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Danish Sayed

Researcher at Rutgers University

Publications -  31
Citations -  3782

Danish Sayed is an academic researcher from Rutgers University. The author has contributed to research in topics: Gene expression & Regulation of gene expression. The author has an hindex of 14, co-authored 27 publications receiving 3506 citations. Previous affiliations of Danish Sayed include University of Medicine and Dentistry of New Jersey.

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MicroRNAs in development and disease.

TL;DR: The discovery, structure, and mode of function of miRNAs in mammalian cells are described, before elaborating on their roles and significance during development and pathogenesis in the various mammalian organs, while attempting to reconcile their functions with the existing knowledge of their targets.
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MicroRNAs Play an Essential Role in the Development of Cardiac Hypertrophy

TL;DR: It is proposed that microRNAs play an essential regulatory role in the development of cardiac hypertrophy, wherein downregulation of miR-1 is necessary for the relief of growth-related target genes from its repressive influence and induction ofhypertrophy.
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Downregulation of MiR-199a Derepresses Hypoxia-Inducible Factor-1α and Sirtuin 1 and Recapitulates Hypoxia Preconditioning in Cardiac Myocytes

TL;DR: It is reported here that miR-199a is acutely downregulated in cardiac myocytes on a decline in oxygen tension and this reduction is required for the rapid upregulation of its target, hypoxia-inducible factor (Hif)-1α.
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MicroRNA-21 Targets Sprouty2 and Promotes Cellular Outgrowths

TL;DR: It is proposed that an increase in miR-21 enhances the formation of various types of cellular protrusions through directly targeting and down-regulating SPRY2.
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MicroRNA-21 Is a Downstream Effector of AKT That Mediates Its Antiapoptotic Effects via Suppression of Fas Ligand

TL;DR: It is demonstrated here for the first time that miR-21 is positively regulated via an AKT-dependent pathway, which is depressed during prolonged hypoxia, and identified a unique aspect of the function of AKT by which it inhibits apoptosis through mi R-21-dependent suppression of FasL.