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Nancy G. Forger

Researcher at Georgia State University

Publications -  113
Citations -  4884

Nancy G. Forger is an academic researcher from Georgia State University. The author has contributed to research in topics: Sexual differentiation & Stria terminalis. The author has an hindex of 40, co-authored 104 publications receiving 4468 citations. Previous affiliations of Nancy G. Forger include State University of New York System & University of California, Berkeley.

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The epigenetics of sex differences in the brain.

TL;DR: The study of epigenetics of sex differences is in its earliest stages, with needed advances in understanding of the hormonal regulation of enzymes controlling acetylation and methylation, coregulatory proteins, transient versus stable DNA methylation patterns, and sex differences across the epigenome to fully understand sex differences in brain and behavior.
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Deletion of Bax eliminates sex differences in the mouse forebrain

TL;DR: Bax-dependent cell death is required for sexual differentiation of cell number, regardless of whether testosterone decreases or increases cell death, and the sex difference in AVPV dopaminergic cell number was not affected by Bax gene deletion, demonstrating heterogeneity of mechanisms controlling cell number within a single nucleus.
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Seasonal variation in mammalian striated muscle mass and motoneuron morphology.

TL;DR: Photoperiod-induced fluctuations in gonadal function of white-footed mice were associated with morphological changes in perineal muscles and their motoneurons, and Androgen-mediated annual changes in muscle mass and motoneuron morphology appear to be a natural part of this species' physiology.
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Epigenetic control of sexual differentiation of the bed nucleus of the stria terminalis.

TL;DR: It is suggested that a disruption in histone deacetylation may lead to long-term alterations in gene expression that block the masculinizing actions of testosterone in the BNSTp.
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Cell death and sexual differentiation of the nervous system

TL;DR: Evidence is presented for the hormonal regulation of neurotrophic factors and involvement of Bcl-2 family proteins in the determination of sex differences in neuron number and molecular mechanisms by which gonadal steroids may control cell survival.