Ectopic expression of Hel-N1 an RNA-binding protein increases glucose transporter (GLUT1) expression in 3T3-L1 adipocytes.

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)
Lucy G. Andrews (Creator)
Renu G. Jain (Creator)
Jack D. Keene (Creator)
Kevin M. McGowan (Creator)
Phillip H. Pekala (Creator)
Institution
East Carolina University (ECU )
Web Site: http://www.ecu.edu/lib/

Abstract: 3T3-L1 preadipocytes ectopically expressing the mammalian RNA-binding protein Hel-N1 expressed up to 10-fold more glucose transporter (GLUT1) protein and exhibited elevated rates of basal glucose uptake. Hel-N1 is a member of the ELAV-like family of proteins associated with the induction and maintenance of differentiation in various species. ELAV proteins are known to bind in vitro to short stretches of uridylates in the 3' untranslated regions (3'UTRs) of unstable mRNAs encoding growth-regulatory proteins involved in transcription and signal transduction. GLUT1 mRNA also contains a large 3'UTR with a U-rich region that binds specifically to Hel-N1 in vitro. Analysis of the altered GLUT1 expression at the translational and posttranscriptional levels suggested a mechanism involving both mRNA stabilization and accelerated formation of translation initiation complexes. These findings are consistent with the hypothesis that the Hel-N1 family of proteins modulate gene expression at the level of mRNA in the cytoplasm. Originally published Molecular and Cellular Biology Vol. 17 No. 2 Feb 1997

Additional Information

Publication
Other
Molecular and Cellular Biology. 17:2(February 1997) p. 954-962.
Language: English
Date: 2011
Keywords
RNA binding protein, glucose transporter, Gene expression

Email this document to

This item references:

TitleLocation & LinkType of Relationship
Ectopic expression of Hel-N1 an RNA-binding protein increases glucose transporter (GLUT1) expression in 3T3-L1 adipocytes.http://hdl.handle.net/10342/3304The described resource references, cites, or otherwise points to the related resource.