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There are at least four distinct but related alkaline phosphatases: intestinal, placental, placental-like, and liver/bone/kidney (tissue non-specific). Additionally we are shipping ALPL Antibodies (219) and ALPL Proteins (19) and many more products for this protein.
Showing 10 out of 45 products:
Mouse (Murine) ALPL ELISA Kit for Sandwich ELISA - ABIN415660
Wu, Lin, Liou, Lu, Chen, Fu, Yang: Dextromethorphan inhibits osteoclast differentiation by suppressing RANKL-induced nuclear factor-?B activation. in Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA 2013
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Rat (Rattus) ALPL ELISA Kit for Sandwich ELISA - ABIN416228
Gradosova, Zivna, Svejkovska, Palicka, Tichy, Zivny: The role of atorvastatin in bone metabolism in male albino Wistar rats. in Die Pharmazie 2011
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Rat (Rattus) ALPL ELISA Kit for Competition ELISA - ABIN580965
Abuohashish, Al-Rejaie, Al-Hosaini, Parmar, Ahmed: Alleviating effects of morin against experimentally-induced diabetic osteopenia. in Diabetology & metabolic syndrome 2013
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Adults with persistent hypophosphatasemia frequently harbor alkaline phosphatase mutations and have elevated ALP (show ALP ELISA Kits) substrates.
Mutations in ALPL which reduce alkaline phosphatase activity are responsible for Hypophosphatasia , a rare disorder characterized by defective bone and teeth mineralization and early tooth loss.
ALDH appears to be involved in the interaction between lung and Osteosarcoma (OS) cells, and ALP (show ALP ELISA Kits) may be a valuable biomarker for monitoring functional OS changes during metastasis.
These results show that an increase of TNAP activity in ACDC (arterial calcification due to deficiency of CD73) contributes to ectopic calcification by disrupting the extracellular balance of PPi and Pi and identify potential therapeutic targets for ACDC.
the identification of 11 novel ALPL mutations in the five different HPP (show SPTA1 ELISA Kits) forms and the observation of a recurrent mutation, p. (Thr166Ile) in the Spanish population expand our knowledge of pathogenic ALPL mutations.
Preoperative calcitonin (show CALCA ELISA Kits) levels were correlated with the presence of tumor, whereas alkaline phosphatase (ALP) levels were not. There were no significant associations between tumor volume and ALP (show ALP ELISA Kits) or calcitonin (show CALCA ELISA Kits) levels in the preoperative or postoperative periods. During long-term follow-up, serum ALP (show ALP ELISA Kits) was significantly associated with tumor recurrence, but serum calcitonin (show CALCA ELISA Kits) was not.
His ALPL gene mutation came from c.228delG mutation in his mother and c.407G>A compound heterozygous mutation in his father
Both PPARgamma (show PPARG ELISA Kits) gene expression and TNALP activity increased during intracellular lipid accumulation in HepG2 and 3T3-L1 cells. Inhibition of TNALP blocked intracellular lipid accumulation but did not alter expression of the PPARgamma (show PPARG ELISA Kits) gene.
ALPL is a major contributor to the pathogenesis of Prostate cancer progression.
ALPL expression is significantly upregulated in human masticatory mucosa during wound healing
Our results offer clear evidence that TNAP modulates T lymphocyte function and specifically T cell-dependent colitis.
The results are the first to demonstrate a role for ENC1 (show ENC1 ELISA Kits) in the control of osteoblast differentiation. Additionally, the contrasting mineralization phenotypes and transcriptional patterns seen with coordinate knockdown of both ENC1 (show ENC1 ELISA Kits) isoforms vs selective knockdown of 67 kDa ENC1 (show ENC1 ELISA Kits) suggest opposing roles for the isoforms in regulation of osteoblastic differentiation, through effects on Alpl expression and phosphate cellular
TNAP overexpression in vascular endothelium in mice leads to an unusual course of coronary atherosclerosis and was accompanied by the reduction in body weight and left ventricular ejection fraction.
Data, including data from studies using cells from transgenic/knockout mice, suggest that Med1 plays role in enamel formation; Med1 induces Alpl via stimulation of Notch1 signaling by forming Notch1-RBP-Jk complex on Alpl promoter. (Med1 = mediator complex subunit 1; Alpl = alkaline phosphatase, liver-bone-kidney; Notch1 = Notch gene homolog 1; RBP-Jk = kappa J region recombining binding protein suppressor of hairless)
These analyses revealed that TNAP deficient mice present an increased proliferation of neural precursors, an altered neuronal morphology, and an augmented neuronal activity. We found that these alterations were associated with a partial downregulation of the purinergic P2X7 receptor (P2X7R (show P2RX7 ELISA Kits)).
Despite similar deficiencies in alkaline phosphatase, Alpl(-/-) mice develop craniosynostosis and a brachycephalic/acrocephalic craniofacial shape of variable penetrance.
Prevention of lethal murine hypophosphatasia by neonatal ex vivo gene therapy using lentivirally transduced bone marrow cells expressing Akp-2.
TNAP in the vasculature contributes to the pathology of medial vascular calcification and that it is a druggable target.
In cardiac fibroblasts, TNAP expression and activity is induced by sFRP2 (show SFRP2 ELISA Kits).
p107 (show RBL1 ELISA Kits) is required for the efficient recruitment of an activating SWI/SNF (show SNRPA ELISA Kits) chromatin-remodeling complex, an essential event in Alpl induction.
The peri (show PLIN1 ELISA Kits)-partum characteristics of serum bone-specific alkaline phosphatase (BAP (show PHB2 ELISA Kits)) and urinary deoxypyridinoline (DPD (show DPYD ELISA Kits)) in dairy cattle are reported.
GPI (show GPI ELISA Kits)-anchored proteins are localized on the outer layer of plasma membranes and clustered in microdomains generally called lipid rafts.
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.
tissue-nonspecific alkaline phosphatase
, alkaline phosphatase, tissue-nonspecific isozyme
, tissue non-specific alkaline phosphatase
, alkaline phosphatase, liver/bone/kidney
, alkaline phosphatase, tissue-nonspecific isozyme-like
, alkaline phosphatase liver/bone/kidney isozyme
, alkaline phosphomonoesterase
, liver/bone/kidney-type alkaline phosphatase
, tissue-nonspecific ALP
, alkaline phosphatase 2, liver
, Tissue-nonspecific ALP alkaline phosphatase
, alkaline phosphatase tissue non-specific isoform
, liver/bone/kidney isozyme