Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of rat pancreatic beta-cells in response to cytokine exposure and NF-kappa B activation blocking


ABSTRACT: Type 1 diabetes mellitus results from an autoimmune destruction of pancreatic beta-cells. Based on findings suggesting NF-kappa B plays a role in beta cell apoptosis, we blocked NF-kappa B activation in cytokine-exposed FACS sorted beta cells by a recombinant adenovirus (AdI kappa B((SA)2)) containing an inhibitor of NF kappa B alpha (I kappa Bac) super-repressor (S32A/S36A). The expression profile was then analyzed with the Affymetrix RG U34a microarray.

ORGANISM(S): Rattus norvegicus

SUBMITTER: John Brestelli 

PROVIDER: E-CBIL-9 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

A comprehensive analysis of cytokine-induced and nuclear factor-kappa B-dependent genes in primary rat pancreatic beta-cells.

Cardozo A K AK   Heimberg H H   Heremans Y Y   Leeman R R   Kutlu B B   Kruhøffer M M   Ørntoft T T   Eizirik D L DL  

The Journal of biological chemistry 20011030 52


Type 1 diabetes mellitus results from an autoimmune destruction of pancreatic beta-cells. Cytokines, such as interleukin-1 beta and interferon-gamma, are putative mediators of immune-induced beta-cell death and, under in vitro conditions, cause beta-cell apoptosis. We have recently shown that interleukin-1 beta + interferon-gamma modifies the expression of >200 genes in beta-cells. Several of these genes are putative targets for the transcription factor nuclear factor-kappa B (NF-kappa B), and i  ...[more]

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