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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Alkaline phosphatase, liver/bone/kidney

tissue-nonspecific alkaline phosphatase, TNSALP, TNAP, ALPL, liver/bone/kidney alkaline phosphatase, glycerophosphatase
There are at least four distinct but related alkaline phosphatases: intestinal, placental, placental-like, and liver/bone/kidney (tissue non-specific). The first three are located together on chromosome 2, while the tissue non-specific form is located on chromosome 1. The product of this gene is a membrane bound glycosylated enzyme that is not expressed in any particular tissue and is, therefore, referred to as the tissue-nonspecific form of the enzyme. The exact physiological function of the alkaline phosphatases is not known. A proposed function of this form of the enzyme is matrix mineralization; however, mice that lack a functional form of this enzyme show normal skeletal development. This enzyme has been linked directly to hypophosphatasia, a disorder that is characterized by hypercalcemia and includes skeletal defects. The character of this disorder can vary, however, depending on the specific mutation since this determines age of onset and severity of symptoms. Alternatively spliced transcript variants have been described. [provided by RefSeq, Apr 2010] (from NCBI)
Top mentioned proteins: ACID, CAN, HAD, Runx2, HPP
Papers using tissue-nonspecific alkaline phosphatase antibodies
Papers on tissue-nonspecific alkaline phosphatase
Asfotase Alfa: A Review in Paediatric-Onset Hypophosphatasia.
Scott, Auckland, New Zealand. In Drugs, Feb 2016
Hypophosphatasia (HPP) is a rare inheritable disease that results from loss-of-function mutations in the ALPL gene encoding tissue-nonspecific alkaline phosphatase (TNSALP).
Skeletal Mineralization Deficits and Impaired Biogenesis and Function of Chondrocyte-Derived Matrix Vesicles in Phospho1(-/-) and Phospho1/Pit1 Double Knockout Mice.
Millán et al., Roma, Italy. In J Bone Miner Res, Feb 2016
UNASSIGNED: We have previously shown that ablation of either the Phospho1 or Alpl gene, encoding PHOSPHO1 and tissue-nonspecific alkaline phosphatase (TNAP) respectively, lead to hyperosteoidosis but that their chondrocyte- and osteoblast-derived matrix vesicles (MVs) are able to initiate mineralization.
Development of biodegradable poly(citrate)-polyhedral oligomeric silsesquioxanes hybrid elastomers with high mechanical properties and osteoblastic differentiation activity.
Lei et al., In Acs Appl Mater Interfaces, Feb 2016
POC-POSS hybrids exhibit significantly enhanced osteogenic differentiation through upregulating alkaline phosphatase (ALP) activity, calcium deposition and expression of osteogenic markers (ALPL, BGLAP and Runx2).
Anabolic and anti-resorptive modulation of bone homeostasis by the epigenetic modulator sulforaphane, a naturally occurring isothiocyanate.
van Wijnen et al., United States. In J Biol Chem, Feb 2016
SFN enhances active DNA demethylation via Tet1 and Tet2 and promotes pre-osteoblast differentiation by enhancing extracellular matrix mineralization and the expression of osteoblastic markers (Runx2, Col1a1, Bglap2, Sp7, Atf4 and Alpl).
Clinical, biochemical and genetic spectrum of low alkaline phosphatase levels in adults.
Riancho et al., Santander, Spain. In Eur J Intern Med, Feb 2016
BACKGROUND: Low serum levels of alkaline phosphatase (ALP) are a hallmark of hypophosphatasia.
Unilateral Anterior Crossbite Induces Aberrant Mineral Deposition in Degenerative Temporomandibular Cartilage in Rats.
Wang et al., Xi'an, China. In Osteoarthritis Cartilage, Jan 2016
In contrast, the expression of Tnap and MMP13 was increased 4-weeks post-UAC.
Hypophosphatasia: an overview of the disease and its treatment.
Bianchi, Milano, Italy. In Osteoporos Int, Dec 2015
This review presents the current knowledge on hypophosphatasia, a rare genetic disease of very variable severity (from lethal to mild) and clinical presentation, caused by defective production of tissue-non-specific alkaline phosphatase (TNSALP).
Alkaline Phosphatase and Hypophosphatasia.
Whyte et al., Los Angeles, United States. In Calcif Tissue Int, Dec 2015
UNASSIGNED: Hypophosphatasia (HPP) results from ALPL mutations leading to deficient activity of the tissue-non-specific alkaline phosphatase isozyme (TNAP) and thereby extracellular accumulation of inorganic pyrophosphate (PPi), a natural substrate of TNAP and potent inhibitor of mineralization.
TNAP Plays a Key Role in Neural Differentiation as well as in Neurodegenerative Disorders.
Avila et al., Madrid, Spain. In Subcell Biochem, 2014
New evidences have been reported that point to the ecto-enzyme, tissue-nonspecific alkaline phosphatase (TNAP), as a key element at the origin of two opposite phenomena, neuronal differentiation and neuronal degeneration.
Neurological Symptoms of Hypophosphatasia.
Taketani, Izumo, Japan. In Subcell Biochem, 2014
Hypophosphatasia (HPP) is a bone metabolic disorder caused by mutations in the liver/bone/kidney alkaline phosphatase gene (ALPL), which encodes tissue-nonspecific alkaline phosphatase (TNAP).
Reprogramming of pericyte-derived cells of the adult human brain into induced neuronal cells.
Berninger et al., München, Germany. In Cell Stem Cell, 2012
Genetic fate-mapping in mice expressing an inducible Cre recombinase under the tissue-nonspecific alkaline phosphatase promoter corroborated the pericytic origin of the reprogrammed cells.
Systems genetics of metabolism: the use of the BXD murine reference panel for multiscalar integration of traits.
Auwerx et al., Lausanne, Switzerland. In Cell, 2012
Traits and networks were linked to loci encompassing both known variants and novel candidate genes, including alkaline phosphatase (ALPL), here linked to hypophosphatasia.
All-trans retinoic acid induces chromatin remodeling at the promoter of the mouse liver, bone, and kidney alkaline phosphatase gene in C3H10T 1/2 cells.
Hong et al., Guangzhou, China. In Biochem Genet, 2012
a link between ATRA-induced mL/B/K-ALP gene transcription and chromatin remodeling
Enzyme-replacement therapy in life-threatening hypophosphatasia.
Landy et al., Saint Louis, United States. In N Engl J Med, 2012
BACKGROUND: Hypophosphatasia results from mutations in the gene for the tissue-nonspecific isozyme of alkaline phosphatase (TNSALP).
Mechanism for release of alkaline phosphatase caused by glycosylphosphatidylinositol deficiency in patients with hyperphosphatasia mental retardation syndrome.
Kinoshita et al., Ōsaka, Japan. In J Biol Chem, 2012
GPI transamidase recognizes incomplete GPI bearing mannose and cleaves a hydrophobic signal peptide, resulting in secretion of soluble ALP explaining the molecular mechanism of hyperphosphatasia in hyperphosphatasia mental retardation syndrome.
Prophylactic treatment with alkaline phosphatase in cardiac surgery induces endogenous alkaline phosphatase release.
Oeveren et al., Maastricht, Netherlands. In Int J Artif Organs, 2012
Intravenous bolus administration plus 8 hours continuous infusion of alkaline phosphatase in patients undergoing coronary artery bypass grafting with cardiopulmonary bypass results in endogenous alkaline phosphatase release.
Identification of the mutations in the tissue-nonspecific alkaline phosphatase gene in two Chinese families with hypophosphatasia.
Zhang et al., Shanghai, China. In Arch Med Res, 2012
A novel de novo splicing mutation in intron 4 and a missense mutation in exon 11 of the ALPL gene are responsible for hypophosphatasia in some Chinese patients.
Serum bone alkaline phosphatase in assessing illness severity of infected neonates in the neonatal intensive care unit.
Chen et al., Chongqing, China. In Int J Biol Sci, 2011
Serum BALP level is associated with the severity of illness in infected neonates.
Characterization of human embryonic stem cell lines by the International Stem Cell Initiative.
Zhang et al., United Kingdom. In Nat Biotechnol, 2007
They expressed the glycolipid antigens SSEA3 and SSEA4, the keratan sulfate antigens TRA-1-60, TRA-1-81, GCTM2 and GCT343, and the protein antigens CD9, Thy1 (also known as CD90), tissue-nonspecific alkaline phosphatase and class 1 HLA, as well as the strongly developmentally regulated genes NANOG, POU5F1 (formerly known as OCT4), TDGF1, DNMT3B, GABRB3 and GDF3.
Mice lacking tissue non-specific alkaline phosphatase die from seizures due to defective metabolism of vitamin B-6.
MacGregor et al., Atlanta, United States. In Nat Genet, 1995
In humans, deficiency of the tissue non-specific alkaline phosphatase (TNAP) gene is associated with defective skeletal mineralization.
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