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Matthew N. Poy

Researcher at Max Delbrück Center for Molecular Medicine

Publications -  41
Citations -  10398

Matthew N. Poy is an academic researcher from Max Delbrück Center for Molecular Medicine. The author has contributed to research in topics: microRNA & Insulin. The author has an hindex of 25, co-authored 38 publications receiving 9839 citations. Previous affiliations of Matthew N. Poy include University of Toledo Medical Center & ETH Zurich.

Papers
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Journal ArticleDOI

Combinatorial microRNA target predictions.

TL;DR: PicTar, a computational method for identifying common targets of micro RNAs, is presented and widespread coordinate control executed by microRNAs is suggested, thus providing evidence for coordinate microRNA control in mammals.
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A pancreatic islet-specific microRNA regulates insulin secretion

TL;DR: It is shown that overexpression of miR-375 suppressed glucose-induced insulin secretion, and conversely, inhibition of endogenous mi R-375 function enhanced insulin secretion and may constitute a novel pharmacological target for the treatment of diabetes.
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A skin microRNA promotes differentiation by repressing ‘stemness’

TL;DR: It is shown that microRNA-203 is induced in the skin concomitantly with stratification and differentiation and defines a molecular boundary between proliferative basal progenitors and terminally differentiating suprabasal cells, ensuring proper identity of neighbouring layers.
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miR-375 maintains normal pancreatic α- and β-cell mass

TL;DR: It is shown that microRNA-375 (miR-375), which is highly expressed in pancreatic islets, is required for normal glucose homeostasis and adaptive β-cell expansion in response to increasing insulin demand in insulin resistance.
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Apolipoprotein M is required for prebeta-HDL formation and cholesterol efflux to HDL and protects against atherosclerosis.

TL;DR: Overexpression of apoM in Ldlr−/− mice protected against atherosclerosis when the mice were challenged with a cholesterol-enriched diet, showing that apo M is important for the formation of preβ-HDL and cholesterol efflux to HDL, and thereby inhibits formation of atherosclerotic lesions.