Colin Farquharson

Gradual reactivation over time of vascular tissue angiotensin I to angiotensin II conversion during chronic lisinopril therapy in chronic heart failure.

Allopurinol improves endothelial dysfunction in chronic heart failure.

Differences in metabolic parameters and gene expression related to osteochondrosis/osteoarthrosis in pigs fed 25-hydroxyvitamin D3.

Aldosterone induces acute endothelial dysfunction in vivo in humans: evidence for an aldosterone-induced vasculopathy.

Comparative modelling of human PHOSPHO1 reveals a new group of phosphatases within the haloacid dehalogenase superfamily.

PHOSPHO1-A novel phosphatase specifically expressed at sites of mineralisation in bone and cartilage.

Human PHOSPHO1 exhibits high specific phosphoethanolamine and phosphocholine phosphatase activities.

Tonic levels of angiotensin II reduce tonic levels of vascular nitric oxide even in salt-replete man.

Identification of a novel class of mammalian phosphoinositol-specific phospholipase C enzymes.

Probing the substrate specificities of human PHOSPHO1 and PHOSPHO2.

Elevated expression of hypoxia inducible factor-2alpha in terminally differentiating growth plate chondrocytes.

The presence of PHOSPHO1 in matrix vesicles and its developmental expression prior to skeletal mineralization.

Effect of spironolactone on C-reactive protein levels in patients with heart disease.

Functional involvement of PHOSPHO1 in matrix vesicle-mediated skeletal mineralization.

IGF-I signalling in bone growth: inhibitory actions of dexamethasone and IL-1beta.

Phospholipase C-eta enzymes as putative protein kinase C and Ca2+ signalling components in neuronal and neuroendocrine tissues.

Identification of a novel splice variant of the haloacid dehalogenase: PHOSPHO1.

Genetic selection for fast growth generates bone architecture characterised by enhanced periosteal expansion and limited consolidation of the cortices but a diminution in the early responses to mechanical loading.

Kinetic analysis of substrate utilization by native and TNAP-, NPP1-, or PHOSPHO1-deficient matrix vesicles.

Inhibition of PHOSPHO1 activity results in impaired skeletal mineralization during limb development of the chick.

Loss of skeletal mineralization by the simultaneous ablation of PHOSPHO1 and alkaline phosphatase function: a unified model of the mechanisms of initiation of skeletal calcification.

PHOSPHO1 is essential for mechanically competent mineralization and the avoidance of spontaneous fractures.

The appearance and modulation of osteocyte marker expression during calcification of vascular smooth muscle cells.

Social networking between cells of the foetal skeleton: the importance of thyroid hormones.

Sodium fluoride induces apoptosis and alters bcl-2 family protein expression in MC3T3-E1 osteoblastic cells.

The skeleton: no bones about it.

SOCS2 is the critical regulator of GH action in murine growth plate chondrogenesis.

Altered bone development and an increase in FGF-23 expression in Enpp1(-/-) mice.

Extracellular matrix mineralization promotes E11/gp38 glycoprotein expression and drives osteocytic differentiation.

The importance of the SIBLING family of proteins on skeletal mineralisation and bone remodelling.

Cartilage development and degeneration: a Wnt Wnt situation.

Inflammation and linear bone growth: the inhibitory role of SOCS2 on GH/IGF-1 signaling.

Pharmacological inhibition of PHOSPHO1 suppresses vascular smooth muscle cell calcification.

Mechanisms and clinical consequences of vascular calcification.

Suppression of mammalian bone growth by membrane transport inhibitors.

A protective role for FGF-23 in local defence against disrupted arterial wall integrity?

Identification of novel regulators of osteoblast matrix mineralization by time series transcriptional profiling.

Total protein analysis as a reliable loading control for quantitative fluorescent Western blotting.

Upregulation of IGF2 expression during vascular calcification.

Ablation of osteopontin improves the skeletal phenotype of phospho1(-/-) mice.

Design, synthesis and evaluation of benzoisothiazolones as selective inhibitors of PHOSPHO1.

Reference point indentation is not indicative of whole mouse bone measures of stress intensity fracture toughness.

BMP-9 regulates the osteoblastic differentiation and calcification of vascular smooth muscle cells through an ALK1 mediated pathway.

Deficiency of the bone mineralization inhibitor NPP1 protects against obesity and diabetes.

An investigation of the mineral in ductile and brittle cortical mouse bone.

Piroxicam treatment augments bone abnormalities in interleukin-10 knockout mice.

Increased linear bone growth by GH in the absence of SOCS2 is independent of IGF-1.

The Functional co-operativity of Tissue-Nonspecific Alkaline Phosphatase (TNAP) and PHOSPHO1 during initiation of Skeletal Mineralization.

E11/Podoplanin Protein Stabilization Through Inhibition of the Proteasome Promotes Osteocyte Differentiation in Murine in Vitro Models.

Skeletal Mineralization Deficits and Impaired Biogenesis and Function of Chondrocyte-Derived Matrix Vesicles in Phospho1(-/-) and Phospho1/Pi t1 Double-Knockout Mice.

Dmp1 Promoter-Driven Diphtheria Toxin Receptor Transgene Expression Directs Unforeseen Effects in Multiple Tissues.

End stage renal disease-induced hypercalcemia may promote aortic valve calcification via Annexin VI enrichment of valve interstitial cell derived-matrix vesicles.

Skeletal energy homeostasis: a paradigm of endocrine discovery.

Hypomorphic conditional deletion of E11/Podoplanin reveals a role in osteocyte dendrite elongation.

A distinctive patchy osteomalacia characterises Phospho1-deficient mice.

PLA2 and ENPP6 may act in concert to generate phosphocholine from the matrix vesicle membrane during skeletal mineralization.

Animal models to explore the effects of glucocorticoids on skeletal growth and structure.

Intravesicular Phosphatase PHOSPHO1 Function in Enamel Mineralization and Prism Formation.