The Transcription Factor Early Growth-response Factor 1 Modulates Tumor Necrosis Factor- α , Immunoglobulin E, and Airway Responsiveness in Mice

2001 ◽  
Vol 163 (3) ◽  
pp. 778-785 ◽  
Author(s):  
ERIC S. SILVERMAN ◽  
GEORGE T. DE SANCTIS ◽  
JOSHUA BOYCE ◽  
JAMES A. MACLEAN ◽  
AIPING JIAO ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Tumor Necrosis ◽  
Growth Response ◽  
Tumor Necrosis Factor Α ◽  
Immunoglobulin E ◽  
Early Growth ◽  
Response Factor ◽  
Early Growth Response ◽  
Factor Α ◽  
Necrosis Factor

Tumor Necrosis Factor-α Provokes a Hypertrophic Growth Response in Adult Cardiac Myocytes

Circulation ◽  
1997 ◽  
Vol 95 (5) ◽  
pp. 1247-1252 ◽  
Author(s):  
Tomoyuki Yokoyama ◽  
Masayuki Nakano ◽  
John L. Bednarczyk ◽  
Bradley W. McIntyre ◽  
Mark Entman ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Cardiac Myocytes ◽  
Tumor Necrosis ◽  
Growth Response ◽  
Tumor Necrosis Factor Α ◽  
Hypertrophic Growth ◽  
Adult Cardiac Myocytes ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Yersinia enterocolitica Impairs Activation of Transcription Factor NF-κB: Involvement in the Induction of Programmed Cell Death and in the Suppression of the Macrophage Tumor Necrosis Factor α Production

1998 ◽  
Vol 187 (7) ◽  
pp. 1069-1079 ◽  
Author(s):  
Klaus Ruckdeschel ◽  
Suzanne Harb ◽  
Andreas Roggenkamp ◽  
Mathias Hornef ◽  
Robert Zumbihl ◽  
...  
Keyword(s):  
Cell Death ◽  
Transcription Factor ◽  
Tumor Necrosis Factor ◽  
Programmed Cell Death ◽  
Proteasome Inhibitor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

In this study, we investigated the activity of transcription factor NF-κB in macrophages infected with Yersinia enterocolitica. Although triggering initially a weak NF-κB signal, Y. enterocolitica inhibited NF-κB activation in murine J774A.1 and peritoneal macrophages within 60 to 90 min. Simultaneously, Y. enterocolitica prevented prolonged degradation of the inhibitory proteins IκB-α and IκB-β observed by treatment with lipopolysaccharide (LPS) or nonvirulent, plasmid-cured yersiniae. Analysis of different Y. enterocolitica mutants revealed a striking correlation between the abilities of these strains to inhibit NF-κB and to suppress the tumor necrosis factor α (TNF-α) production as well as to trigger macrophage apoptosis. When NF-κB activation was prevented by the proteasome inhibitor MG-132, nonvirulent yersiniae as well as LPS became able to trigger J774A.1 cell apoptosis and inhibition of the TNF-α secretion. Y. enterocolitica also impaired the activity of NF-κB in epithelial HeLa cells. Although neither Y. enterocolitica nor TNF-α could induce HeLa cell apoptosis alone, TNF-α provoked apoptosis when activation of NF-κB was inhibited by Yersinia infection or by the proteasome inhibitor MG-132. Together, these data demonstrate that Y. enterocolitica suppresses cellular activation of NF-κB, which inhibits TNF-α release and triggers apoptosis in macrophages. Our results also suggest that Yersinia infection confers susceptibility to programmed cell death to other cell types, provided that the appropriate death signal is delivered.

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