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Yogesh Saletore

Researcher at Cornell University

Publications -  9
Citations -  5097

Yogesh Saletore is an academic researcher from Cornell University. The author has contributed to research in topics: Gene & RNA. The author has an hindex of 9, co-authored 9 publications receiving 3661 citations. Previous affiliations of Yogesh Saletore include 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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The N 6 -methyladenosine (m 6 A)-forming enzyme METTL3 controls myeloid differentiation of normal hematopoietic and leukemia cells

TL;DR: It is shown that shRNA-mediated depletion of the m6A-forming enzyme METTL3 in human hematopoietic stem/progenitor cells (HSPCs) promotes cell differentiation, coupled with reduced cell proliferation, and this results provide a rationale for the therapeutic targeting of MET TL3 in myeloid leukemia.
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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.
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The birth of the Epitranscriptome: deciphering the function of RNA modifications

TL;DR: A perspective on current work and new single-molecule sequencing methods for detecting RNA base modifications is presented, and methyl-6-adenosine is shown to be most pronounced near the beginning of the 3' UTR.
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Dynamics of the human and viral m 6 A RNA methylomes during HIV-1 infection of T cells

TL;DR: It is shown that viral infection triggers a massive increase in m6A in both host and viral mRNAs, which identifies a new mechanism for the control of HIV-1 replication and its interaction with the host immune system.