scholarly journals Functional Interaction of STAT3 Transcription Factor with the Coactivator NcoA/SRC1a

2001 ◽  
Vol 277 (10) ◽  
pp. 8004-8011 ◽  
Author(s):  
Sandrine Giraud ◽  
Frédéric Bienvenu ◽  
Sylvie Avril ◽  
Hugues Gascan ◽  
David M. Heery ◽  
...  
Cytokine ◽  
2009 ◽  
Vol 48 (1-2) ◽  
pp. 127
Author(s):  
Velasco Cimica ◽  
Janaki Iyer ◽  
Nancy C. Reich

2018 ◽  
Vol 19 (6) ◽  
pp. 1608 ◽  
Author(s):  
David Lee ◽  
Rachel O’Keefe ◽  
Patrick Ha ◽  
Jennifer Grandis ◽  
Daniel Johnson

2007 ◽  
Vol 27 (24) ◽  
pp. 8770-8782 ◽  
Author(s):  
Jianhai Jiang ◽  
Yuanyan Wei ◽  
Jialin Shen ◽  
Dan Liu ◽  
Xiaoning Chen ◽  
...  

ABSTRACT Transcription factor E1AF is widely known to play critical roles in tumor metastasis via directly binding to the promoters of genes involved in tumor migration and invasion. Here, we report for the first time E1AF as a novel binding partner for ubiquitously expressed Sp1 transcription factor. E1AF forms a complex with Sp1, contributes to Sp1 phosphorylation and transcriptional activity, and functions as a mediator between epidermal growth factor and Sp1 phosphorylation and activity. Sp1 functions as a carrier bringing E1AF to the promoter region, thus activating transcription of glioma-related gene for β1,4-galactosyltransferase V (GalT V; EC 2.4.1.38). Biologically, E1AF functions as a positive invasion regulator in glioma in cooperation with Sp1 partly via up-regulation of GalT V. This report describes a new mechanism of glioma invasion involving a cooperative effort between E1AF and Sp1 transcription factors.


2003 ◽  
Vol 278 (31) ◽  
pp. 28758-28764 ◽  
Author(s):  
Toru Suzuki ◽  
Shinsuke Muto ◽  
Saku Miyamoto ◽  
Kenichi Aizawa ◽  
Masami Horikoshi ◽  
...  

Oncogene ◽  
2013 ◽  
Vol 33 (9) ◽  
pp. 1158-1166 ◽  
Author(s):  
T M Becker ◽  
S C Boyd ◽  
B Mijatov ◽  
K Gowrishankar ◽  
S Snoyman ◽  
...  

2006 ◽  
Vol 80 (1) ◽  
pp. 108-118 ◽  
Author(s):  
Nam-Hyuk Cho ◽  
Dior Kingston ◽  
Heesoon Chang ◽  
Eun-Kyung Kwon ◽  
Jo-Min Kim ◽  
...  

ABSTRACT Lipid rafts are membrane microdomains that are proposed to function as platforms for both receptor signaling and trafficking. Our previous studies have demonstrated that Tip of herpesvirus saimiri (HVS), which is a T-lymphotropic tumor virus, is constitutively targeted to lipid rafts and interacts with cellular Lck tyrosine kinase and p80 WD repeat-containing endosomal protein. Through the interactions with Lck and p80, HVS Tip modulates diverse T-cell functions, which leads to the downregulation of T-cell receptor (TCR) and CD4 coreceptor surface expression, the inhibition of TCR signal transduction, and the activation of STAT3 transcription factor. In this study, we investigated the functional significance of Tip association with lipid rafts. We found that Tip expression remarkably increased lipid raft fractions in human T cells by enhancing the recruitment of lipid raft-resident proteins. Genetic analysis showed that the carboxyl-terminal transmembrane, but not p80 and Lck interaction, of Tip was required for the lipid raft localization and that lipid raft localization of Tip was necessary for the efficient downregulation of TCR and CD4 surface expression. Correlated with this, treatment with Filipin III, a lipid raft-disrupting agent, effectively reversed the downregulation of CD3 and CD4 surface expression induced by Tip. On the other hand, Tip mutants that were no longer present in lipid rafts were still capable of inhibiting TCR signaling and activating STAT3 transcription factor activity as efficiently as wild-type (wt) Tip. These results indicate that the association of Tip with lipid rafts is essential for the downregulation of TCR and CD4 surface expression but not for the inhibition of TCR signal transduction and the activation of STAT3 transcription factor. These results also suggest that the signaling and targeting activities of HVS Tip rely on functionally and genetically separable mechanisms, which may independently modulate T-cell function for viral persistence or pathogenesis.


2006 ◽  
Vol 119 (24) ◽  
pp. 5098-5105 ◽  
Author(s):  
E. Kavanagh ◽  
M. Buchert ◽  
A. Tsapara ◽  
A. Choquet ◽  
M. S. Balda ◽  
...  

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