Transcriptional regulation of estrogen-responsive genes by non-steroidal estrogens: Doisynolic and allenolic acids

Meyers, Cal Y.; Lutfi, Hisham G.; Adler, Stuart B.

doi:10.1016/s0960-0760(97)00063-0

Cited by 18 publications

(13 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…10,11,13,18 (2) In animals (±)-cis-bisdehydrodoisynolic acid [(±)-1] and its 3-methyl ether [(±)-4] are highly estrogenic. 1,3,5,7,[13][14][15][16]20 However, a sensitive transcription assay showed that (±)-4 was 250-fold less active in human cell lines than in a nonhuman cell line.…”

Section: Discussion and Resultsmentioning

confidence: 99%

Absolute Structure Determination of the Highly Biologically Active Bisdehydrodoisynolic Acids

Meyers

Hou

Robinson

et al. 2000

Journal of Pharmaceutical Sciences

Self Cite

View full text Add to dashboard Cite

Section: Discussion and Resultsmentioning

confidence: 99%

Absolute Structure Determination of the Highly Biologically Active Bisdehydrodoisynolic Acids

Meyers

Hou

Robinson

et al. 2000

Journal of Pharmaceutical Sciences

Self Cite

View full text Add to dashboard Cite

“…Although the ERα and ERβ are similar in structure and function, mechanistic differences between the two receptor subtypes may augment or minimize the effects of polymorphisms on cognition and mood. These differences include the binding and transcription efficacy for non-steroidal ligands118, the levels of circulating 17β estradiol needed to activate a particular promoter119 and cofactors that help to initiate transcription 120. Although ESR2 is highly polymorphic, there may be fewer functional polymorphisms on the ESR2 versus ESR1 gene.…”

Section: Discussionmentioning

confidence: 99%

A review of estrogen receptor α gene (ESR1) polymorphisms, mood, and cognition

Sundermann¹,

Maki²,

Bishop³

2010

Menopause

137

View full text Add to dashboard Cite

OBJECTIVE There are significant individual differences in the extent to which mood and cognition change as a function of reproductive stage, menstrual phase, postpartum, and hormone therapy. This review explores the extent to which variations or polymorphisms in the estrogen receptor α gene (ESR1) predict cognitive and mood outcomes. METHODS A literature search was conducted from 1995 to November 2009 through PubMed, EMBASE, and PsychINFO. Twenty-five manuscripts were reviewed that summarize investigations of ESR1 in mental health. RESULTS Among studies investigating ESR1 in relation to cognition, 11 of 14 case-control studies reported an association between ESR1 polymorphisms and risk for developing dementia. Three of four prospective cohort studies reported an association between ESR1 polymorphisms and significant cognitive decline. There are inconsistencies between case-control and cohort studies regarding whether specific ESR1 alleles increase or decrease the risk for cognitive dysfunction. The relationships between ESR1 and cognitive impairment tend to be specific to or driven by women and restricted to risk for Alzheimer’s disease rather than other dementia causes. Three of five studies examining ESR1 polymorphisms in relation to anxiety or depressive symptoms found significant associations. Significant associations have also been reported between ESR1 polymorphisms and childhood-onset mood disorder and premenstrual dysphoric disorder. CONCLUSIONS A strong relationship between ESR1 variants and cognitive outcomes is evident and preliminary evidence suggests a role of the ESR1 gene in certain mood outcomes. Insights into the discordant results will come from future studies that include haplotype analyses, analyses within specific ethnic/racial populations, and gender-stratified analyses.

show abstract

“…CAT, β-galactosidase, and luciferase activities were measured as described by Godambe et al (35), Hall et al (36), and Meyers et al (33), respectively. Results were expressed as normalized CAT or luciferase activity after correction for transfection efficiency using the cotransfected β-galactosidase control for each well.…”

Section: Methodsmentioning

confidence: 99%

Estrogen decreases TNF gene expression by blocking JNK activity and the resulting production of c-Jun and JunD

Srivastava¹,

Weitzmann²,

Cenci³

et al. 1999

J. Clin. Invest.

Self Cite

232

142

View full text Add to dashboard Cite

Central to the bone-sparing effect of estrogen (E 2 ) is its ability to block the monocytic production of the osteoclastogenic cytokine TNF-α (TNF). However, the mechanism by which E 2 downregulates TNF production is presently unknown. Transient transfection studies in HeLa cells, an E 2 receptor-negative line, suggest that E 2 inhibits TNF gene expression through an effect mediated by estrogen receptor β (ERβ). We also report that in RAW 264.7 cells, an E 2 receptor-positive murine monocytic line, E 2 downregulates cytokine-induced TNF gene expression by decreasing the activity of the Jun NH 2 -terminal kinase (JNK). The resulting diminished phosphorylation of c-Jun and JunD at their NH 2 -termini decreases the ability of these nuclear proteins to autostimulate the expression of the c-Jun and JunD genes, thus leading to lower production of c-Jun and JunD. The consequent decrease in the nuclear levels of c-Jun and JunD leads to diminished binding of c-Jun/c-Fos and JunD/c-Fos heterodimers to the AP-1 consensus sequence in the TNF promoter and, thus, to decreased transactivation of the TNF gene.

show abstract

Transcriptional regulation of estrogen-responsive genes by non-steroidal estrogens: Doisynolic and allenolic acids

Cited by 18 publications

References 25 publications

Absolute Structure Determination of the Highly Biologically Active Bisdehydrodoisynolic Acids

Absolute Structure Determination of the Highly Biologically Active Bisdehydrodoisynolic Acids

A review of estrogen receptor α gene (ESR1) polymorphisms, mood, and cognition

Estrogen decreases TNF gene expression by blocking JNK activity and the resulting production of c-Jun and JunD

Contact Info

Product

Resources

About