132820 @default.
• W2048589552 cites W2122265031 @default.
• W2048589552 cites W2122969246 @default.
• W2048589552 cites W2128003724 @default.
• W2048589552 cites W2136812627 @default.
• W2048589552 cites W2139844763 @default.
• W2048589552 cites W2142252785 @default.
• W2048589552 cites W2142459690 @default.
• W2048589552 cites W2156281856 @default.
• W2048589552 cites W2157019406 @default.
• W2048589552 cites W2162612828 @default.
• W2048589552 cites W2166404930 @default.
• W2048589552 cites W2169102073 @default.
• W2048589552 cites W2169458819 @default.
• W2048589552 cites W2172200901 @default.
• W2048589552 doi "https://doi.org/10.1074/jbc.m114.619098" @default.
• W2048589552 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4424363" @default.
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• W2048589552 hasPublicationYear "2015" @default.
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