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The progressive ankylosis gene product ANK regulates extracellular ATP levels in primary articular chondrocytes

Overview of attention for article published in Arthritis Research & Therapy, October 2013
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Title
The progressive ankylosis gene product ANK regulates extracellular ATP levels in primary articular chondrocytes
Published in
Arthritis Research & Therapy, October 2013
DOI 10.1186/ar4337
Pubmed ID
Authors

Ann K Rosenthal, Claudia M Gohr, Elizabeth Mitton-Fitzgerald, Megan K Lutz, George R Dubyak, Lawrence M Ryan

Abstract

Extracellular ATP (eATP) is released by articular chondrocytes under physiological and pathological conditions. High eATP levels cause pathologic calcification, damage cartilage, and mediate pain. We recently showed that stable over-expression of the progressive ankylosis gene product, ANK, increased chondrocyte eATP levels, but the mechanisms of this effect remained unexplored. The purpose of this work was to further investigate mechanisms of eATP efflux in primary articular chondrocytes and to better define the role of ANK in this process.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 35 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 3%
Unknown 34 97%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 9 26%
Student > Master 4 11%
Student > Bachelor 3 9%
Professor 3 9%
Lecturer 2 6%
Other 4 11%
Unknown 10 29%
Readers by discipline Count As %
Agricultural and Biological Sciences 8 23%
Medicine and Dentistry 4 11%
Biochemistry, Genetics and Molecular Biology 3 9%
Immunology and Microbiology 2 6%
Chemistry 2 6%
Other 4 11%
Unknown 12 34%