Specific Inhibition of Nuclear Factor-κB–Dependent Inflammatory Responses by Cell Type-Specific Mechanisms upon A2A Adenosine Receptor Gene Transfer

2004 ◽  
Vol 66 (5) ◽  
pp. 1147-1159 ◽  
Author(s):  
William A. Sands ◽  
Anthony F. Martin ◽  
Elaine W. Strong ◽  
Timothy M. Palmer
Keyword(s):  
Gene Transfer ◽  
Adenosine Receptor ◽  
Inflammatory Responses ◽  
Receptor Gene ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Specific Inhibition ◽  
Cell Type ◽  
A2a Adenosine Receptor ◽  
Cell Type Specific

The restricted promoter activity of the liver transcription factor hepatocyte nuclear factor 3 beta involves a cell-specific factor and positive autoactivation

1992 ◽  
Vol 12 (2) ◽  
pp. 552-562
Author(s):  
L Pani ◽  
X B Quian ◽  
D Clevidence ◽  
R H Costa
Keyword(s):  
Transcription Factor ◽  
Promoter Activity ◽  
Binding Activity ◽  
Specific Factor ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Cell Type ◽  
Specific Expression ◽  
Cell Type Specific Expression ◽  
Cell Type Specific

The transcription factor hepatocyte nuclear factor 3 (HNF-3) is involved in the coordinate expression of several liver genes. HNF-3 DNA binding activity is composed of three different liver proteins which recognize the same DNA site. The HNF-3 proteins (designated alpha, beta, and gamma) possess homology in the DNA binding domain and in several additional regions. To understand the cell-type-specific expression of HNF-3 beta, we have defined the regulatory sequences that elicit hepatoma-specific expression. Promoter activity requires -134 bp of HNF-3 beta proximal sequences and binds four nuclear proteins, including two ubiquitous factors. One of these promoter sites interacts with a novel cell-specific factor, LF-H3 beta, whose binding activity correlates with the HNF-3 beta tissue expression pattern. Furthermore, there is a binding site for the HNF-3 protein within its own promoter, suggesting that an autoactivation mechanism is involved in the establishment of HNF-3 beta expression. We propose that both the LF-H3 beta and HNF-3 sites play an important role in the cell-type-specific expression of the HNF-3 beta transcription factor.

scholarly journals Rel Induces Interferon Regulatory Factor 4 (IRF-4) Expression in Lymphocytes

2000 ◽  
Vol 191 (8) ◽  
pp. 1281-1292 ◽  
Author(s):  
Raelene J. Grumont ◽  
Steve Gerondakis
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Nuclear Factor Κb ◽  
Wild Type ◽  
Cell Type ◽  
Regulatory Factor ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific ◽  
Interferon Regulatory Factor 4

In lymphocytes, the Rel transcription factor is essential in establishing a pattern of gene expression that promotes cell proliferation, survival, and differentiation. Here we show that mitogen-induced expression of interferon (IFN) regulatory factor 4 (IRF-4), a lymphoid-specific member of the IFN family of transcription factors, is Rel dependent. Consistent with IRF-4 functioning as a repressor of IFN-induced gene expression, the absence of IRF-4 expression in c-rel−/− B cells coincided with a greater sensitivity of these cells to the antiproliferative activity of IFNs. In turn, enforced expression of an IRF-4 transgene restored IFN modulated c-rel−/− B cell proliferation to that of wild-type cells. This cross-regulation between two different signaling pathways represents a novel mechanism that Rel/nuclear factor κB can repress the transcription of IFN-regulated genes in a cell type–specific manner.

scholarly journals Cell type-specific inhibition of p53-mediated apoptosis by mdm2.

1996 ◽  
Vol 15 (7) ◽  
pp. 1596-1606 ◽  
Author(s):  
Y. Haupt ◽  
Y. Barak ◽  
M. Oren
Keyword(s):  
Specific Inhibition ◽  
Cell Type ◽  
Cell Type Specific

scholarly journals Therapeutic efficacy of soluble receptor activator of nuclear factor-κB-Fc delivered by nonviral gene transfer in a mouse model of osteolytic osteosarcoma

2008 ◽  
Vol 7 (10) ◽  
pp. 3389-3398 ◽  
Author(s):  
François Lamoureux ◽  
Gaëlle Picarda ◽  
Julie Rousseau ◽  
Clothilde Gourden ◽  
Séverine Battaglia ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Mouse Model ◽  
Therapeutic Efficacy ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Soluble Receptor ◽  
Nonviral Gene Transfer ◽  
Receptor Activator
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