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NLRC5 is a transcriptional regulator of MHC class I genes

ABSTRACT: NLRC5 is a member of the NLR family of proteins. The observation that NLRC5 is found in the nucleus prompted us to perform a gene array to identify putative target genes of NLRC5. We generated Jurkat T cell lines that stably express either the wild-type or mutant forms of NLRC5 harboring mutations in the nucleotide binding domain (NBD): Walker A (deficient in nucleotide binding), Walker B (deficient in nucleotide hydrolysis), and the combined Walker AB, carrying both mutations. Site-directed mutagenesis was used to create the NLRC5 NBD mutants: Walker A (K234A), Walker B (E311Q), and Walker AB (both mutations). We compared the expression profiles of Jurkat T cells expressing GFP, or the GFP-tagged wild-type, Walker A, Walker B, or Walker AB forms of NLRC5. GFP and the Walker A and Walker AB forms of NLRC5 were considered functionally inactive, while the wild-type and Walker B forms of NLRC5 were considered functionally active. These groups were used as biological replicates to assess the effect of NLRC5 activity on gene expression.

ORGANISM(S): Homo sapiens

SUBMITTER: Amy Li

PROVIDER: E-GEOD-22064 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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NLRC5 is a transcriptional regulator of MHC class I genes

Project description:NLRC5 is a member of the NLR family of proteins. The observation that NLRC5 is found in the nucleus prompted us to perform a gene array to identify putative target genes of NLRC5. We generated Jurkat T cell lines that stably express either the wild-type or mutant forms of NLRC5 harboring mutations in the nucleotide binding domain (NBD): Walker A (deficient in nucleotide binding), Walker B (deficient in nucleotide hydrolysis), and the combined Walker AB, carrying both mutations. Site-directed mutagenesis was used to create the NLRC5 NBD mutants: Walker A (K234A), Walker B (E311Q), and Walker AB (both mutations).

2010-06-30 | GSE22064 | GEO

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Project description:Bronchial asthma is associated with type 2 immune responses induced by components of adaptive as well as innate immunity. Although innate cytokines such as IL-25 have been shown to play key roles in development of airway hyperreactivity (AHR), little is known of innate molecules that regulate IL-25-mediated airway inflammation. We found that blockade of repulsive guidance molecule b (RGMb) in an experimental murine model of asthma blocked the development of AHR, a cardinal feature of asthma, and that RGMb is expressed on F4/80+CD11b+CD11cneg macrophages (RGMb+ macrophages), which accumulated in the lungs of OVA-sensitized and challenged mice, but not in naÃ¯ve mice. Moreover, we found that a large fraction of the RGMb+ macrophages expressed the IL-25 receptor IL-17RB and produced IL-13. IL-25 was critical for the development of AHR in our model, since mice deficient in IL-17RB did not develop AHR. Finally, treatment with anti-RGMb mAb during the challenge phase of the protocol after allergen sensitization effectively prevented the development of AHR and airway inflammation, suggesting for the first time that RGMb+ cells, including RGMb+ macrophages, play critical roles in allergen-induced asthma. We used microarrays to compare the gene expression patterns in WT mice sensitized and challenged with OVA that were treated with either RGMb mAb or an isotype control. First replicate: 3 control samples (mice sensitized and challenged with saline), 3 RGMb mAb samples, 3 isotype samples; 2nd replicate: 3 control samples, 3 RGMb mAb samples, 2 isotype samples. Lung tissues were harvested at the same treatment time point in all groups.

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2014-10-20 | E-GEOD-62218 | biostudies-arrayexpress

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2008-04-07 | E-GEOD-9717 | biostudies-arrayexpress

Differential gene expression by NKX2-1 suppression in NCI-H2009 cells

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2012-08-16 | E-GEOD-29181 | biostudies-arrayexpress

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