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Luke Whitesell

Researcher at Massachusetts Institute of Technology

Publications -  75
Citations -  8817

Luke Whitesell is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: HSF1 & Drug resistance. The author has an hindex of 36, co-authored 75 publications receiving 7756 citations. Previous affiliations of Luke Whitesell include University of Arizona & University of Toronto.

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HSP90 and the chaperoning of cancer.

TL;DR: Pharmacologically 'bribing' the essential guard duty of the chaperone HSP90 (heat-shock protein of 90 kDa) seems to offer a unique anticancer strategy of considerable promise.
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Heat shock factor 1 is a powerful multifaceted modifier of carcinogenesis.

TL;DR: It is reported that eliminating HSF1 protects mice from tumors induced by mutations of the RAS oncogene or a hot spot mutation in the tumor suppressor p53, and human cancer lines of diverse origins show much greater dependence onHSF1 function to maintain proliferation and survival than their nontransformed counterparts.
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HSF1 Drives a Transcriptional Program Distinct from Heat Shock to Support Highly Malignant Human Cancers

TL;DR: In this paper, the authors identify an HSF1-regulated transcriptional program specific to highly malignant cells and distinct from heat shock, which supports oncogenic processes: cell-cycle regulation, signaling, metabolism, adhesion and translation.
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Widespread Macromolecular Interaction Perturbations in Human Genetic Disorders

TL;DR: This work functionally profile several thousand missense mutations across a spectrum of Mendelian disorders using various interaction assays, suggesting that disease-associated alleles that perturb distinct protein activities rather than grossly affecting folding and stability are relatively widespread.
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Harnessing Hsp90 function as a powerful, broadly effective therapeutic strategy for fungal infectious disease

TL;DR: Hsp90 provides a much-needed strategy for improving the treatment of fungal disease because it enhances the efficacy of existing antifungals, blocks the emergence of drug resistance, and exerts broad-spectrum activity against diverse fungal pathogens.