M
Michael G. Rosenfeld
Researcher at University of California, San Diego
Publications - 522
Citations - 112098
Michael G. Rosenfeld is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Transcription factor & Regulation of gene expression. The author has an hindex of 178, co-authored 504 publications receiving 107707 citations. Previous affiliations of Michael G. Rosenfeld include Tokai University & Salk Institute for Biological Studies.
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Journal ArticleDOI
A pituitary POU domain protein, Pit-1, activates both growth hormone and prolactin promoters transcriptionally.
Harry J. Mangalam,Vivian R. Albert,Holly A. Ingraham,Michael S. Kapiloff,Laura Wilson,Charles A. Nelson,Harry P. Elsholtz,Michael G. Rosenfeld +7 more
TL;DR: It is found that when the pituitary-specific 33-kD transcription factor Pit-1 is expressed in either the heterologous HeLa cell line or in bacteria, it binds to and activates transcription from both growth hormone and prolactin promoters in vitro at levels even 10-fold lower than those normally present in pituitaries.
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Nuclear receptor coregulators: multiple modes of modification.
TL;DR: This review focuses on the different modes of regulation of nuclear receptor coregulators and the implications for tissue- and context-specific transcriptional responses to hormone and membrane receptor signaling.
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Nuclear Integration of Glucocorticoid Receptor and Nuclear Factor-κB Signaling by CREB-binding Protein and Steroid Receptor Coactivator-1
Kelly-Ann Sheppard,Kathleen M. Phelps,Amy J. Williams,Dimitris Thanos,Christopher K. Glass,Michael G. Rosenfeld,Mary E. Gerritsen,Tucker Collins +7 more
TL;DR: It is proposed that cross-talk between the p65 component of NF-κB and glucocorticoid receptors is due, at least in part, to nuclear competition for limiting amounts of the coactivators CBP and SRC-1, thus providing a novel mechanism for decreasing expression of genes involved in the inflammatory response.
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Pit-1-dependent expression of the receptor for growth hormone releasing factor mediates pituitary cell growth.
TL;DR: The cloning of mouse and rat complementary DNAs encoding a new member of the seven-transmembrane-helix, G-protein-coupled receptor family restricted to the pituitary gland, which mediates increases in intracellular cAMP and cAMP-dependent gene transcription in response to GRF is reported.
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N-CoR controls differentiation of neural stem cells into astrocytes.
TL;DR: It is proposed that repression by N-CoR, modulated by opposing enzymatic activities, is a critical mechanism in neural stem cells that underlies the inhibition of glial differentiation.