scholarly journals Critical role of tumor necrosis factor receptor 1 in the pathogenesis of pulmonary emphysema in mice

2016 ◽  
Vol Volume 11 ◽  
pp. 1705-1712 ◽  
Author(s):  
Masaki Fujita ◽  
Ouchi Hiroshi ◽  
Satoshi Ikemage ◽  
Eiji Harada ◽  
Takemasa Matsumoto ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Pulmonary Emphysema ◽  
Tumor Necrosis ◽  
Critical Role ◽  
Tumor Necrosis Factor Receptor ◽  
Necrosis Factor

The Role of the Tumor Necrosis Factor Receptor in 2,4,6-Trinitrobenzene Sulfonic Acid (TNBS)-Induced Colitis in Mice

2005 ◽  
Vol 50 (9) ◽  
pp. 1669-1676 ◽  
Author(s):  
Minoru Nakai ◽  
Kaori Sudo ◽  
Yasuhiro Yamada ◽  
Yasushi Kojima ◽  
Tomohiro Kato ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Sulfonic Acid ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Trinitrobenzene Sulfonic Acid ◽  
Necrosis Factor

scholarly journals Opposing role of tumor necrosis factor receptor 1 signaling in T cell-mediated hepatitis and bacterial infection in mice

Hepatology ◽  
2016 ◽  
Vol 64 (2) ◽  
pp. 508-521 ◽  
Author(s):  
Raluca Wroblewski ◽  
Marietta Armaka ◽  
Vangelis Kondylis ◽  
Manolis Pasparakis ◽  
Henning Walczak ◽  
...  
Keyword(s):  
T Cell ◽  
Tumor Necrosis Factor ◽  
Bacterial Infection ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Necrosis Factor

scholarly journals A Critical Role of the p75 Tumor Necrosis Factor Receptor (p75TNF-R) in Organ Inflammation Independent of  TNF, Lymphotoxin α, or the p55TNF-R

1998 ◽  
Vol 188 (7) ◽  
pp. 1343-1352 ◽  
Author(s):  
Eleni Douni ◽  
George Kollias
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Critical Role ◽  
Tumor Necrosis Factor Receptor ◽  
Peripheral Blood Mononuclear ◽  
Enhanced Production ◽  
Wide Range ◽  
Lymphotoxin Α ◽  
Necrosis Factor

Despite overwhelming evidence that enhanced production of the p75 tumor necrosis factor receptor (p75TNF-R) accompanies development of specific human inflammatory pathologies such as multi-organ failure during sepsis, inflammatory liver disease, pancreatitis, respiratory distress syndrome, or AIDS, the function of this receptor remains poorly defined in vivo. We show here that at levels relevant to human disease, production of the human p75TNF-R in transgenic mice results in a severe inflammatory syndrome involving mainly the pancreas, liver, kidney, and lung, and characterized by constitutively increased NF-κB activity in the peripheral blood mononuclear cell compartment. This process is shown to evolve independently of the presence of TNF, lymphotoxin α, or the p55TNF-R, although coexpression of a human TNF transgene accelerated pathology. These results establish an independent role for enhanced p75TNF-R production in the pathogenesis of inflammatory disease and implicate the direct involvement of this receptor in a wide range of human inflammatory pathologies.

A Critical Role of Luteolin-Induced Reactive Oxygen Species in Blockage of Tumor Necrosis Factor-Activated Nuclear Factor-κB Pathway and Sensitization of Apoptosis in Lung Cancer Cells

2007 ◽  
Vol 71 (5) ◽  
pp. 1381-1388 ◽  
Author(s):  
Wei Ju ◽  
Xia Wang ◽  
Honglian Shi ◽  
Wenshu Chen ◽  
Steven A. Belinsky ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Critical Role ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Necrosis Factor

scholarly journals Role of SODD in Regulation of Tumor Necrosis Factor Responses

2003 ◽  
Vol 23 (11) ◽  
pp. 4026-4033 ◽  
Author(s):  
Hidetoshi Takada ◽  
Nien-Jung Chen ◽  
Christine Mirtsos ◽  
Shinobu Suzuki ◽  
Nobutaka Suzuki ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Signaling Proteins ◽  
Ligand Stimulation ◽  
Cytotoxic Responses ◽  
Necrosis Factor

ABSTRACT Signaling from tumor necrosis factor receptor type 1 (TNFR1) can elicit potent inflammatory and cytotoxic responses that need to be properly regulated. It was suggested that the silencer of death domains (SODD) protein constitutively associates intracellularly with TNFR1 and inhibits the recruitment of cytoplasmic signaling proteins to TNFR1 to prevent spontaneous aggregation of the cytoplasmic death domains of TNFR1 molecules that are juxtaposed in the absence of ligand stimulation. In this study, we demonstrate that mice lacking SODD produce larger amounts of cytokines in response to in vivo TNF challenge. SODD-deficient macrophages and embryonic fibroblasts also show altered responses to TNF. TNF-induced activation of NF-κB is accelerated in SODD-deficient cells, but TNF-induced c-Jun N-terminal kinase activity is slightly repressed. Interestingly, the apoptotic arm of TNF signaling is not hyperresponsive in the SODD-deficient cells. Together, these results suggest that SODD is critical for the regulation of TNF signaling.

scholarly journals Critical role of tumor necrosis factor receptor 1, but not 2, in hepatic stellate cell proliferation, extracellular matrix remodeling, and liver fibrogenesis

Hepatology ◽  
2011 ◽  
Vol 54 (1) ◽  
pp. 319-327 ◽  
Author(s):  
Núria Tarrats ◽  
Anna Moles ◽  
Albert Morales ◽  
Carmen García-Ruiz ◽  
José C. Fernández-Checa ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Necrosis ◽  
Stellate Cell ◽  
Critical Role ◽  
Tumor Necrosis Factor Receptor ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Liver Fibrogenesis ◽  
Necrosis Factor
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