Journal
RNA BIOLOGY
Volume 15, Issue 7, Pages 849-855Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15476286.2018.1465795
Keywords
chtop; transcription; mRNA export; PRMT1; PRMT5; intron retention; NMD; splicing; -thalassemia; glioblastoma
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Funding
- Japan Science and Technology Agency (JP) [JPMJCR13M2]
- grant for Core Research for Evolutionary Science and Technology (CREST) from Japan Science and Technology Agency [JPMJCR13M2]
- Ministry of Education, Culture, Sports, Science, & Technology of Japan (MEXT)
- JSPS KAKENHI [16K18489]
- Core Research for Evolutionary Science and Technology (CREST), Japan Science and Technology Agency
- Grants-in-Aid for Scientific Research [16K18489] Funding Source: KAKEN
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Chtop binds competitively to the arginine methyltransferases PRMT1 and PRMT5, thereby promoting the asymmetric or symmetric methylation of arginine residues, respectively. In cooperation with PRMT1, Chtop activates transcription of certain gene groups, such as the estrogen-inducible genes in breast cancer cells, the 5-hydroxymethylcytosine-modified genes involved in glioblastomagenesis, or the Zbp-89-dependent genes in erythroleukemia cells. Chtop also represses expression of the fetal -globin gene. In addition, Chtop is a component of the TREX complex that links transcription elongation to mRNA export. The regulation of Chtop expression is, therefore, a key process during the expression of certain gene groups and pathogenesis of certain diseases. Our recent study revealed that cellular levels of Chtop are strictly autoregulated by a mechanism involving intron retention and nonsense-mediated mRNA decay. Here, we summarize roles of Chtop in gene-specific expression and highlight our recent findings concerning the autoregulation of Chtop.
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