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Distinct control of MyD88 adapter-dependent and Akt kinase-regulated responses by the interleukin (IL)-1RI co-receptor, TILRR

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Distinct control of MyD88 adapter-dependent and Akt kinase-regulated responses by the interleukin (IL)-1RI co-receptor, TILRR. / Zhang, Xiao; Montagut Pino, Gemma; Shephard, Freya; Kiss-Toth, Endre; Qwarnstrom, Eva E.

In: Journal of Biological Chemistry, Vol. 287, No. 15, 06.04.2012, p. 12348-12352.

Research output: Contribution to journalArticle

Harvard

Zhang, X, Montagut Pino, G, Shephard, F, Kiss-Toth, E & Qwarnstrom, EE 2012, 'Distinct control of MyD88 adapter-dependent and Akt kinase-regulated responses by the interleukin (IL)-1RI co-receptor, TILRR' Journal of Biological Chemistry, vol 287, no. 15, pp. 12348-12352.

APA

Zhang, X., Montagut Pino, G., Shephard, F., Kiss-Toth, E., & Qwarnstrom, E. E. (2012). Distinct control of MyD88 adapter-dependent and Akt kinase-regulated responses by the interleukin (IL)-1RI co-receptor, TILRR. Journal of Biological Chemistry, 287(15), 12348-12352doi: 10.1074/jbc.C111.321711

Vancouver

Zhang X, Montagut Pino G, Shephard F, Kiss-Toth E, Qwarnstrom EE. Distinct control of MyD88 adapter-dependent and Akt kinase-regulated responses by the interleukin (IL)-1RI co-receptor, TILRR. Journal of Biological Chemistry. 2012 Apr 6;287(15):12348-12352.

Author

Zhang, Xiao; Montagut Pino, Gemma; Shephard, Freya; Kiss-Toth, Endre; Qwarnstrom, Eva E. / Distinct control of MyD88 adapter-dependent and Akt kinase-regulated responses by the interleukin (IL)-1RI co-receptor, TILRR.

In: Journal of Biological Chemistry, Vol. 287, No. 15, 06.04.2012, p. 12348-12352.

Research output: Contribution to journalArticle

Bibtex - Download

@article{978d59054b034c31b997dc33356cb90f,
title = "Distinct control of MyD88 adapter-dependent and Akt kinase-regulated responses by the interleukin (IL)-1RI co-receptor, TILRR",
author = "Xiao Zhang and {Montagut Pino}, Gemma and Freya Shephard and Endre Kiss-Toth and Qwarnstrom, {Eva E.}",
year = "2012",
volume = "287",
number = "15",
pages = "12348--12352",
journal = "Journal of Biological Chemistry",
issn = "0021-9258",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - Distinct control of MyD88 adapter-dependent and Akt kinase-regulated responses by the interleukin (IL)-1RI co-receptor, TILRR

A1 - Zhang,Xiao

A1 - Montagut Pino,Gemma

A1 - Shephard,Freya

A1 - Kiss-Toth,Endre

A1 - Qwarnstrom,Eva E.

AU - Zhang,Xiao

AU - Montagut Pino,Gemma

AU - Shephard,Freya

AU - Kiss-Toth,Endre

AU - Qwarnstrom,Eva E.

PY - 2012/4/6

Y1 - 2012/4/6

N2 - Inflammatory responses are controlled through members of the interleukin-1 receptor (IL-1R)/Toll-like receptor superfamily. Our earlier work demonstrates that the IL-1 receptor type 1 (IL-1RI) co-receptor, Toll-like and IL-1 receptor regulator (TILRR), amplifies IL-1 activation of NF-?B and inflammatory genes. Here we show that TILRR similarly promotes IL-1-induced anti-apoptotic signals and reduces caspase-3 activity. Further, the TILRR-induced effects on cell survival and inflammatory responses are controlled through distinct parts of the IL-1RI regulatory Toll IL-1 receptor (TIR) domain. Alanine-scanning mutagenesis identified a functional TILRR mutant (R425A), which blocked increases in cell survival and upstream activation of Akt but had no effect on amplification of MyD88- dependent inflammatory responses. A second mutant (D448A) blocked TILRR potentiation of MyD88-dependent signals and inflammatory activation but had no impact on cell survival. Secondary structure predictions suggested that the mutations induce distinct alterations in the a-helical structure of the TILRR core protein. The results indicate a role for TILRR in selective amplification of NF-?B responses through IL-1RI and suggest that the specificity is determined by changes in receptor conformation and adapter protein recruitment. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.

AB - Inflammatory responses are controlled through members of the interleukin-1 receptor (IL-1R)/Toll-like receptor superfamily. Our earlier work demonstrates that the IL-1 receptor type 1 (IL-1RI) co-receptor, Toll-like and IL-1 receptor regulator (TILRR), amplifies IL-1 activation of NF-?B and inflammatory genes. Here we show that TILRR similarly promotes IL-1-induced anti-apoptotic signals and reduces caspase-3 activity. Further, the TILRR-induced effects on cell survival and inflammatory responses are controlled through distinct parts of the IL-1RI regulatory Toll IL-1 receptor (TIR) domain. Alanine-scanning mutagenesis identified a functional TILRR mutant (R425A), which blocked increases in cell survival and upstream activation of Akt but had no effect on amplification of MyD88- dependent inflammatory responses. A second mutant (D448A) blocked TILRR potentiation of MyD88-dependent signals and inflammatory activation but had no impact on cell survival. Secondary structure predictions suggested that the mutations induce distinct alterations in the a-helical structure of the TILRR core protein. The results indicate a role for TILRR in selective amplification of NF-?B responses through IL-1RI and suggest that the specificity is determined by changes in receptor conformation and adapter protein recruitment. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.

U2 - 10.1074/jbc.C111.321711

DO - 10.1074/jbc.C111.321711

M1 - Article

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 15

VL - 287

SP - 12348

EP - 12352

ER -

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