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Mouse Bone-specific Alkaline Phosphatase (BALP) ELISA Kit

Product#: CS-CSB-E11914m-IS
$993.92
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Low Signal Optimization Reagents

4 core reagents below are included with every order, plus 1 of the 2 detection-specific reagents (matched automatically to your kit type) — 5 components, every time.

DCP-PIC100X

Protease Inhibitor Cocktail (100X)

Included with every order
 DCP-SM1AbTBS1X

SigMax 1Ab-TBS

Included with every order
 DCP-UTBS1X

Universal Blocking Buffer

Included with every order
 DCP-SM2AbTBS1X

SigMax 2Ab-TBS

Included with every order

+ the 5th component, matched to your kit's detection method:

DCP-HRPTBS1X

HRPQuench-TBS

Exclusively for HRP-based kits
OR
DCP-ALPTBS1X

ALPQuench-TBS

Exclusively for ALP-based kits

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Mouse ELISA Kit · Metabolism‌

Mouse Bone-specific Alkaline Phosphatase (BALP) ELISA Kit

Sandwich quantitative immunoassay for Bone-specific alkaline phosphatase in mouse serum, plasma, tissue homogenates  available in multiple catalog sizes:

Trial 24T 96T

Note: Please send inquiries regarding Trial 24T orders to support@diagnocine.com.

Detection Range
0.78-50 U/L
Sensitivity
0.39 U/L
Assay Time
3.5 hours
Sample Volume
50-100 μL
Product specifications
Target nameBone-specific alkaline phosphatase
Uniprot No.P09242
SpeciesMus musculus (Mouse)
Sample typesserum, plasma, tissue homogenates
Detection range0.78U/L-50U/L
Sensitivity0.39U/L
Assay time3.5h
Sample loading volume50-100μL
Detection wavelength450 nm
Assay principleSandwich (Quantitative)
Data analysisStandard curve + Curve Expert software
Research areaMetabolism‌
Storage condition2-8°C (see protocol for full details)
Shipping condition4 °C
Shelf life6 months
Bone-specific alkaline phosphatase serum plasma tissue homogenates Metabolism‌ Mouse ELISA
Lead Time

10 business days

Processing + 3-5 days shipping

Availability

In Stock : USA

Worldwide shipping available

Assay principle
Sample prep
Antibody capture
450 nm detection
Standard curve
Quantification

In this sandwich ELISA, Bone-specific alkaline phosphatase in the sample is captured between a pre-coated capture antibody and a detection antibody. Signal intensity is proportional to analyte concentration. Quantification uses a standard curve fitted with Curve Expert software, covering 0.78U/L-50U/L with a minimum detectable dose of 0.39U/L.

For research use only (RUO). Not intended for diagnostic or therapeutic purposes. Validated in mouse serum, plasma, tissue homogenates matrices only.
Alternative Names
Alpl ELISA Kit; Akp-2 ELISA Kit; Akp2 ELISA Kit; Alkaline phosphatase ELISA Kit; tissue-nonspecific isozyme ELISA Kit; AP-TNAP ELISA Kit; TNSALP ELISA Kit; EC 3.1.3.1 ELISA Kit; Alkaline phosphatase 2 ELISA Kit; Alkaline phosphatase liver/bone/kidney isozyme ELISA Kit
Function
Alkaline phosphatase that metabolizes various phosphate compounds and plays a key role in skeletal mineralization and adaptive thermogenesis. Has broad substrate specificity and can hydrolyze a considerable variety of compounds: however, only a few substrates, such as diphosphate (inorganic pyrophosphate; PPi), pyridoxal 5'-phosphate (PLP) and N-phosphocreatine are natural substrates. Plays an essential role in skeletal and dental mineralization via its ability to hydrolyze extracellular diphosphate, a potent mineralization inhibitor, to phosphate: it thereby promotes hydroxyapatite crystal formation and increases inorganic phosphate concentration. Acts in a non-redundant manner with PHOSPHO1 in skeletal mineralization: while PHOSPHO1 mediates the initiation of hydroxyapatite crystallization in the matrix vesicles (MVs), ALPL/TNAP catalyzes the spread of hydroxyapatite crystallization in the extracellular matrix. Also promotes dephosphorylation of osteopontin (SSP1), an inhibitor of hydroxyapatite crystallization in its phosphorylated state; it is however unclear whether ALPL/TNAP mediates SSP1 dephosphorylation via a direct or indirect manner. Catalyzes dephosphorylation of PLP to pyridoxal (PL), the transportable form of vitamin B6, in order to provide a sufficient amount of PLP in the brain, an essential cofactor for enzymes catalyzing the synthesis of diverse neurotransmitters. Additionally, also able to mediate ATP degradation in a stepwise manner to adenosine, thereby regulating the availability of ligands for purinergic receptors. Also capable of dephosphorylating microbial products, such as lipopolysaccharides (LPS) as well as other phosphorylated small-molecules, such as poly-inosine:cytosine (poly I:C). Acts as a key regulator of adaptive thermogenesis as part of the futile creatine cycle: localizes to the mitochondria of thermogenic fat cells and acts by mediating hydrolysis of N-phosphocreatine to initiate a futile cycle of creatine dephosphorylation and phosphorylation. During the futile creatine cycle, creatine and N-phosphocreatine are in a futile cycle, which dissipates the high energy charge of N-phosphocreatine as heat without performing any mechanical or chemical work.
Gene References into Functions
  1. correction of bone mineralization abnormalities in knockout mice null for both the TNAP (Akp2) and PC-1 (Enpp1) genes PMID: 12082181
  2. The Alpl (Akp2) gene is located within the quantitative trait locus region for alkaline phosphatase activity on chromosome 4. PMID: 16159911
  3. alkaline phosphatase 2(Hpp/Hpp) mice develop late-onset skeletal disease, notably defective endochondral ossification and bone mineralization that leads to arthropathies of knees and shoulders PMID: 17539739
  4. The process selectively internalizes IAP and may contribute to the appearance of the enzyme in serum and surfactant-like particles. PMID: 17947448
  5. Results show that inorganic phosphate (P(i)) levels and TNSALP activity increased in response to androgen/androgen receptor (AR), and P(i) signals increase the expression and translocation of AR. PMID: 18838539
  6. TNAP-AID mice expressed alpha-fetoprotein and had deleterious mutations in the tumour suppressor gene Trp53, some of which corresponded to those found in human cancer. PMID: 18997814
  7. Tissue-nonspecific alkaline phosphatase is the enzyme that hydrolyzes both ATP and inorganic pyrophosate in matrix vesicles. PMID: 19874193
  8. Once the HT2B receptor is expressed, it constitutively controls tissue-nonspecific alkaline phosphatase activity at a post-translational level along the overall period of bone mineral deposition PMID: 20573958
  9. These results demonstrate that calcium ions released from apatite are important in the synergistic effect of 20alpha-HC and apatite. PMID: 20683129
  10. We show that TNAP knockdown reduces cell proliferation and differentiation into neurons or oligodendrocytes PMID: 20849921
  11. Data show that alkaline phosphatase (AP) activity in brain vessels and parenchyma in which AP exhibits specific patterns is attributable to TNAP. PMID: 21191615
  12. Results demonstrate that TNAP, regulating both ligand availability and protein expression of P2X7 receptor, is essential for axonal development. PMID: 21289095
  13. a link between ATRA-induced mL/B/K-ALP gene transcription and chromatin remodeling PMID: 22270475
  14. In the cerebral cortex, myelinated axons, while present in wild-type, were absent in the Akp2( -/- ) mice and these animals also displayed a significantly increased proportion of immature cortical synapses. PMID: 22696173
  15. data suggest that the promineralization role of TNAP may be related not only to its accepted pyrophosphatase activity but also to its ability to modify the phosphorylation status of OPN. PMID: 23427088
  16. mineralization abnormalities of dentin; reduced overall mineralization with decreased matrix vesicle mineralization in the Phospho1(-/-) mice; almost complete absence of matrix vesicles in mice; further reduction in mineralization. PMID: 23694930
  17. Inhibition of rhBMP-2-induced ALP activity by intracellular delivery of SMURF1 in murine calvarial preosteoblast cells. PMID: 24288199
  18. Taken together, these data indicate that ATF3 is a novel negative regulator of osteoblast differentiation by specifically suppressing ALP gene expression in preosteoblasts. PMID: 24315873
  19. CD73 and TNAP play interactive roles to metabolize luminally applied 5'-AMP in the renal vasculature such that inhibition of both is required to inhibit the production of adenosine. PMID: 24990899
  20. Findings demonstrate that Alpl(-/-) mice exhibit a craniofacial skeletal phenotype similar to that seen in infants with HPP, including true bony craniosynostosis in the context of severely diminished bone mineralization PMID: 25014884
  21. TNAP plays a role in governing the phosphorylation status of phospholamban in the sarcoplasmic reticulum. PMID: 25015959
  22. p107 is required for the efficient recruitment of an activating SWI/SNF chromatin-remodeling complex, an essential event in Alpl induction. PMID: 25182511
  23. TNAP in the vasculature contributes to the pathology of medial vascular calcification and that it is a druggable target. PMID: 25428889
  24. In cardiac fibroblasts, TNAP expression and activity is induced by sFRP2. PMID: 25972450
  25. Prevention of lethal murine hypophosphatasia by neonatal ex vivo gene therapy using lentivirally transduced bone marrow cells expressing Akp-2. PMID: 26467745
  26. Despite similar deficiencies in alkaline phosphatase, Alpl(-/-) mice develop craniosynostosis and a brachycephalic/acrocephalic craniofacial shape of variable penetrance. PMID: 26605996
  27. 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). PMID: 27466191
  28. TNAP activation in vascular smooth muscle cells (VSMCs) appears sufficient to induce calcification. TNAP activation in VSMCs stimulates expression of chondrocyte markers. PMID: 27932058
  29. The results are the first to demonstrate a role for ENC1 in the control of osteoblast differentiation. Additionally, the contrasting mineralization phenotypes and transcriptional patterns seen with coordinate knockdown of both ENC1 isoforms vs selective knockdown of 67 kDa ENC1 suggest opposing roles for the isoforms in regulation of osteoblastic differentiation, through effects on Alpl expression and phosphate cellular PMID: 27996212
  30. Our results offer clear evidence that TNAP modulates T lymphocyte function and specifically T cell-dependent colitis. PMID: 28039309
  31. 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) PMID: 28673966
  32. 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. PMID: 29023576
  33. intestinal alkaline phosphatase knockout mice display higher intestinal Ca uptake, which over time appears to correlate with a positive effect on the biomechanical properties of trabecular bone. PMID: 29234952
  34. Study results from cerulein induced pancreatitis model in TNAP+/- mice show that altered TNAP expression results in heightened pancreatic inflammation, which may be explained by an augmented response of neutrophils and by a higher sensitivity of acinar cells to cerulein injury. PMID: 30251694
Tissue Specificity
Widely expressed. Expressed in DRG neurons and spinal cord neurons.
Subcellular Location
Cell membrane; Lipid-anchor, GPI-anchor. Extracellular vesicle membrane; Lipid-anchor, GPI-anchor. Mitochondrion membrane; Lipid-anchor, GPI-anchor. Mitochondrion intermembrane space.
Protein Families
Alkaline phosphatase family
Database Links

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