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- Publisher Website: 10.1128/MCB.23.11.4026-4033.2003
- Scopus: eid_2-s2.0-0037569619
- PMID: 12748303
- WOS: WOS:000183031900028
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Article: Role of SODD in regulation of tumor necrosis factor responses
Title | Role of SODD in regulation of tumor necrosis factor responses |
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Authors | |
Issue Date | 2003 |
Citation | Molecular and Cellular Biology, 2003, v. 23, n. 11, p. 4026-4033 How to Cite? |
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. |
Persistent Identifier | http://hdl.handle.net/10722/291634 |
ISSN | 2023 Impact Factor: 3.2 2023 SCImago Journal Rankings: 1.452 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Takada, Hidetoshi | - |
dc.contributor.author | Chen, Nien Jung | - |
dc.contributor.author | Mirtsos, Christine | - |
dc.contributor.author | Suzuki, Shinobu | - |
dc.contributor.author | Suzuki, Nobutaka | - |
dc.contributor.author | Wakeham, Andrew | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Yeh, Wen Chen | - |
dc.date.accessioned | 2020-11-17T14:54:47Z | - |
dc.date.available | 2020-11-17T14:54:47Z | - |
dc.date.issued | 2003 | - |
dc.identifier.citation | Molecular and Cellular Biology, 2003, v. 23, n. 11, p. 4026-4033 | - |
dc.identifier.issn | 0270-7306 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291634 | - |
dc.description.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. | - |
dc.language | eng | - |
dc.relation.ispartof | Molecular and Cellular Biology | - |
dc.title | Role of SODD in regulation of tumor necrosis factor responses | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1128/MCB.23.11.4026-4033.2003 | - |
dc.identifier.pmid | 12748303 | - |
dc.identifier.pmcid | PMC155221 | - |
dc.identifier.scopus | eid_2-s2.0-0037569619 | - |
dc.identifier.volume | 23 | - |
dc.identifier.issue | 11 | - |
dc.identifier.spage | 4026 | - |
dc.identifier.epage | 4033 | - |
dc.identifier.isi | WOS:000183031900028 | - |
dc.identifier.issnl | 0270-7306 | - |