V
Vinay V. Eapen
Researcher at Brandeis University
Publications - 25
Citations - 6133
Vinay V. Eapen is an academic researcher from Brandeis University. The author has contributed to research in topics: DNA damage & Autophagy. The author has an hindex of 15, co-authored 22 publications receiving 5499 citations. Previous affiliations of Vinay V. Eapen include Harvard University.
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Journal ArticleDOI
Caffeine impairs resection during DNA break repair by reducing the levels of nucleases Sae2 and Dna2
Michael Tsabar,Vinay V. Eapen,Jennifer M. Mason,Gonen Memisoglu,David P. Waterman,Marcus J. C. Long,Douglas K. Bishop,James E. Haber +7 more
TL;DR: In response to chromosomal double-strand breaks, eukaryotic cells activate the DNA damage checkpoint, which is orchestrated by the PI3 kinase-like protein kinases ATR and ATM (Mec1 and Tel1 in budding yeast), and caffeine is used to inhibit the checkpoint kinases after DSB induction.
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PP2C phosphatases promote autophagy by dephosphorylation of the Atg1 complex
TL;DR: Two redundant PP2C-type phosphatases, Ptc2 and Ptc3, regulate macroautophagy by dephosphorylating Atg13 and Atg1 and are suggested to play a previously uncharacterized and central role in the regulation of core autophagy proteins.
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Quantitative proteomics reveals the selectivity of ubiquitin-binding autophagy receptors in the turnover of damaged lysosomes by lysophagy.
TL;DR: In this article, the authors employ quantitative organelle capture and proximity biotinylation proteomics of autophagy adaptors, cargo receptors, and galectins in response to acute lysosomal damage.
Posted ContentDOI
Quantitative proteomics reveals the selectivity of ubiquitin-binding autophagy receptors in the turnover of damaged lysosomes by lysophagy
TL;DR: In this paper, the authors employ quantitative organelle capture and proximity biotinylation proteomics of autophagy adaptors, cargo receptors, and Galectins in response to acute lysosomal damage.
Journal ArticleDOI
Live cell monitoring of double strand breaks in S. cerevisiae.
David P. Waterman,Felix Zhou,Kevin Li,Cheng-Sheng Lee,Michael Tsabar,Vinay V. Eapen,Allison J. Mazzella,James E. Haber +7 more
TL;DR: It is concluded that co-localization of foci in cells with 3 DSBs does not represent formation of a homologous recombination “repair center,” as the same distribution of Ddc2-GFP foci was found in the absence of the Rad52 protein.