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Anti-MTG16 antibodies reveal MTG16 subcellular distribution and nucleocytoplasmic transport in erythroleukemia cells

Authors Nguyen H, Mariotti J, Bareyan D, Carnahan R, Cooper T, Williams C, Engel M

Received 16 September 2014

Accepted for publication 9 October 2014

Published 19 February 2015 Volume 2015:5 Pages 27—41

DOI https://doi.org/10.2147/ANTI.S74419

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Professor Shixia Wang


Hong Nguyen,1 Jolene Mariotti,1 Diana Bareyan,2 Robert H Carnahan,3 Tracy Cooper,3 Christopher S Williams,4 Michael E Engel2,5

1Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN, 2Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT, 3Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, 4Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, 5Department of Pediatrics, University of Utah School of Medicine and Primary Children's Hospital, Salt Lake City, UT, USA

Abstract: The myeloid translocation gene (MTG) family of transcriptional corepressors consists of three highly conserved members: MTG8, MTG16, and MTGR1, each evolutionarily related to the Drosophila protein NERVY and with orthologs across the mammalian hierarchy. By coordinating coincident interactions between DNA binding proteins, other corepressors, and epigenetic effectors, MTG proteins occupy a critical nexus in transcriptional control complexes to profoundly impact the specification of cell fate. MTG family members are most conserved within nervy homology regions (NHRs) 1–4, with each region fulfilling functions common to the family. Studies of functional differences between MTG proteins require carefully qualified immunologic reagents specific to each family member. We have developed a group of a-MTG16 antibodies and carefully characterized their specificity for MTG16. These tools reveal that MTG16 is concentrated in the cytoplasm of erythroleukemia cell lines from human and mouse. Using the chromosome region maintenance 1 (CRM1) antagonist leptomycin B, we show that MTG16 levels rise in the nucleus of murine erythroleukemia cells and decline in the cytoplasm. Together, these data indicate bidirectional movement of MTG16 between cytoplasmic and nuclear compartments. Our work reveals an unrecognized feature of MTG16 regulation that may impact cell fate specification and provides reagents to address important questions regarding MTG16 functions in vivo.

Keywords: antibody, nucleus, cytoplasm, transport


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