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Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE29947 | GEO | 2011/08/31

SECONDARY ACCESSION(S): PRJNA140785

REPOSITORIES: GEO

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Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses

Project description:This SuperSeries is composed of the following subset Series: GSE29888: Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses (Agilent) GSE29891: Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses (Affymetrix) Refer to individual Series

2011-08-30 | E-GEOD-29947 | biostudies-arrayexpress

Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses (Affymetrix)

Project description:Our systems analysis reported here demonstrates that TLR-responses in macrophages are markedly impaired by SHARPIN deficiency, and that SHARPIN controls expression of a subset of TLR2-induced, NF-kB and AP-1 dependent genes that overlaps with those affected by the hypomorphic panr2 mutation in NEMO. 46 total RNA samples from murine bone marrow derived macrophages were analyzed (32 by Agilent array, 14 by Affymetrix Exon array) On Affymetrix Exon array, the responses of macrophages to 12hr stimulation with the TLR2 ligand PAM3CSK4 (300ng/mL) were analyzed in biological duplicates for the Map3k8(sluggish) mutant and respective controls and in singlet for the Tnf(KO) mutant compared to two respective WT controls.

2011-08-30 | E-GEOD-29891 | biostudies-arrayexpress

Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses (Agilent)

Project description:Our systems analysis reported here demonstrates that TLR-responses in macrophages are markedly impaired by SHARPIN deficiency, and that SHARPIN controls expression of a subset of TLR2-induced, NF-kB and AP-1 dependent genes that overlaps with those affected by the hypomorphic panr2 mutation in NEMO. 46 total RNA samples from murine bone marrow derived macrophages were analyzed (32 by Agilent array, 14 by Affymetrix Exon array) On Agilent array, the responses of macrophages to 12hr stimulation with the TLR2 ligand PAM3CSK4 (300ng/mL) were analyzed in biological duplicates for five mutant mouse strains and respective controls: Sharpin(cpdm), Ikbkg(panr2), Atf3(KO), Il10(KO), and Nfkb1(KO).

2011-08-30 | E-GEOD-29888 | biostudies-arrayexpress

Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses (Affymetrix)

2011-08-31 | GSE29891 | GEO

Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses (Agilent)

2011-08-31 | GSE29888 | GEO

Systems analysis identifies an essential role for SHANK-associated RH domain-interacting protein (SHARPIN) in macrophage Toll-like receptor 2 (TLR2) responses.

Project description:Precise control of the innate immune response is essential to ensure host defense against infection while avoiding inflammatory disease. Systems-level analyses of Toll-like receptor (TLR)-stimulated macrophages suggested that SHANK-associated RH domain-interacting protein (SHARPIN) might play a role in the TLR pathway. This hypothesis was supported by the observation that macrophages derived from chronic proliferative dermatitis mutation (cpdm) mice, which harbor a spontaneous null mutation in the Sharpin gene, exhibited impaired IL-12 production in response to TLR activation. Systems biology approaches were used to define the SHARPIN-regulated networks. Promoter analysis identified NF-κB and AP-1 as candidate transcription factors downstream of SHARPIN, and network analysis suggested selective attenuation of these pathways. We found that the effects of SHARPIN deficiency on the TLR2-induced transcriptome were strikingly correlated with the effects of the recently described hypomorphic L153P/panr2 point mutation in Ikbkg [NF-κB Essential Modulator (NEMO)], suggesting that SHARPIN and NEMO interact. We confirmed this interaction by co-immunoprecipitation analysis and furthermore found it to be abrogated by panr2. NEMO-dependent signaling was affected by SHARPIN deficiency in a manner similar to the panr2 mutation, including impaired p105 and ERK phosphorylation and p65 nuclear localization. Interestingly, SHARPIN deficiency had no effect on IκBα degradation and on p38 and JNK phosphorylation. Taken together, these results demonstrate that SHARPIN is an essential adaptor downstream of the branch point defined by the panr2 mutation in NEMO.

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