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Lidenys Varela

Researcher at Johns Hopkins University

Publications -  6
Citations -  213

Lidenys Varela is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Macrophage migration inhibitory factor & Proto-oncogene tyrosine-protein kinase Src. The author has an hindex of 5, co-authored 6 publications receiving 179 citations. Previous affiliations of Lidenys Varela include University of Texas Medical Branch.

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Organelle-Specific, Rapid Induction of Molecular Activities and Membrane Tethering

TL;DR: This work activated Ras GTPase at distinct intracellular locations and induced tethering of membranes from two organelles, endoplasmic reticulum and mitochondria, using new chemically inducible dimerization probes.
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Macrophage Migration Inhibitory Factor Is a Novel Determinant of Cigarette Smoke–Induced Lung Damage

TL;DR: Taken together, MIF appears to antagonize CS-induced toxicity in the lung and resultant emphysematous tissue remodeling by suppressing EC DNA damage and controlling p53-mediated apoptosis, highlighting a critical role of MIF in EC homeostasis within the lung.
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Macrophage Migration Inhibitory Factor: A Novel Inhibitor of Apoptosis Signal-Regulating Kinase 1-p38-Xanthine Oxidoreductase-Dependent Cigarette Smoke-Induced Apoptosis.

TL;DR: It is demonstrated that both the activity of xanthine oxidoreductase (XOR), a superoxide-generating enzyme obligatory for CS-induced DNA damage and EndoC apoptosis, and superoxide concentrations are increased after CS exposure in the absence of MIF.
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mTOR Signaling Feedback Modulates Mammary Epithelial Differentiation and Restrains Invasion Downstream of PTEN Loss

TL;DR: It is found that mTOR signaling promoted basal-like differentiation and repressed nuclear hormone receptor expression after short-term PTEN loss in murine cell cultures analyzed ex vivo, and that PTEN inactivation inhibited growth factor-induced epithelial invasion and that downstream mTOR-mediated signaling feedback was both necessary and sufficient for this effect.
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Functional Impact of Human Genetic Variants of COL18A1/Endostatin on Pulmonary Endothelium.

TL;DR: It is demonstrated that ES inhibits PEC migration, proliferation and cell survival, with significant differences between human variants, indicating they are functional genetic variants.