Pradip Sinha

This paper identifies SARS-CoV-2 PLpro as a driver of epithelial stress and tissue damage across species by activating metabolic and inflammatory pathways in Drosophila and mammalian models.

This study shows that RasG12V-induced epithelial senescence in Drosophila triggers host metabolic syndrome through cytokine signaling, linking oncogene-induced senescence to metabolic disorders.

The paper shows that Yorkie acts as a tumor suppressor in Drosophila squamous epithelia by suppressing TOR-driven α-tubulin acetylation, which is tissue-specific and distinct from other epithelial lineages.

This study shows that Yki signaling suppresses PI3K/Akt/TOR in Drosophila squamous epithelia, preventing tumor formation, and that its loss leads to cancer-like changes in multiple tubular organs.

The paper shows human ERG oncoprotein represses the LIM-domain binding gene Chip/LDB1 in Drosophila, with implications for prostate cancer, through histone modification and disruption of the Chip-Tailup complex.

The paper shows that degenerating larval epidermal cells generate pull forces that drive thorax closure in Drosophila by contracting and shrinking, facilitating HE migration and zipping.

The paper shows that Drosophila male accessory gland shares developmental genetic toolkits with mammalian prostate, revealing deep homology.