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Robyn Branicky
Researcher at McGill University
Publications - 19
Citations - 1488
Robyn Branicky is an academic researcher from McGill University. The author has contributed to research in topics: Caenorhabditis elegans & Superoxide dismutase. The author has an hindex of 11, co-authored 18 publications receiving 948 citations. Previous affiliations of Robyn Branicky include Laboratory of Molecular Biology.
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Superoxide dismutases: Dual roles in controlling ROS damage and regulating ROS signaling.
TL;DR: Studies in model organisms and humans are discussed, which reveal the dual roles of SOD enzymes in controlling damage and regulating signaling and the need for fine local control of ROS signaling.
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Redox Regulation of Germline and Vulval Development in Caenorhabditis elegans
TL;DR: Two pathways by which the altered redox chemistry of the clk-1 mutants of Caenorhabditis elegans acts in vivo on germline development are identified and the oncogenic ras signaling pathway appears to be modulated by cytoplasmic ROS.
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clk-1, mitochondria, and physiological rates.
TL;DR: The evidence supporting the regulatory role of clk-1 in physiological timing is reviewed, and possible models for the action of CLK-1 are discussed, in particular, one proposing that CL k-1 is involved in the coordination of mitochondrial and nuclear function.
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What keeps C. elegans regular: the genetics of defecation.
Robyn Branicky,Siegfried Hekimi +1 more
TL;DR: A review of Caenorhabditis elegans highlights how the function of a system even this simple results from the integration of many aspects of an organism's biology and involves the action of diverse genes.
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The anti-neurodegeneration drug clioquinol inhibits the aging-associated protein CLK-1.
Ying Wang,Robyn Branicky,Zaruhi Stepanyan,Melissa Carroll,Marie-Pierre Guimond,Abdelmadjid K. Hihi,Steve Hayes,Kevin M. McBride,Siegfried Hekimi +8 more
TL;DR: The results suggest that the surprising action of clioquinol on several age-dependent neurodegenerative diseases with distinct etiologies might result from a slowing down of the aging process through action of the drug on CLK-1.