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A recent study from the The Black Family Stem Cell Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; The Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; and Department of Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA shows that A Genome-wide RNAi Screen Identifies Opposing Functions of Snai1 and Snai2 on the Nanog Dependency in Reprogramming. 

This study was published in the 2 October issue of 2014 Molecular Cell  by Prof Wang J,  Gingold JA and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD reports that: Insights into the regulation of Embroyonic stem cell differentiation, reprogramming, insulin resistance and autophagy: Tumor suppressor p53 inhibits pluripotency-associated genes Lin-28 and miR-290-295 through its target gene. 

Idea Proposed/Formulated byDr L Boominathan Ph.D.

CitationBoominathan, Insights into the regulation of Embroyonic stem cell differentiation, reprogramming, insulin resistance and autophagy: Tumor suppressor p53 inhibits pluripotency-associated genes Lin-28 and miR-290-295 through its target gene, 17/October/2014, 10.10 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

Web: http://genomediscovery.org

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Significance: The RNA-binding and reprogramming protein Lin-28 has been shown to be overexpressed in a number of cancer cells. miRNA-290-295 has been shown to promote self renewal and reprogramming. This study suggests that tumor suppressor p53, by increasing the expression of its target gene, it may decrease the expression of a number of pluripotency genes, including Lin-28 and miR-290-295. Thereby, it may inhibit cancer stem cell proliferation, promote embroyonic stem cell differentiation, insulin resistance and autophagy. Thus, pharmacological formulations encompassing “p53 modulators may be used to treat a number of disease conditions, including cancer and insulin resistance.


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