Render Target: STATIC
Render Timestamp: 2024-11-21T13:13:58.832Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-11-18 16:03:12.508
Product last modified at: 2024-11-19T09:00:32.060Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
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) 35
    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 SMN1 protein.

    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).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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