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Kate D. Meyer

Researcher at Duke University

Publications -  32
Citations -  6889

Kate D. Meyer is an academic researcher from Duke University. The author has contributed to research in topics: RNA & Medicine. The author has an hindex of 14, co-authored 21 publications receiving 4779 citations. Previous affiliations of Kate D. Meyer include Northwestern University & Max Planck Society.

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Comprehensive Analysis of mRNA Methylation Reveals Enrichment in 3′ UTRs and near Stop Codons

TL;DR: A method is presented for transcriptome-wide m(6)A localization, which combines m( 6)A-specific methylated RNA immunoprecipitation with next-generation sequencing (MeRIP-Seq) and reveals insights into the epigenetic regulation of the mammalian transcriptome.
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5′ UTR m6A Promotes Cap-Independent Translation

TL;DR: It is shown that mRNAs containing N(6)-methyladenosine (m(6)A) in their 5' UTR can be translated in a cap-independent manner, and that diverse cellular stresses induce a transcriptome-wide redistribution of m( 6)A, resulting in increased numbers of m RNAs with 5'UTR m(6), which bypasses 5' cap-binding proteins to promote translation under stresses.
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The dynamic epitranscriptome: N6-methyladenosine and gene expression control

TL;DR: This work has shown that m6A is present in a large subset of the transcriptome in specific regions of mRNA, which suggests that mRNA may undergo post-transcriptional methylation to regulate its fate and function, which is analogous to methyl modifications in DNA.
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Rethinking m6A Readers, Writers, and Erasers.

TL;DR: In this review, recent advances in m6A research are summarized, and it is highlighted how these new findings have reshaped the understanding of how m 6A is regulated in the transcriptome.
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The fat mass and obesity associated gene (Fto) regulates activity of the dopaminergic midbrain circuitry

TL;DR: It is demonstrated that inactivation of the Fto gene, encoding a nucleic acid demethylase, impairs dopamine receptor type 2 (D2R) and type 3 (D3R) (collectively, 'D2-like receptor')-dependent control of neuronal activity and behavioral responses.