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Steven P. Gygi

Researcher at Harvard University

Publications -  778
Citations -  147003

Steven P. Gygi is an academic researcher from Harvard University. The author has contributed to research in topics: Proteome & Phosphorylation. The author has an hindex of 172, co-authored 704 publications receiving 129173 citations. Previous affiliations of Steven P. Gygi include University of Rochester Medical Center & Cell Signaling Technology.

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Regulation of MicroRNA Machinery and Development by Interspecies S-Nitrosylation

TL;DR: The microbiota can shape the post-translational landscape of the host proteome to regulate microRNA activity, gene expression, and host development, and suggest a general mechanism by which the microbiota may control host cellular functions, as well as a new role for gasotransmitters.
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PIASy Mediates SUMO-2/3 Conjugation of Poly(ADP-ribose) Polymerase 1 (PARP1) on Mitotic Chromosomes

TL;DR: A novel SUMO-2/3-modified mitotic chromosomal protein is isolated and identified as poly(ADP-ribose) polymerase 1 (PARP1), and a residue within the BRCA1 C-terminal domain of PARP1 (lysine 482) is identified as its primary SUMOylation site.
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MLK3 regulates bone development downstream of the faciogenital dysplasia protein FGD1 in mice

TL;DR: The results provide a putative biochemical mechanism for the skeletal defects in human FGDY and suggest that modulating MAPK signaling may benefit these patients.
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Survey of Activated FLT3 Signaling in Leukemia

TL;DR: It is shown that oncogenic FLT3 regulates proteins involving diverse cellular processes and affects multiple signaling pathways in human leukemia that were previously appreciated, such as Fc epsilon RI-mediated signaling, BCR, and CD40 signaling pathways.
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C. elegans SIRT6/7 homolog SIR-2.4 promotes DAF-16 relocalization and function during stress.

TL;DR: SIR-2.4 is identified as a critical regulator of DAF-16 specifically in the context of stress responses, and a novel role for acetylation is revealed, modulated by the antagonistic activities of CBP-1 and SIR- 2.4, in modulating D AF-16 localization and function.