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© 2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

The ST2 gene was originally identified as a primary responsive gene induced by stimulation with growth factors and by oncogenic stress. The ST2 gene harbors two distinct promoters – a distal promoter and a proximal promoter. In this study, we identified a novel type of serum‐responsive element in the ST2 proximal promoter using reporter gene analysis; this element includes a possible responsive element for STAT family proteins. Indeed, enforced expression of constitutively active STAT3 activated this promoter element and induced the expression of ST2 gene products. Furthermore, an oncogenic Ras (G12V) mutant also caused the expression of ST2 gene products by utilizing the proximal promoter. We also clarified that activation of the ST2 promoter by either growth stimulation or oncogenic Ras was suppressed by the inhibitors for STAT3 and ERK pathways. Our observations strongly suggest the importance of STAT family and ERK pathways for the induction of ST2 gene products by cell growth stimulation.

Details

Title
STAT 3 and ERK pathways are involved in cell growth stimulation of the ST 2/ IL 1 RL 1 promoter
Author
Tago, Kenji 1 ; Ohta, Satoshi 1 ; Megumi Funakoshi‐Tago 2 ; Chihiro Aoki‐Ohmura 1 ; Matsugi, Jitsuhiro 1 ; Shin‐ichi Tominaga 3 ; Yanagisawa, Ken 1 

 Division of Structural Biochemistry, Jichi Medical University, Shimotsuke, Tochigi, Japan 
 Department of Hygienic Chemistry, Faculty of Pharmacy, Keio University, Minato‐ku, Tokyo, Japan 
 Medical Biochemistry, Department of Biochemistry, Jichi Medical University, Shimotsuke, Tochigi, Japan 
Pages
293-302
Section
Research Articles
Publication year
2017
Publication date
Feb 2017
Publisher
John Wiley & Sons, Inc.
e-ISSN
22115463
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2289570634
Copyright
© 2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.