Modulation of exosome-mediated mRNA turnover by interaction of gtp-binding protein 1 (GTPBP1) with its target mrnas

Cited 20 time in scopus
Metadata Downloads
Title
Modulation of exosome-mediated mRNA turnover by interaction of gtp-binding protein 1 (GTPBP1) with its target mrnas
Author(s)
K C Woo; Tae-Don Kim; K H Lee; D Y Kim; S Kim; H R Lee; H J Kang; Sang Jeon Chung; S Senju; Y Nishimura; K T Kim
Bibliographic Citation
FASEB Journal, vol. 25, no. 8, pp. 2757-2769
Publication Year
2011
Abstract
Eukaryotic mRNA turnover is among most critical mechanisms that affect mRNA abundance and are regulated by mRNA-binding proteins and the cytoplasmic exosome. A functional protein, guanosine-triphosphate-binding protein 1 (GTPBP1), which associates with both the exosome and target mRNAs, was identified. The overexpression of GTPBP1 accelerated the target mRNA decay, whereas the reduction of the GTPBP1 expression with RNA interference stabilized the target mRNA. GTPBP1 has a putative guanosine-triphosphate (GTP)-binding domain, which is found in members of the G-protein family and Ski7p, a well-known core factor of the exosome-mediated mRNA turnover pathway in yeast. Analyses of protein interactions and mRNA decay demonstrated that GTPBP1 modulates mRNA degradation via GTP-binding-dependent target loading. Moreover, GTPBP1-knockout models displayed multiple mRNA decay defects, including elevated nocturnal levels of Aanat mRNA in pineal glands, and retarded degradation of TNF-α mRNA in lipopolysaccharide-treated splenocytes. The results of this study suggest that GTPBP1 is a regulator and adaptor of the exosome-mediated mRNA turnover pathway.
Keyword
Circadian rhythmUntranslated region
ISSN
0892-6638
Publisher
Wiley
DOI
http://dx.doi.org/10.1096/fj.10-178715
Type
Article
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.