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Quinn P. Peterson

Researcher at Harvard University

Publications -  36
Citations -  2942

Quinn P. Peterson is an academic researcher from Harvard University. The author has contributed to research in topics: Cell & Cancer cell. The author has an hindex of 18, co-authored 32 publications receiving 2497 citations. Previous affiliations of Quinn P. Peterson include Mayo Clinic & Howard Hughes Medical Institute.

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Journal ArticleDOI

Generation of functional human pancreatic β cells in vitro

TL;DR: A scalable differentiation protocol is reported that can generate hundreds of millions of glucose-responsive β cells from hPSC in vitro that secrete human insulin into the serum of mice shortly after transplantation in a glucose-regulated manner, and transplantation of these cells ameliorates hyperglycemia in diabetic mice.
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Artery/Vein Specification Is Governed by Opposing Phosphatidylinositol-3 Kinase and MAP Kinase/ERK Signaling

TL;DR: Chemical genetic analysis has uncovered unanticipated opposing roles of PI3K and ERK in artery/vein specification.
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PAC-1 Activates Procaspase-3 in Vitro through Relief of Zinc-Mediated Inhibition

TL;DR: The discovery of a compound, PAC-1, which enhances procaspase-3 activity in vitro and induces apoptotic death in cancer cells in culture and in mouse xenograft models is reported, indicating this discovery of the in vitro mechanism of action ofPAC-1 is critical to the development and optimization of other procaspases-activating compounds.
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Procaspase-3 Activation as an Anti-Cancer Strategy: Structure-Activity Relationship of Procaspase-Activating Compound 1 (PAC-1) and its Cellular Co-Localization with Caspase-3

TL;DR: The data presented herein further bolster the hypothesis that PAC-1 induces apoptosis in cancer cells through the direct activation of procaspase-3, has implications for the design and discovery of next-generation procaspases-3 activating compounds, and sheds light on the anti-apoptotic role of cellular zinc.
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AML1-ETO reprograms hematopoietic cell fate by downregulating scl expression

TL;DR: A transgenic zebrafish line that enables inducible expression of the human AML1-ETO oncogene is described, and it is demonstrated that scl is an important mediator of the ability of AML 1-ETo to reprogram hematopoietic cell fate decisions, suggesting that sCl may be an important contributor to AML-1- ETO-associated leukemia.