M
Miles F. Wilkinson
Researcher at University of California, San Diego
Publications - 169
Citations - 11661
Miles F. Wilkinson is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Gene & Homeobox. The author has an hindex of 57, co-authored 163 publications receiving 10617 citations. Previous affiliations of Miles F. Wilkinson include University of California, Berkeley & University of Puerto Rico, Medical Sciences Campus.
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Journal ArticleDOI
The Nonsense-Mediated Decay RNA Surveillance Pathway
TL;DR: Whether these proofreading events preferentially occur during a "pioneer" round of translation in higher and lower eukaryotes, their cellular location, and whether they can use alternative EJC factors or act independent of the EJC are discussed.
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Targeted DNA demethylation and activation of endogenous genes using programmable TALE-TET1 fusion proteins
Morgan L. Maeder,James Angstman,Marcy E. Richardson,Samantha J Linder,Vincent M Cascio,Shengdar Q. Tsai,Quan H Ho,Jeffry D. Sander,Deepak Reyon,Bradley E. Bernstein,Joseph F. Costello,Miles F. Wilkinson,J. Keith Joung +12 more
TL;DR: It is demonstrated that modification of critical methylated promoter CpG positions can lead to substantial increases in the expression of endogenous human genes using fusions of engineered transcription activator–like effector repeat arrays and the TET1 hydroxylase catalytic domain.
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Messenger RNA regulation: to translate or to degrade.
TL;DR: While NMD and miRNA‐mediated mRNA silencing use different decision‐making processes to determine the fate of their targets, both are greatly influenced by mRNP dynamics and are linked to RNA processing bodies.
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Molecular mechanism for distinct neurological phenotypes conveyed by allelic truncating mutations.
Ken Inoue,Mehrdad Khajavi,Tomoko Ohyama,Shin ichi Hirabayashi,John T. Wilson,James D. Reggin,Pedro Mancias,Ian J. Butler,Miles F. Wilkinson,Michael Wegner,James R. Lupski,James R. Lupski +11 more
TL;DR: It is reported that although all nonsense and frameshift mutations that cause premature termination of translation generate truncated SOX10 proteins with potent dominant-negative activity, the more severe disease phenotype, PCWH, is realized only when the mutant mRNAs escape the nonsense-mediated decay (NMD) pathway.
Journal ArticleDOI
A Regulatory Mechanism That Detects Premature Nonsense Codons in T-cell Receptor Transcripts in Vivo Is Reversed by Protein Synthesis Inhibitors in Vitro
Mark S. Carter,Jessica Doskow,Phillip Morris,Shulin Li,Ronald P. Nhim,Sara Sandstedt,Miles F. Wilkinson +6 more
TL;DR: In this paper, the authors performed sequence analysis of reverse transcriptase-polymerase chain reaction products from fetal and adult thymus and found that newly transcribed T-cell receptor-β pre-mRNAs (intron-bearing) are frequently derived from ptc-bearing genes but such transcripts rarely accumulate as mature (fully spliced) TCR-β transcripts.