Anti-SMN Antibody, clone 62E7

35 kDa was observed; however, the calculated molecular weight is 31.849 kDa

The survival of motor neurons (SMN) protein is essential for the biogenesis of small nuclear RNA (snRNA)-ribonucleoproteins (snRNPs), the major components of the pre-mRNA splicing machinery. Though it is ubiquitously expressed, SMN deficiency causes the motor neuron degenerative disease spinal muscular atrophy (SMA). SMN deficiency, similar to that which occurs in severe SMA, has unexpected cell type-specific effects on the repertoire of snRNAs and mRNAs. It alters the stoichiometry of snRNAs and causes widespread pre-mRNA splicing defects in numerous transcripts of diverse genes, preferentially those containing a large number of introns, in SMN-deficient mouse tissues. These findings reveal a key role for the SMN complex in RNA metabolism and in splicing regulation and indicate that SMA is a general splicing disease that is not restricted to motor neurons.

Epitope: Unknown

His-tagged recombinant protein corresponding to human SMN.

Immunocytochemistry Analysis: 1:500 dilution from a representative lot detected SMN in HeLa cells.

Research Category
Epigenetics & Nuclear Function

Research Sub Category
RNA Metabolism & Binding Proteins

Use Anti-SMN Antibody, clone 62E7 (Mouse Monoclonal Antibody) validated in WB, ICC, IP to detect SMN also known as Spinal muscular atrophy (Werdnig-Hoffmann disease Kugelberg-Welander disease).

Recognizes SMN.

Format: Purified

Protein G Purified

Purified mouse monoclonal IgG1κ in buffer containing 0.1 M Tris-Glycine (pH 7.4, 150 mM NaCl) with 0.05% sodium azide.

Stable for 1 year at 2-8°C from date of receipt.

Control
HeLa cell lysate

Evaluated by Western Blot in HeLa cell lysate.

Western Blot Analysis: 0.5 µg/ml of this antibody detected SMN on 10 µg of HeLa cell lysate.

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

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