SMN ELISA kit (ab136947)
Key features and details
- Sensitivity: 50 pg/ml
- Range: 50 pg/ml - 3200 pg/ml
- Sample type: Cell Lysate, Tissue Extracts
- Detection method: Colorimetric
- Assay type: Sandwich (quantitative)
- Reacts with: Mouse, Human
Overview
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Product name
SMN ELISA kit -
Detection method
Colorimetric -
Precision
Intra-assay Sample n Mean SD CV% 928 pg/ml 20 0.8% 322 pg/ml 20 1.1% 122 pg/ml 20 3.2% Inter-assay Sample n Mean SD CV% 983 pg/ml 12 7.1% 378 pg/ml 12 8.9% 134 pg/ml 12 11.4% -
Sample type
Tissue Extracts, Cell Lysate -
Assay type
Sandwich (quantitative) -
Sensitivity
50 pg/ml -
Range
50 pg/ml - 3200 pg/ml -
Recovery
Sample specific recovery Sample type Average % Range Human PBMC Lysate 79% - 134% Mouse brain extract 83% - 112% Mouse muscle extract 76% - 146% Mouse spinal cord extract 39% - 69% -
Assay duration
Multiple steps standard assay -
Species reactivity
Reacts with: Mouse, Human -
Product overview
Abcam’s SMN ELISA (Enzyme-Linked Immunosorbent Assay) kit is an in vitro enzyme-linked immunosorbent assay for the quantitative measurement of SMN in Human and mouse cell and tissue extracts.
An anti-Human SMN antibody is precoated onto 96-well plates, standards or test samples are added to the wells and incubated at room temperature. The wells are washed and a polyclonal detector antibody specific to SMN is added, followed by incubation at room temperature. After further washing, a horseradish peroxidase (HRP) conjugated anti-species antibody is added to each well and incubated at room temperature. After incubation the excess reagents are washed away. TMB substrate is added to each well and after a short incubation the enzyme reaction is stopped and the yellow color generated is read at 450 nm. The intensity of the yellow coloration is directly proportional to the amount of SMN captured in the plate.
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Notes
Abcam has not and does not intend to apply for the REACH Authorisation of customers’ uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses. -
Platform
Microplate
Properties
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Storage instructions
Please refer to protocols. -
Components 1 x 96 tests 20X Wash Buffer Concentrate 1 x 100ml Anti-rabbit IgG-HRP conjugate 1 x 10ml Assay Buffer 13 1 x 100ml Extraction Reagent 4 1 x 100ml Human SMN Standard 2 vials Microplate coated with anti-SMN monoclonal antibody (12 x 8 wells) 1 x 96 tests Plate Sealer 1 x 3 units Rabbit polyclonal anti-Human SMN antibody 1 x 10ml Stop Solution 2 1 x 10ml TMB Substrate 1 x 10ml -
Research areas
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Function
The SMN complex plays an essential role in spliceosomal snRNP assembly in the cytoplasm and is required for pre-mRNA splicing in the nucleus. It may also play a role in the metabolism of snoRNPs. -
Tissue specificity
Expressed in a wide variety of tissues. Expressed at high levels in brain, kidney and liver, moderate levels in skeletal and cardiac muscle, and low levels in fibroblasts and lymphocytes. Also seen at high levels in spinal cord. Present in osteoclasts and mononuclear cells (at protein level). -
Involvement in disease
Defects in SMN1 are the cause of spinal muscular atrophy autosomal recessive type 1 (SMA1) [MIM:253300]. Spinal muscular atrophy refers to a group of neuromuscular disorders characterized by degeneration of the anterior horn cells of the spinal cord, leading to symmetrical muscle weakness and atrophy. Autosomal recessive forms are classified according to the age of onset, the maximum muscular activity achieved, and survivorship. The severity of the disease is mainly determined by the copy number of SMN2, a copy gene which predominantly produces exon 7-skipped transcripts and only low amount of full-length transcripts that encode for a protein identical to SMN1. Only about 4% of SMA patients bear one SMN1 copy with an intragenic mutation. SMA1 is a severe form, with onset before 6 months of age. SMA1 patients never achieve the ability to sit.
Defects in SMN1 are the cause of spinal muscular atrophy autosomal recessive type 2 (SMA2) [MIM:253550]. SMA2 is an autosomal recessive spinal muscular atrophy of intermediate severity, with onset between 6 and 18 months. Patients do not reach the motor milestone of standing, and survive into adulthood.
Defects in SMN1 are the cause of spinal muscular atrophy autosomal recessive type 3 (SMA3) [MIM:253400]. SMA3 is an autosomal recessive spinal muscular atrophy with onset after 18 months. SMA3 patients develop ability to stand and walk and survive into adulthood.
Defects in SMN1 are the cause of spinal muscular atrophy autosomal recessive type 4 (SMA4) [MIM:271150]. SMA4 is an autosomal recessive spinal muscular atrophy characterized by symmetric proximal muscle weakness with onset in adulthood and slow disease progression. SMA4 patients can stand and walk. -
Sequence similarities
Belongs to the SMN family.
Contains 1 Tudor domain. -
Cellular localization
Cytoplasm. Nucleus > gem. Localized in subnuclear structures next to coiled bodies, called Gemini of Cajal bodies. - Information by UniProt
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Alternative names
- BCD541
- Component of gems 1
- Gemin 1
see all -
Database links
- Entrez Gene: 6606 Human
- Entrez Gene: 6607 Human
- Entrez Gene: 20595 Mouse
- Omim: 600354 Human
- SwissProt: Q16637 Human
- SwissProt: P97801 Mouse
- Unigene: 202179 Human
- Unigene: 535788 Human
see all
Images
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Typical Standard Curve
Representative Standard Curve using ab136947.
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Typical Parallelism GraphA parallelism experiment was carried out to determine if the recombinant Human SMN standard accurately determines SMN concentrations in biological matrices. To assess parallelism, values for Human PBMC lysate and mouse tissue extract was obtained from a standard curve using four parameter logistic curve fitting. The observed concentration was plotted against the dilution factor. Parallelism of the curves demonstrates that the antibody binding characteristics are similar enough to allow the accurate determination of analyte levels in diluted samples.