Key features and details
- Sensitivity: 14 pg/ml
- Range: 12.29 pg/ml - 25000 pg/ml
- Sample type: Cell culture supernatant, Plasma, Serum
- Detection method: Colorimetric
- Assay type: Sandwich (quantitative)
- Reacts with: Mouse
Product nameMouse PSAP ELISA Kit
See all PSAP kits
Intra-assay Sample n Mean SD CV% General < 10% Inter-assay Sample n Mean SD CV% General < 12%
Sample typeCell culture supernatant, Serum, Plasma
Assay typeSandwich (quantitative)
Range12.29 pg/ml - 25000 pg/ml
Sample specific recovery Sample type Average % Range Serum 119.1 109% - 132% Plasma 111.9 95% - 123% Cell culture media 87.94 68% - 112%
Assay durationMultiple steps standard assay
Species reactivityReacts with: Mouse
Mouse PSAP ELISA Kit (ab277399) is an in-vitro enzyme-linked immunosorbent assay for the quantitative measurement of Mouse PSAP in serum, plasma and cell culture supernatants.
This assay employs an antibody specific for Mouse PSAP coated on a 96-well plate. Standards and samples are pipetted into the wells and Mouse PSAP present in a sample is bound to the wells by the immobilized antibody. The wells are washed, and biotinylated anti-Mouse PSAP antibody is added. After washing away unbound biotinylated antibody, HRP-conjugated streptavidin is pipetted to the wells. The wells are again washed, a TMB substrate solution is added to the wells and color develops in proportion to the amount of Mouse PSAP bound. The Stop Solution changes the color from blue to yellow, and the intensity of the color is measured at 450 nm.
Tested applicationsSuitable for: Sandwich ELISAmore details
PlatformPre-coated microplate (12 x 8 well strips)
Storage instructionsStore at -20°C. Please refer to protocols.
Components 1 x 96 tests 20X Wash Buffer Concentrate 1 x 25ml 5X Assay Diluent 1 x 15ml 700X HRP-Streptavidin Concentrate 1 x 200µl Biotinylated Anti-Mouse PSAP Antibody 2 vials Anti-Mouse PSAP coated Microplate 1 unit Mouse PSAP standard protein (Lyophilized) 2 vials Stop Solution 1 x 8ml TMB One-Step Substrate Reagent 1 x 12ml
FunctionThe lysosomal degradation of sphingolipids takes place by the sequential action of specific hydrolases. Some of these enzymes require specific low-molecular mass, non-enzymic proteins: the sphingolipids activator proteins (coproteins).
Saposin-A and saposin-C stimulate the hydrolysis of glucosylceramide by beta-glucosylceramidase (EC 126.96.36.199) and galactosylceramide by beta-galactosylceramidase (EC 188.8.131.52). Saposin-C apparently acts by combining with the enzyme and acidic lipid to form an activated complex, rather than by solubilizing the substrate.
Saposin-B stimulates the hydrolysis of galacto-cerebroside sulfate by arylsulfatase A (EC 184.108.40.206), GM1 gangliosides by beta-galactosidase (EC 220.127.116.11) and globotriaosylceramide by alpha-galactosidase A (EC 18.104.22.168). Saposin-B forms a solubilizing complex with the substrates of the sphingolipid hydrolases.
Saposin-D is a specific sphingomyelin phosphodiesterase activator (EC 22.214.171.124).
Involvement in diseaseDefects in PSAP are the cause of combined saposin deficiency (CSAPD) [MIM:611721]; also known as prosaposin deficiency. CSAPD is due to absence of all saposins, leading to a fatal storage disorder with hepatosplenomegaly and severe neurological involvement.
Defects in PSAP saposin-B region are the cause of leukodystrophy metachromatic due to saposin-B deficiency (MLD-SAPB) [MIM:249900]. MLD-SAPB is an atypical form of metachromatic leukodystrophy. It is characterized by tissue accumulation of cerebroside-3-sulfate, demyelination, periventricular white matter abnormalities, peripheral neuropathy. Additional neurological features include dysarthria, ataxic gait, psychomotr regression, seizures, cognitive decline and spastic quadriparesis.
Defects in PSAP saposin-C region are the cause of atypical Gaucher disease (AGD) [MIM:610539]. Affected individuals have marked glucosylceramide accumulation in the spleen without having a deficiency of glucosylceramide-beta glucosidase characteristic of classic Gaucher disease, a lysosomal storage disorder.
Defects in PSAP saposin-A region are the cause of atypical Krabbe disease (AKRD) [MIM:611722]. AKRD is a disorder of galactosylceramide metabolism. AKRD features include progressive encephalopathy and abnormal myelination in the cerebral white matter resembling Krabbe disease.
Note=Defects in PSAP saposin-D region are found in a variant of Tay-Sachs disease (GM2-gangliosidosis).
Sequence similaritiesContains 2 saposin A-type domains.
Contains 4 saposin B-type domains.
modificationsThis precursor is proteolytically processed to 4 small peptides, which are similar to each other and are sphingolipid hydrolase activator proteins.
N-linked glycans show a high degree of microheterogeneity.
The one residue extended Saposin-B-Val is only found in 5% of the chains.
- Information by UniProt
- A1 activator
- Cerebroside sulfate activator
Our Abpromise guarantee covers the use of ab277399 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|Sandwich ELISA||Use at an assay dependent concentration.|
ab277399 has not yet been referenced specifically in any publications.