Key result
The mouse ank locus encodes a multipass transmembrane protein that controls pyrophosphate levels, identifying a possible mechanism regulating tissue calcification and susceptibility to arthritis.
The identification of the ANK protein reveals a mechanism for controlling pyrophosphate levels, which regulates tissue calcification and susceptibility to arthritis.
No immediate clinical implications for arthritis; leaves open ANK relevance to human calcification pathways.
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.
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Ho et al. (2000) studied Arthritis and tissue calcification. ank gene mutation / ANK protein was evaluated on Pyrophosphate levels and tissue calcification. The mouse ank locus encodes a multipass transmembrane protein that controls pyrophosphate levels, identifying a possible mechanism regulating tissue calcification and susceptibility to arthritis.
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