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Joseph R. Nevins

Researcher at Duke University

Publications -  261
Citations -  44398

Joseph R. Nevins is an academic researcher from Duke University. The author has contributed to research in topics: E2F & Transcription factor. The author has an hindex of 105, co-authored 261 publications receiving 42988 citations. Previous affiliations of Joseph R. Nevins include Thomas Jefferson University & Durham University.

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Journal ArticleDOI

Genomic strategies for personalized cancer therapy

TL;DR: The ability to develop gene expression signatures will likely allow us to guide the use of currently available cancer drugs, develop new targeted therapeutics, and provide an opportunity to better match the most effective drug or drugs with the molecular characteristics of the individual patient.
Journal ArticleDOI

Division of labour between Myc and G1 cyclins in cell cycle commitment and pace control

TL;DR: This work model the potential roles of individual components together with the use of an integrated system to follow E2F dynamics at the single-cell level and in real time and finds that Myc is critical in modulating the amplitude, whereas cyclin D/E activities have little effect on amplitude but do contribute to the modulation of duration of E 2F activation, thereby affecting the pace of cell cycle progression.
Book ChapterDOI

Mechanisms of viral-mediated trans-activation of transcription.

TL;DR: The features and characteristics of the E1A trans -activation system besides the related details deriving from other relevant viral systems are discussed, including a role for these proteins in altering cell proliferation control can be imagined.
Journal ArticleDOI

Diagnosis of partial body radiation exposure in mice using peripheral blood gene expression profiles.

TL;DR: It is demonstrated that partial body irradiation, even to a single limb, generates a characteristic PB signature of radiation injury and thus may necessitate the use of multiple signatures, both partial body and total body, to accurately assess the status of an individual exposed to radiation.
Journal ArticleDOI

The Rb-related p107 protein can suppress E2F function independently of binding to cyclin A/cdk2.

TL;DR: An analysis of the ability of the p107 mutant proteins to suppress cell growth suggests that both E1F-dependent and E2F-independent events correlate with this activity.