catalog number :
MBS747610
products type :
ELISA Kit
products full name :
Mouse Aminolevulinate Delta Dehydratase ELISA Kit
products short name :
[Aminolevulinate Delta Dehydratase]
other names :
[aminolevulinate, delta-, dehydratase, isoform CRA_a; Delta-aminolevulinic acid dehydratase; delta-aminolevulinic acid dehydratase; porphobilinogen synthase; aminolevulinate, delta-, dehydratase; aminolevulinate dehydratase; Porphobilinogen synthase]
products gene name :
[ALAD]
other gene names :
[ALAD; ALAD; PBGS; ALADH; ALADH]
uniprot entry name :
HEM2_HUMAN
specificity :
This assay has high sensitivity and excellent specificity for detection of ALAD. No significant cross-reactivity or interference between ALAD and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between ALAD and all the analogues, therefore, cross reaction may still exist in some cases.
storage stability :
Store all reagents at 2-8 degree C.
image1 heading :
Typical Testing Data/Standard Curve
other info1 :
Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Detection Range: 25-500ng/mL. Sensitivity: 1.0ng/mL
products categories :
Cardiovascular
products description :
Intended Uses: This ALAD ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Mouse ALAD. This ELISA kit for research use only, not for therapeutic or diagnostic applications!. Principle of the Assay ALAD ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-ALAD antibody and an ALAD-HRP conjugate. The assay sample and buffer are incubated together with ALAD-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the ALAD concentration since ALAD from samples and ALAD-HRP conjugate compete for the anti-ALAD antibody binding site. Since the number of sites is limited, as more sites are occupied by ALAD from the sample, fewer sites are left to bind ALAD-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The ALAD concentration in each sample is interpolated from this standard curve.
ncbi acc num :
EAW87380.1
ncbi mol weight :
39,034 Da
ncbi pathways :
Heme Biosynthesis Pathway (198818); Heme Biosynthesis Pathway (106326); Metabolic Pathways (132956); Metabolism Pathway (477135); Metabolism Of Porphyrins Pathway (106325); Porphyrin And Chlorophyll Metabolism Pathway (83021); Porphyrin And Chlorophyll Metabolism Pathway (407); Heme Biosynthesis II Pathway (545289); Superpathway Of Heme Biosynthesis From Glycine (138401); Tetrapyrrole Biosynthesis II Pathway (142231)
ncbi summary :
The ALAD enzyme is composed of 8 identical subunits and catalyzes the condensation of 2 molecules of delta-aminolevulinate to form porphobilinogen (a precursor of heme, cytochromes and other hemoproteins). ALAD catalyzes the second step in the porphyrin and heme biosynthetic pathway; zinc is essential for enzymatic activity. ALAD enzymatic activity is inhibited by lead and a defect in the ALAD structural gene can cause increased sensitivity to lead poisoning and acute hepatic porphyria. [provided by RefSeq, Jul 2008]
uniprot summary :
ALAD: Catalyzes an early step in the biosynthesis of tetrapyrroles. Binds two molecules of 5-aminolevulinate per subunit, each at a distinct site, and catalyzes their condensation to form porphobilinogen. Defects in ALAD are the cause of acute hepatic porphyria (AHEPP). A form of porphyria. Porphyrias are inherited defects in the biosynthesis of heme, resulting in the accumulation and increased excretion of porphyrins or porphyrin precursors. They are classified as erythropoietic or hepatic, depending on whether the enzyme deficiency occurs in red blood cells or in the liver. AHP is characterized by attacks of gastrointestinal disturbances, abdominal colic, paralysis, and peripheral neuropathy. Most attacks are precipitated by drugs, alcohol, caloric deprivation, infections, or endocrine factors. Belongs to the ALADH family. 2 isoforms of the human protein are produced by alternative splicing. Protein type: EC 4.2.1.24; Lyase; Cofactor and Vitamin Metabolism - porphyrin and chlorophyll. Chromosomal Location of Human Ortholog: 9q33.1. Cellular Component: nucleus; cytosol. Molecular Function: identical protein binding; porphobilinogen synthase activity; zinc ion binding; lead ion binding; catalytic activity. Biological Process: porphyrin metabolic process; protoporphyrinogen IX biosynthetic process; protein homooligomerization; heme biosynthetic process. Disease: Porphyria, Acute Hepatic
size4 :
10x96-Strip-Wells