Targeted Disruption of Metallothionein I and II Genes Increases Sensitivity to Cadmium

We inactivated the mouse metallothionein (MT)-I and MT-II genes in embryonic stem cells and generated mice homozygous for these mutant alleles. These mice were viable and reproduced normally when reared under normal laboratory conditions. They were, however, more susceptible to hepatic poisoning by...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1994-01, Vol.91 (2), p.584-588
Main Authors: Masters, Brian A., Kelly, Edward J., Quaife, Carol J., Brinster, Ralph L., Palmiter, Richard D.
Format: Article
Language:English
Subjects:
Alanine Transaminase - blood
Alleles
Amino Acid Sequence
Analytical, structural and metabolic biochemistry
Animals
Aspartate Aminotransferases - blood
Base Sequence
Biochemistry
Biological and medical sciences
Cadmium
Cadmium Poisoning - genetics
Cadmium Poisoning - metabolism
Cadmium Poisoning - pathology
DNA - genetics
Exons
Female
Fundamental and applied biological sciences. Psychology
Genes
Histology
Liver
Liver - drug effects
Liver - pathology
Male
Male animals
Metalloproteins
Metallothionein - genetics
Metallothionein - metabolism
Mice
Mice, Inbred C57BL
Mice, Mutant Strains
Molecular Sequence Data
Mutagenesis, Insertional
Mutation
Oligonucleotides
Other metalloproteins
Protein Biosynthesis
Proteins
Rodents
Transcription, Genetic
Zinc
Citations: Items that cite this one
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Description
Summary:We inactivated the mouse metallothionein (MT)-I and MT-II genes in embryonic stem cells and generated mice homozygous for these mutant alleles. These mice were viable and reproduced normally when reared under normal laboratory conditions. They were, however, more susceptible to hepatic poisoning by cadmium. This proves that these widely expressed MTs are not essential for development but that they do protect against cadmium toxicity. These mice provide a means for testing other proposed functions of MT in vivo.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.91.2.584