Please use this identifier to cite or link to this item: https://doi.org/10.1074/jbc.M600224200
Title: αCP1 mediates stabilization of hTERT mRNA by autocrine human growth hormone
Authors: Emerald, B.S.
Chen, Y.
Zhu, T. 
Zhu, Z.
Lee, K.-O. 
Gluckman, P.D.
Lobie, P.E.
Issue Date: 5-Jan-2007
Citation: Emerald, B.S., Chen, Y., Zhu, T., Zhu, Z., Lee, K.-O., Gluckman, P.D., Lobie, P.E. (2007-01-05). αCP1 mediates stabilization of hTERT mRNA by autocrine human growth hormone. Journal of Biological Chemistry 282 (1) : 680-690. ScholarBank@NUS Repository. https://doi.org/10.1074/jbc.M600224200
Abstract: We herein demonstrate that autocrine human growth hormone production in human mammary carcinoma cells results in increased telomerase activity as a result of specific up-regulation of telomerase catalytic subunit (human telomerase reverse transcriptase (hTERT)) mRNA and protein. This increase in hTERT gene expression is not due to increased transcriptional activation of the hTERT promoter but is the result of increased stability of hTERT mRNA exerted by CU-rich cis-regulatory sequences present in the 3′-untranslated region of TERT mRNA. Autocrine human growth hormone up-regulates two poly(C)-binding proteins, αCP1 and αCP2, which bind to these cis-regulatory elements and stabilize hTERT mRNA. We have therefore demonstrated that post-transcriptional modulation of the level of hTERT mRNA is one mechanism for regulation of cellular telomerase activity. © 2007 by The American Society for Biochemistry and Molecular Biology, Inc.
Source Title: Journal of Biological Chemistry
URI: http://scholarbank.nus.edu.sg/handle/10635/130577
ISSN: 00219258
DOI: 10.1074/jbc.M600224200
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.

SCOPUSTM   
Citations

20
checked on Nov 19, 2018

WEB OF SCIENCETM
Citations

20
checked on Nov 19, 2018

Page view(s)

17
checked on Nov 9, 2018

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.