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Journal ArticleDOI

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

Andrew M. Ho, +2 more
- 14 Jul 2000 - 
- Vol. 289, Iss: 5477, pp 265-270
TLDR
It is shown that the mouse progressive ankylosis locus encodes a multipass transmembrane protein (ANK) that is expressed in joints and other tissues and controls pyrophosphate levels in cultured cells.
Abstract
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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Citations
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Journal ArticleDOI

The serum protein α2–Heremans-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification

TL;DR: A critical role is demonstrated of the serum protein alpha2-Heremans-Schmid glycoprotein (Ahsg) as an inhibitor of unwanted mineralization and a novel therapeutic concept to prevent ectopic calcification accompanying various diseases is provided.
Journal ArticleDOI

Bisphosphonates: The first 40 years

TL;DR: The discovery and development of the bisphosphonates (BPs) as a major class of drugs for the treatment of bone diseases has been a fascinating story, and a paradigm of a successful journey from 'bench to bedside'.
Journal ArticleDOI

Vascular Calcification Pathobiology of a Multifaceted Disease

TL;DR: Clinically, vascular calcification is now accepted as a valuable predictor of coronary heart disease, and, conversely, many treatments for cardiovascular disease such as statins, antioxidants, hormone replacement therapy, ACE inhibitors, fish oils, and calcium channel blockers may affect bone health.
Journal ArticleDOI

Tissue-nonspecific alkaline phosphatase and plasma cell membrane glycoprotein-1 are central antagonistic regulators of bone mineralization

TL;DR: The results suggest that inhibiting PC-1 function may be a viable therapeutic strategy for hypophosphatasia, and interfere with TNAP activity may correct pathological hyperossification because of PPi insufficiency.
Journal ArticleDOI

The mechanism of mineralization and the role of alkaline phosphatase in health and disease.

TL;DR: Although hypophosphatasia is untreatable at present, the recent success of enzyme replacement therapy offers promise, and strategies for preventing pathologic calcification using TNAP and NPP1 are in development.
References
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Journal ArticleDOI

SV40-transformed simian cells support the replication of early SV40 mutants.

TL;DR: Three transformed lines of simian cells were established and found to contain T antigen; retain complete permissiveness for lytic growth of SV40; support the replication of tsA209 virus at 40 degrees C; and support the replicate of pure populations of SV 40 mutants with deletions in the early region.
Journal ArticleDOI

Characterizing the quantitative genetic contribution to rheumatoid arthritis using data from twins

TL;DR: There is no evidence in these twin data that the overall genetic contribution to RA differs by sex, age, age at disease onset, and disease severity.
Journal ArticleDOI

Toppred ii: an improved software for membrane protein structure predictions

TL;DR: The aim of developing TopPred II is to compile all existing knowledge about topology in order to permit easy access to prediction of membrane protein topologies.
Journal ArticleDOI

Genetic influences on osteoarthritis in women: a twin study

TL;DR: These results demonstrate for the first time a clear genetic effect for radiographic osteoarthritis of the hand and knee in women, with a genetic influence ranging from 39-65%, independent of known environmental or demographic confounders.
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