Abnormal vitamin B6 metabolism in alkaline phosphatase knock-out mice causes multiple abnormalities, but not the impaired bone mineralization.
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Inflammation causes tissue-specific depletion of vitamin B6.TNAP and EHD1 are over-expressed in bovine brain capillary endothelial cells after the re-induction of blood-brain barrier propertiesLoss of skeletal mineralization by the simultaneous ablation of PHOSPHO1 and alkaline phosphatase function: a unified model of the mechanisms of initiation of skeletal calcificationA hypomorphic PIGA gene mutation causes severe defects in neuron development and susceptibility to complement-mediated toxicity in a human iPSC modelEnzyme replacement therapy on hypophosphatasia mouse model.Enzyme replacement therapy for murine hypophosphatasiaCellular function and molecular structure of ecto-nucleotidases.Tissue-nonspecific alkaline phosphatase and plasma cell membrane glycoprotein-1 are central antagonistic regulators of bone mineralizationIntestinal alkaline phosphatase release is not associated with chylomicron formation.Improvement of the skeletal and dental hypophosphatasia phenotype in Alpl-/- mice by administration of soluble (non-targeted) chimeric alkaline phosphatase.Plasma alkaline phosphatase is elevated in Alzheimer's disease and inversely correlates with cognitive function.Dose response of bone-targeted enzyme replacement for murine hypophosphatasia.Impaired calcification around matrix vesicles of growth plate and bone in alkaline phosphatase-deficient mice.Concerted regulation of inorganic pyrophosphate and osteopontin by akp2, enpp1, and ank: an integrated model of the pathogenesis of mineralization disorders.Catalytic signature of a heat-stable, chimeric human alkaline phosphatase with therapeutic potential.Enzyme replacement therapy prevents dental defects in a model of hypophosphatasia.Prolonged survival and phenotypic correction of Akp2(-/-) hypophosphatasia mice by lentiviral gene therapy.Rescue of severe infantile hypophosphatasia mice by AAV-mediated sustained expression of soluble alkaline phosphatasePrevention of Lethal Murine Hypophosphatasia by Neonatal Ex Vivo Gene Therapy Using Lentivirally Transduced Bone Marrow CellsNeonatal seizures: controversies and challenges in translating new therapies from the lab to the isolette.Enzyme replacement prevents enamel defects in hypophosphatasia miceAccelerated fat absorption in intestinal alkaline phosphatase knockout mice.Ablation of TNAP function compromises myelination and synaptogenesis in the mouse brainTreatment of hypophosphatasia by muscle-directed expression of bone-targeted alkaline phosphatase via self-complementary AAV8 vector.Alkaline Phosphatase and Hypophosphatasia.In vivo overexpression of tissue-nonspecific alkaline phosphatase increases skeletal mineralization and affects the phosphorylation status of osteopontinA Critical Role of TRPM7 As an Ion Channel Protein in Mediating the Mineralization of the Craniofacial Hard Tissues.Ablation of osteopontin improves the skeletal phenotype of phospho1(-/-) mice.Neurodevelopmental alterations and seizures developed by mouse model of infantile hypophosphatasia are associated with purinergic signalling deregulation.Identification of altered brain metabolites associated with TNAP activity in a mouse model of hypophosphatasia using untargeted NMR-based metabolomics analysis.Infantile hypophosphatasia secondary to a novel compound heterozygous mutation presenting with pyridoxine-responsive seizures.Tissue-nonspecific Alkaline Phosphatase Regulates Purinergic Transmission in the Central Nervous System During Development and Disease.Hypophosphatasia: an overview of the disease and its treatment.ATP catabolism by tissue non-specific alkaline phosphatase contributes to development of ARDS in influenza-infected mice.Hypophosphatasia - pathophysiology and treatment.Fingerprinting-based metabolomic approach with LC-MS to sleep apnea and hypopnea syndrome: a pilot study.Alkaline phosphatase is increased in both brain and plasma in Alzheimer's disease.Disruption of the murine intestinal alkaline phosphatase gene Akp3 impairs lipid transcytosis and induces visceral fat accumulation and hepatic steatosis.Metabolic etiologies in West syndrome.Haploinsufficient TNAP Mice Display Decreased Extracellular ATP Levels and Expression of Pannexin-1 Channels.
P2860
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P2860
Abnormal vitamin B6 metabolism in alkaline phosphatase knock-out mice causes multiple abnormalities, but not the impaired bone mineralization.
description
2001 nî lūn-bûn
@nan
2001 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
Abnormal vitamin B6 metabolism ...... impaired bone mineralization.
@ast
Abnormal vitamin B6 metabolism ...... impaired bone mineralization.
@en
type
label
Abnormal vitamin B6 metabolism ...... impaired bone mineralization.
@ast
Abnormal vitamin B6 metabolism ...... impaired bone mineralization.
@en
prefLabel
Abnormal vitamin B6 metabolism ...... impaired bone mineralization.
@ast
Abnormal vitamin B6 metabolism ...... impaired bone mineralization.
@en
P2093
P2860
P1476
Abnormal vitamin B6 metabolism ...... impaired bone mineralization.
@en
P2093
P2860
P304
P356
10.1002/1096-9896(2000)9999:9999<::AID-PATH722>3.0.CO;2-Y
P577
2001-01-01T00:00:00Z