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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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Molecular determinants of resistance to antiandrogen therapy

TL;DR: Using microarray-based profiling of isogenic prostate cancer xenograft models, it is found that a modest increase in androgen receptor mRNA was the only change consistently associated with the development of resistance to antiandrogen therapy.
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Production of a novel neuropeptide encoded by the calcitonin gene via tissue-specific RNA processing

TL;DR: The approach described here permits the application of recombinant DNA technology to analyses of complex neurobiological systems in the absence of prior structural or biological information.
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The coregulator exchange in transcriptional functions of nuclear receptors

TL;DR: Based on their importance in biology and medicine, as well as the relatively simple mechanism of regulation, NR represent one of the most intensively studied and best-understood classes of transcription factors at the molecular level.
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A CBP Integrator Complex Mediates Transcriptional Activation and AP-1 Inhibition by Nuclear Receptors

TL;DR: It is suggested that CBP/p300 serves as an integrator of multiple signal transduction pathways within the nucleus, in addition to distinct coactivators for function of nuclear receptors, CREB, and AP-1.
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Ligand-independent repression by the thyroid hormone receptor mediated by a nuclear receptor co-repressor

TL;DR: A nuclear receptor co-repressor (N-CoR) of relative molecular mass 270K has been identified which mediates ligand-independent inhibition of gene transcription by these receptors, suggesting that the molecular mechanisms of repression by thyroid-hormone and retinoic-acid receptors are analogous to the co- repressor-dependent transcriptional inhibitory mechanisms of yeast and Drosophila.