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

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

Authors

  • Ho AM
  • Johnson MD
  • Kingsley DM

Journal

Science (New York, N.Y.)

Publication Data

July 14, 2000

Associated Grants

  • Agency: NIGMS NIH HHS, Id: 5T32GM07365

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