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Role of the mouse ank gene in control of tissue calcification and arthritis.

Science (New York, N.Y.) | Jul 14, 2000

Mutation at the mouse progressive ankylosis (ank) locus causes a generalized, progressive form of arthritis accompanied by mineral deposition, formation of bony outgrowths, and joint destruction. Here, we show that the ank locus encodes a multipass transmembrane protein (ANK) that is expressed in joints and other tissues and controls pyrophosphate levels in cultured cells. A highly conserved gene is present in humans and other vertebrates. These results identify ANK-mediated control of pyrophosphate levels as a possible mechanism regulating tissue calcification and susceptibility to arthritis in higher animals.

Pubmed ID: 10894769 RIS Download

Mesh terms: Animals | Arthritis | Base Sequence | Biological Transport | COS Cells | Calcinosis | Chromosome Mapping | Cloning, Molecular | DNA | Diphosphates | Durapatite | Gene Expression | Genetic Complementation Test | Humans | Membrane Proteins | Mice | Mice, Transgenic | Molecular Sequence Data | Mutation | Phenotype | Phosphate Transport Proteins | Physical Chromosome Mapping | Sequence Homology, Nucleic Acid | Tissue Distribution

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Associated grants

  • Agency: NIGMS NIH HHS, Id: 5T32GM07365

Mouse Genome Informatics (Data, Gene Annotation)

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