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Sarthak Sahoo

Researcher at Indian Institute of Science

Publications -  40
Citations -  348

Sarthak Sahoo is an academic researcher from Indian Institute of Science. The author has contributed to research in topics: Biology & Medicine. The author has an hindex of 7, co-authored 24 publications receiving 124 citations.

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A Computational Systems Biology Approach Identifies SLUG as a Mediator of Partial Epithelial-Mesenchymal Transition (EMT).

TL;DR: In this paper, an EMT-inducing transcription factor, SLUG (SNAIL2), was shown to stabilize hybrid E/M phenotypes in a computational system biology approach.
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Multi-stability in cellular differentiation enabled by a network of three mutually repressing master regulators.

TL;DR: The dynamics of three master regulators A, B and C inhibiting each other are investigated, thus forming three-coupled toggle switches to form a toggle triad that can lead to co-existence of cells into three differentiated ‘single positive' phenotypes.
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A mechanistic model captures the emergence and implications of non-genetic heterogeneity and reversible drug resistance in ER+ breast cancer cells.

TL;DR: In this article, the authors investigated coupled dynamics of epithelial-mesenchymal transition (EMT) in breast cancer cells and emergence of reversible drug resistance and proposed the potential therapeutic use of mesenchym-epithelial transition inducers besides canonical anti-estrogen therapy to limit the emergence of drug resistance.
Posted ContentDOI

A computational systems biology approach identifies SLUG as a mediator of partial Epithelial-Mesenchymal Transition (EMT)

TL;DR: It is demonstrated that SLUG (SNAIL2) – an EMT-inducing transcription factor – can inhibit cells from undergoing a complete EMT and thus stabilizing them in hybrid E/M phenotype, thereby behaving as a phenotypic stability factor (PSF).
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Let-7a-regulated translational readthrough of mammalian AGO1 generates a microRNA pathway inhibitor.

TL;DR: Overall, the results reveal a negative feedback loop in the mi RNA pathway mediated by the translational readthrough product of AGO1, which can serve as a competitive inhibitor of miRNA pathway.