Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse duodenum and liver with primary (Hfe ?/? and C282Y homozygous mice) and secondary iron overload vs 129S6/SvEvTac wild type controls


ABSTRACT: We determined duodenal and liver gene response patterns in mice with primary (Hfe ?/? and C282Y homozygous mice) and secondary iron overload versus 129S6/SvEvTac wild type controls.

ORGANISM(S): Mus musculus

DISEASE(S): murine hereditary hemochromatosis

SUBMITTER: Nancy Andrews 

PROVIDER: E-MEXP-5 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Regulatory defects in liver and intestine implicate abnormal hepcidin and Cybrd1 expression in mouse hemochromatosis.

Muckenthaler Martina M   Roy Cindy N CN   Custodio Angel O AO   Miñana Belén B   deGraaf Jos J   Montross Lynne K LK   Andrews Nancy C NC   Hentze Matthias W MW  

Nature genetics 20030501 1


Individuals with hereditary hemochromatosis suffer from systemic iron overload due to duodenal hyperabsorption. Most cases arise from a founder mutation in HFE (845G-->A; ref. 2) that results in the amino-acid substitution C282Y and prevents the association of HFE with beta2-microglobulin. Mice homozygous with respect to a null allele of Hfe (Hfe-/-) or homozygous with respect to the orthologous 882G-->A mutation (Hfe(845A/845A)) develop iron overload that recapitulates hereditary hemochromatosi  ...[more]

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