Suppressor of cytokine Signaling-3 inhibits interleukin-1 signaling by targeting the TRAF-6/TAK1 complex

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Fältnamn	Indikatorer	Metadata
000		02635naa a2200313 4500
001		oai:prod.swepub.kib.ki.se:1940219
003		SwePub
008		240701s2006 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a http://kipublications.ki.se/Default.aspx?queryparsed=id:19402192 URI
024	7	a https://doi.org/10.1210/me.2005-03012 DOI
040		a (SwePub)ki
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Frobose, H4 aut
245	1 0	a Suppressor of cytokine Signaling-3 inhibits interleukin-1 signaling by targeting the TRAF-6/TAK1 complex
264	1	b The Endocrine Society,c 2006
520		a IL-1 plays a major role in inflammation and autoimmunity through activation of nuclear factor κ B (NFκB) and MAPKs. Although a great deal is known about the mechanism of activation of NFκB and MAPKs by IL-1, much less is known about the down-regulation of this pathway. Suppressor of cytokine signaling (SOCS)-3 was shown to inhibit IL-1-induced transcription and activation of NFκB and the MAPKs JNK and p38, but the mechanism is unknown. We show here that SOCS-3 inhibits NFκB-dependent transcription induced by overexpression of the upstream IL-1 signaling molecules MyD88, IL-1R-activated kinase 1, TNF receptor-associated factor (TRAF)6, and TGFβ-activated kinase (TAK)1, but not when the MAP3K MAPK/ERK kinase kinase-1 is used instead of TAK1, indicating that the target for SOCS-3 is the TRAF6/TAK1 signaling complex. By coimmunoprecipitation, it was shown that SOCS-3 inhibited the association between TRAF6 and TAK1 and that SOCS-3 coimmunoprecipitated with TAK1 and TRAF6. Furthermore, SOCS-3 inhibited the IL-1-induced catalytic activity of TAK1. Because ubiquitination of TRAF6 is required for activation of TAK1, we analyzed the role of SOCS-3 on TRAF6 ubiquitination and found that SOCS-3 inhibited ubiquitin modification of TRAF6. These results indicate that SOCS-3 inhibits IL-1 signal transduction by inhibiting ubiquitination of TRAF6, thus preventing association and activation of TAK1.
700	1	a Ronn, SG4 aut
700	1	a Heding, PE4 aut
700	1	a Mendoza, H4 aut
700	1	a Cohen, P4 aut
700	1	a Mandrup-Poulsen, T4 aut
700	1	a Billestrup, N4 aut
773	0	t Molecular endocrinology (Baltimore, Md.)d : The Endocrine Societyg 20:7, s. 1587-1596q 20:7<1587-1596x 0888-8809x 1944-9917
856	4	u https://academic.oup.com/mend/article-pdf/20/7/1587/10719437/mend1587.pdf
856	4 8	u http://kipublications.ki.se/Default.aspx?queryparsed=id:1940219
856	4 8	u https://doi.org/10.1210/me.2005-0301

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Av författaren/redakt...: Frobose, H; Ronn, SG; Heding, PE; Mendoza, H; Cohen, P; Mandrup-Poulsen, ...; visa fler...; Billestrup, N; visa färre...

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Av lärosätet: Karolinska Institutet

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