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Ronald M. Evans

Researcher at Salk Institute for Biological Studies

Publications -  729
Citations -  176865

Ronald M. Evans is an academic researcher from Salk Institute for Biological Studies. The author has contributed to research in topics: Nuclear receptor & Receptor. The author has an hindex of 199, co-authored 708 publications receiving 166722 citations. Previous affiliations of Ronald M. Evans include Scripps Research Institute & University of California, Davis.

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Ligation independent cloning irrespective of restriction site compatibility

TL;DR: It is demonstrated that unusual and, in some cases, previously impossible cloning strategies can be readily and efficiently achieved as long as the flanking sequences of the linear vectors are highly related.
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Activin and Its Receptors during Gastrulation and the Later Phases of Mesoderm Development in the Chick Embryo

TL;DR: The results suggest that the importance of activin-related signaling pathways is not confined to pregastrulation stages and that these receptors may be involved in mediating the effects of inducing signals during later stages of development of the mesoderm, limbs, and nervous system.
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Transcriptional inhibition by a glucocorticoid receptor-β-galactosidase fusion protein

TL;DR: The use of human glucocorticoid receptor mutants to identify regions important for trans-repression of the gene encoding the alpha subunit of chorionic gonadotropin suggests a potentially general strategy for creation of sequence-specific transcriptional repressors.
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Retinoid-dependent pathways suppress myocardial cell hypertrophy.

TL;DR: The results suggest the possibility that a pathway for suppression of hypertrophy may exist in vivo, which may have potential therapeutic value.
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Circadian Amplitude Regulation via FBXW7-Targeted REV-ERBα Degradation

TL;DR: It is shown that REV-ERBα, a core inhibitory component of clock transcription, is targeted for ubiquitination and subsequent degradation by the F-box protein FBXW7, which defines an unexpected molecular mechanism for re-engaging the positive transcriptional arm of the clock, as well as a potential route to manipulate clock amplitude via small molecule CDK1 inhibition.