S
Susan Lindquist
Researcher at Massachusetts Institute of Technology
Publications - 443
Citations - 86482
Susan Lindquist is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Heat shock protein & Saccharomyces cerevisiae. The author has an hindex of 147, co-authored 440 publications receiving 81067 citations. Previous affiliations of Susan Lindquist include University of Illinois at Chicago & Howard Hughes Medical Institute.
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Journal ArticleDOI
Phenotypic diversity and altered environmental plasticity in Arabidopsis thaliana with reduced Hsp90 levels.
Todd A. Sangster,Adam K. Bahrami,Amity M. Wilczek,Etsuko Watanabe,Kurt Schellenberg,Catherine A. McLellan,Alicia Kelley,Sek Won Kong,Christine Queitsch,Susan Lindquist +9 more
TL;DR: HSP90 exerts global effects on the environmental responsiveness of plants to many different stimuli, and genome-wide expression analyses suggest a central role for HSP90 in the genesis and maintenance of plastic responses.
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Conservation of Hsp90 macromolecular complexes in Saccharomyces cerevisiae.
TL;DR: Hsp90 functions as part of a highly conserved macromolecular complex in eukaryotes, and homologs of Hsp70, p60, and a 45-kDa immunophilin homolog were isolated by virtue of their specific, stable association with Hsp82.
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Opposing effects of glutamine and asparagine govern prion formation by intrinsically disordered proteins
Randal Halfmann,Simon Alberti,Rajaraman Krishnan,Nicholas Lyle,Charles W. O'Donnell,Oliver D. King,Bonnie Berger,Rohit V. Pappu,Susan Lindquist +8 more
TL;DR: This work uses cell biological, biochemical, and computational techniques to compare Q/N-rich protein variants, and finds that the two residues have strong and opposing effects: N richness promotes assembly of benign self-templating amyloids; Q richness promotes formation of toxic nonamyloid conformers.
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Genetic Architecture of Hsp90-Dependent Drug Resistance
TL;DR: It is determined that both Crz1 and Hph1 modulate azole resistance in the model yeast Saccharomyces cerevisiae and the opportunistic pathogen Candida albicans via calcineurin.
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Changes in the middle region of Sup35 profoundly alter the nature of epigenetic inheritance for the yeast prion [PSI+]
TL;DR: The unique character of these M variants, all carrying the same N-terminalPrion-determining region, demonstrate the importance of M for [PSI+] and suggest that a much wider range of epigenetic phenomena might be based on self-perpetuating, prion-like changes in protein conformation than suggested by current methods for defining prion states.