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Coleen T. Murphy

Researcher at Princeton University

Publications -  123
Citations -  10175

Coleen T. Murphy is an academic researcher from Princeton University. The author has contributed to research in topics: Longevity & Caenorhabditis elegans. The author has an hindex of 38, co-authored 112 publications receiving 8712 citations. Previous affiliations of Coleen T. Murphy include University of California & University of California, San Francisco.

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Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans

TL;DR: The findings suggest that the insulin/IGF-I pathway ultimately exerts its effect on lifespan by upregulating a wide variety of genes, including cellular stress-response, antimicrobial and metabolic genes, and by downregulating specific life-shortening genes.
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Regulation of Aging and Age-Related Disease by DAF-16 and Heat-Shock Factor

TL;DR: The findings suggest that HSF-1 and DAF-16 together activate expression of specific genes, including genes encoding small heat-shock proteins, which in turn promote longevity, which couple the normal aging process to this type of age-related disease.
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Comparing genomic expression patterns across species identifies shared transcriptional profile in aging.

TL;DR: It is found that two highly diverged animals, the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster, implement a shared adult-onset expression program of genes involved in mitochondrial metabolism, DNA repair, catabolism, peptidolysis and cellular transport.
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Insulin/insulin-like growth factor signaling in C. elegans.

TL;DR: Originally identified based on its role in the regulation of larval development and aging, IIS also controls a host of other biological processes and is likely to shed light on its functions and regulation in higher organisms, including humans.
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Condition‐adapted stress and longevity gene regulation by Caenorhabditis elegans SKN‐1/Nrf

TL;DR: It is concluded that under normal conditions SKN‐1 has a wide range of functions in detoxification and other processes, including modulating mechanisms that reduce lifespan, and in response to stress, SKn‐1 and other regulators tailor transcription programs to meet the challenge at hand.