Aggregation of the intracellular domain of the type 1 tumor necrosis factor receptor defined by the two-hybrid system.

Orthodontic tooth movement is dependent on osteoclast activity. Tumor necrosis factor (TNF)-α plays an important role, directly or via chemokine release, in osteoclast recruitment and activation. This study aimed to investigate whether the TNF receptor type 1 (p55) influences these events and, consequently, orthodontic tooth movement. An orthodontic appliance was placed in wild-type mice (WT) and p55-deficient mice (p55−/−). Levels of TNF-α and 2 chemokines (MCP-1/CCL2, RANTES/CCL5) were evaluated in periodontal tissues. A significant increase in CCL2 and TNF-α was observed in both groups after 12 hrs of mechanical loading. However, CCL5 levels remained unchanged in p55−/− mice at this time-point. The number of TRAP-positive osteoclasts in p55−/− mice was significantly lower than that in WT mice. Also, there was a significantly smaller rate of tooth movement in p55−/− mice. Analysis of our data suggests that the TNFR-1 plays a significant role in orthodontic tooth movement that might be associated with changes in CCL5 levels.

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Tumor necrosis factor receptor type-1 in sensory neurons contributes to induction of chronic enhancement of inflammatory hyperalgesia in rat

European Journal of Neuroscience ◽

10.1046/j.1460-9568.2003.02626.x ◽

2003 ◽

Vol 17 (9) ◽

pp. 1847-1852 ◽

Cited By ~ 111

Author(s):

Carlos A. Parada ◽

Jenny J. Yeh ◽

Elizabeth K. Joseph ◽

Jon D. Levine

Keyword(s):

Tumor Necrosis Factor ◽

Sensory Neurons ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Receptor ◽

Receptor Type ◽

Inflammatory Hyperalgesia ◽

Necrosis Factor

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Analysis of liver regeneration in mice lacking type 1 or type 2 tumor necrosis factor receptor: Requirement for type 1 but not type 2 receptor

Hepatology ◽

10.1002/hep.510280410 ◽

1998 ◽

Vol 28 (4) ◽

pp. 959-970 ◽

Cited By ~ 201

Author(s):

Yasuhiro Yamada ◽

Eric M. Webber ◽

Irina Kirillova ◽

Jacques J. Peschon ◽

Nelson Fausto

Keyword(s):

Tumor Necrosis Factor ◽

Liver Regeneration ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Receptor ◽

Necrosis Factor

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Role of SODD in Regulation of Tumor Necrosis Factor Responses

Molecular and Cellular Biology ◽

10.1128/mcb.23.11.4026-4033.2003 ◽

2003 ◽

Vol 23 (11) ◽

pp. 4026-4033 ◽

Cited By ~ 35

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.

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