Lucy C. Robinson
University of Pennsylvania
7 Papers
438 Citations
Lucy C. Robinson is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Saccharomyces cerevisiae & Gene. The author has an hindex of 7, co-authored 7 publications.
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Papers
CDC25: a component of the RAS-adenylate cyclase pathway in Saccharomyces cerevisiae.
TL;DR: The evidence presented here indicates that CDC25, identified by conditional cell cycle arrest mutations, encodes such an upstream function of RAS in the adenylate cyclase pathway.
229
Mammalian and yeast ras gene products: biological function in their heterologous systems
Deborah Defeo-Jones,Kelly Tatchell,Lucy C. Robinson,Irving S. Sigal,William C. Vass,Douglas R. Lowy,Edward M. Scolnick +6 more
TL;DR: Yeast-mammalian hybrid genes and a deletion mutant yeast RASSC-1 gene were shown to induce morphologic transformation of mouse NIH 3T3 cells when the genes had a point mutation analogous to one that increases the transforming activity of mammalian ras genes.
178
RAS2 of Saccharomyces cerevisiae is required for gluconeogenic growth and proper response to nutrient limitation.
TL;DR: It is reported here that strains containing RAS2 disruptions have three distinct phenotypes; they fail to grow efficiently on nonfermentable carbon sources, hyperaccumulate the storage carbohydrates glycogen and trehalose, and sporulate on rich media.
157
Novel suppressors of α-synuclein toxicity identified using yeast
Jun Liang,Cheryl Clark-Dixon,Shaoxiao Wang,Todd R. Flower,Tara Williams-Hart,Richard M. Zweig,Lucy C. Robinson,Kelly Tatchell,Stephan N. Witt +8 more
TL;DR: Four of the five genes are specific for α-syn in that they fail to protect cells from the toxicity of the two inherited mutants A30P or A53T, which suggests that α- syn causes toxicity to cells through a different pathway than these two inherit mutants.
61
Temperature-sensitive ipl1-2/Aurora B mutation is suppressed by mutations in TOR complex 1 via the Glc7/PP1 phosphatase.
TL;DR: The results suggest that TORC1 positively regulates the Glc7 activity that opposes Ipl1 and provide a mechanism to tie nutritional status with mitotic regulation.
31