R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
SMN (F9B6P) Rabbit mAb #74905
Filter:
- WB
- IP
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 38 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:100 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
SMN (F9B6P) Rabbit mAb recognizes endogenous levels of total SMN protein. Based on sequence, this antibody will recognize full-length SMN protein, as well as SMNΔ7, which is the predominant product of the SMN2 gene.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro70 of human SMN protein.
Background
The survival motor neuron (SMN) protein is ubiquitously expressed in mammals and encoded by two genes, SMN1 and SMN2 (1,2). The protein coding sequences of SMN1 and SMN2 are predicted to be identical, as SMN2 differs from SMN1 by only five nucleotides (3). SMN impacts various aspects of RNA metabolism, and is required for biogenesis of small nuclear ribonucleoprotein (snRNP) particles critical for pre-mRNA splicing. Furthermore, SMN, needed for stress granule formation, is found in ribonucleoprotein (RNP) granules moving through neuronal processes and is part of RNP complexes implicated in synaptic local translation (4,5). Mutations in its coding genes, SMN1 or SMN2, are linked to neuromuscular disease spinal muscular atrophy (SMA), a leading genetic cause of infant mortality (2-6). The severity of SMA is inversely proportional to SMN2 copy number. Over 96% of SMA patients have homozygous mutations (deletion, rearrangement, or point mutation) in SMN1, however they retain at least one copy of SMN2 (1).
- Lefebvre, S. et al. (1995) Cell 80, 155-65.
- Singh, R.N. et al. (2017) Biochim Biophys Acta Gene Regul Mech 1860, 299-315.
- Melki, J. (1997) Curr Opin Neurol 10, 381-5.
- Dimitriadi, M. et al. (2016) Proc Natl Acad Sci U S A 113, E4377-86.
- Li, W. (2017) PLoS One 12, e0178519.
- Chaytow, H. et al. (2018) Cell Mol Life Sci 75, 3877-3894.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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