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Alexandre Matov

Researcher at Cornell University

Publications -  19
Citations -  2355

Alexandre Matov is an academic researcher from Cornell University. The author has contributed to research in topics: Microtubule & Prostate cancer. The author has an hindex of 15, co-authored 19 publications receiving 1858 citations. Previous affiliations of Alexandre Matov include University of Wyoming & University of California, San Francisco.

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Drug-tolerant persister cancer cells are vulnerable to GPX4 inhibition

TL;DR: It is demonstrated that a similar therapy-resistant cell state underlies the behaviour of persister cells derived from a wide range of cancers and drug treatments, and it is suggested that targeting of GPX4 may represent a therapeutic strategy to prevent acquired drug resistance.
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plusTipTracker: Quantitative image analysis software for the measurement of microtubule dynamics

TL;DR: The algorithm underlying the reconstruction of full MT trajectories relies on the spatially and temporally global tracking framework described in Jaqaman et al. (2008) and the numerical methods and analytical functionality incorporated in plusTipTracker substantially advance this previous work in terms of flexibility and robustness.
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Analysis of microtubule dynamic instability using a plus-end growth marker

TL;DR: This work introduced spatiotemporal clustering of EB1-EGFP growth tracks to infer microtubule behaviors during phases of pause and shortening and used this method to analyze spatial variations of intracellular microtubules dynamics in migrating epithelial cells.
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Androgen Receptor Splice Variants Determine Taxane Sensitivity in Prostate Cancer

TL;DR: The results suggest that androgen receptor variants that accumulate in CRPC cells utilize distinct pathways of nuclear import that affect the antitumor efficacy of taxanes, suggesting a mechanistic rationale to customize treatments for patients with CRPC, which might improve outcomes.
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GSK3β phosphorylation modulates CLASP–microtubule association and lamella microtubule attachment

TL;DR: It is demonstrated that glycogen synthase kinase 3β (GSK3β) directly phosphorylates CLASPs at multiple sites in the domain required for MT plus end tracking, and that CLASP-mediated stabilization of peripheral MTs may be regulated by local GSK3β inactivation.