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Christine M. Jewell

Researcher at National Institutes of Health

Publications -  30
Citations -  3928

Christine M. Jewell is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Glucocorticoid receptor & Receptor. The author has an hindex of 22, co-authored 30 publications receiving 3811 citations. Previous affiliations of Christine M. Jewell include University of North Carolina at Chapel Hill & Research Triangle Park.

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Journal ArticleDOI

Characterization of mechanisms involved in transrepression of NF-kappa B by activated glucocorticoid receptors.

TL;DR: The data suggest that NF-kappa B, AP-1, and GR interact in a complex regulatory network to modulate gene expression and that cross-coupling of NF- kappa B and GR plays an important role in glucocorticoid-mediated repression of cytokine transcription.
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Proinflammatory cytokines regulate human glucocorticoid receptor gene expression and lead to the accumulation of the dominant negative beta isoform: a mechanism for the generation of glucocorticoid resistance.

TL;DR: The identification of a tumor necrosis factor-responsive NF-κB DNA binding site 5′ to the hGR promoter that leads to a 1.5-fold increase in GRα mRNA and a 2.0-fold rise in GRβ mRNA in HeLaS3 cells is reported, making GRβ the predominant endogenous receptor isoform.
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The Dominant Negative Activity of the Human Glucocorticoid Receptor β Isoform SPECIFICITY AND MECHANISMS OF ACTION

TL;DR: The results suggest that formation of transcriptionally impaired hGRalpha-hGRbeta heterodimers is an important component of the mechanism responsible for the dominant negative activity of hGRbeta.
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Mouse Glucocorticoid Receptor Phosphorylation Status Influences Multiple Functions of the Receptor Protein

TL;DR: Receptors containing seven or eight mutated sites have a markedly extended half-life and do not show the ligand-dependent destabilization seen with wild type receptor, showing that receptor phosphorylation may play a crucial role in regulating receptor levels and hence control receptor functions.
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Multiple glucocorticoid receptor isoforms and mechanisms of post-translational modification.

TL;DR: The recent advances made in identifying the processes that generate and modify multiple GR isoforms and the post-translational modifications that contribute to the increasing diversity in the glucocorticoid signaling pathway are outlined.