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Validated All-in-One™ qPCR Primer for ALPL(NM_000478.5) Search again
Product ID:
HQP006440
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AP-TNAP, APTNAP, HOPS, HPPA, HPPC, HPPI, HPPO, TNALP, TNAP, TNS-ALP, TNSALP
Gene Description:
alkaline phosphatase, biomineralization associated
Target Gene Accession:
NM_000478.5(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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.
Gene References into function
- mutational analysis in patients with various forms of hypophosphatasia
- candidate tumor suppressor gene in meningioma
- regardless of clinical type, deletion in the TNSALP gene occurs frequently among Japanese patients with hypophosphatasia
- the structural differences in human AP isoforms are demonstrated through models
- apical uptake of organic cations in Caco-2 cells is affected by phosphorylation/dephosphorylation mechanisms, and ecto-ALP activity may be involved in this process
- This study indicated that the mutation (G1144A) produced the inactive ALP enzyme and would be a disease-causing mutation of the childhood-type HOPS.
- G317D mutation in the tissue-nonspecific alkaline phosphatase gene associated with childhood hypophosphatasia in a German family.
- Inheritance, absence of malformations, increased serum alkaline phosphatase, peak bone mass decreasing physiologically with age, and involvement of cortical and trabecular bone suggest a new variant of hyperostosis/osteosclerosis.
- Fifteen novel ALPL mutations have been found in a series of 11 families from various origins affected by perinatal and infantile hypophosphatasia.
- Serum BAP should not be considered a good marker for the diagnosis of osteoporosis in men with prostate cancer.
- analysis of residues determining the binding specificity of uncompetitive inhibitors to tissue-nonspecific alkaline phosphatase
- Low serum level in osteochondrodysplasia.
- mutant (A115V) TNSALP gene produced the defective ALP enzyme and it could be recessively transmitted and be a disease-causing mutation of the adult-type hypophosphatasia
- variation in TNSALP may be an important determinant of age-related bone loss in humans
- Our results suggest the involvement of androgen receptor positive chondrocytes in thyroid cartilage mineralization, probably by a testosterone-linked stimulation of alkaline phosphatase.
- saliva AST and ALP may have roles in development of periodontal diseases
- The role of the N-terminus and its microenvironment in determining the enzyme stability and catalysis using human placental (PLAP) and tissue-nonspecific AP (TNAP) as paradigms, is analyzed.
- Our study demonstrates that the novel BALP B1x isoform is occasionally found to be present in children with kidney disease but to a lesser degree in comparison with adults with chronic kidney disease on dialysis.
- Pathologic fractures attributable to hypophosphatasia diagnosed in adulthood, and to missense mutation in TNSALP(C455G>A).
- Serum bone-specific alkaline phosphatase total protein can be considered a sensitive marker of bone turnover and could be especially useful as valuable non-invasive biochemical marker for identifying sickle cell patients with bone complications.
- Nine novel ALPL gene mutations in a series of 8 patients affected by various forms of hypophosphatasia.
- Infantile hypophatasia caused by two novel missense mutations of TNSALP.
- Cysteine inhibited TNAP's phosphatase activity uncompetitively and its inorganic pyrophosphatase activity mix-competitively
- While the wild-type protein reached the cell membrane within the first 24h after transfection, the mutants reached the membrane with delays of 24, 48 or 72 h.
- The results provide an explanation of the lethal phenotype in the patient where the two ALPL alleles are non-functional and in the asymptomatic father where over-expression of the normal allele could counteract the effect of the c.1133A>T mutation.
- Inverse relationships between neuropeptide Y (NPY) and biomarkers (bone and serum alkaline phosphatase) levels of bone turnover suggest that NPY may be implicated in low bone turnover in dialysis patients by a parathyroid-independent mechanism.
- A monoclonal antibody against tissue-nonspecific alkaline phosphatase (ALP) is established that will be a useful tool for effective measurement of liver-ALP, a marker of liver disease, by immunocapture enzymatic assay.
- analysis of the structural importance of the crown domain with respect to the catalytic function of TNSALP
- U(2)OS cells transfected with wild-type TNAP and polymorphism TNAP cDNA showed PHEX (phosphate-regulating gene with homologies to endopeptidases on the X chromosome) induction as in SaOS-2 cells.
- These results suggest that phosphate derived from TNAP-induced hydrolysis of beta-glycerophosphate yields signals that induce TNAP expression.
- Evaluation of a new compound heterozygous TNSALP mutation for its residual enzyme activity and localization in a case of infantile hypophsphatemia.
- Results report for the first time that human B cell express bone specific alkaline phosphatase.
- plasma alkaline phosphatase may have a role in systemic inflammation in Hong Kong Chinese, but it is unknown whether C-reactive protein has a similar role
- These results suggest that the significant difference in Km values between the proteins translated from alkaline phosphatase 787T > C and 787T may contribute to regulatory effects on bone metabolism.
- Neither ALT nor GGT concentrations were correlated with ALP concentration, but AST concentration was moderately correlated with ALP concentration.