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Sophia Hsin-Jung Li

Researcher at Princeton University

Publications -  25
Citations -  2079

Sophia Hsin-Jung Li is an academic researcher from Princeton University. The author has contributed to research in topics: Translation (biology) & Protein biosynthesis. The author has an hindex of 11, co-authored 23 publications receiving 1548 citations. Previous affiliations of Sophia Hsin-Jung Li include Zhejiang University of Science and Technology & Massachusetts Institute of Technology.

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Journal ArticleDOI

Paracrine and autocrine signals induce and maintain mesenchymal and stem cell states in the breast.

TL;DR: In this article, the authors describe three signaling pathways, involving transforming growth factor (TGF)-β and canonical and noncanonical Wnt signaling, that collaborate to induce activation of the EMT program and thereafter function in an autocrine fashion to maintain the resulting mesenchymal state.
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Subfemtotesla scalar atomic magnetometry using multipass cells.

TL;DR: A pump-probe measurement scheme to suppress spin-exchange relaxation and two probe pulses to find the spin precession zero crossing times is used and a magnetic field sensitivity of 0.54 fT/Hz(1/2), which improves by an order of magnitude the best scalar magnetometer sensitivity.
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Mitochondrial translation requires folate-dependent tRNA methylation

TL;DR: It is shown that loss of the catalytic activity of the mitochondrial folate enzyme serine hydroxymethyltransferase 2 (SHMT2), but not of other folate enzymes, leads to defective oxidative phosphorylation in human cells due to impaired mitochondrial translation.
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Human SHMT inhibitors reveal defective glycine import as a targetable metabolic vulnerability of diffuse large B-cell lymphoma

TL;DR: It is shown genetically that dual SHMT1/2 knockout blocks HCT-116 colon cancer tumor xenograft formation and defective glycine import is a targetable metabolic deficiency of DLBCL.
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A Dual-Mechanism Antibiotic Kills Gram-Negative Bacteria and Avoids Drug Resistance.

TL;DR: A compound is characterized that kills both Gram-negative and Gram-positive bacteria through a unique dual-targeting mechanism of action (MoA) with undetectably low resistance frequencies, and suggests that combining multiple MoAs onto a single chemical scaffold may be an underappreciated approach to targeting challenging bacterial pathogens.