S2944

Anti-SMN antibody, Mouse monoclonal

Name: Anti-SMN antibody, Mouse monoclonal
Brand: SIGMA

clone 2B1, purified from hybridoma cell culture

Synonym(s):

Anti-Survival of Motor Neurons

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About This Item

UNSPSC Code:

12352203

NACRES:

NA.41

MDL number:

MFCD01634191

Product Name

Anti-SMN antibody, Mouse monoclonal, clone 2B1, purified from hybridoma cell culture

biological source

mouse

conjugate

unconjugated

antibody form

purified from hybridoma cell culture

antibody product type

primary antibodies

clone

2B1, monoclonal

form

buffered aqueous solution

species reactivity

Xenopus, human, mouse

concentration

~2 mg/mL

technique(s)

microarray: suitable
western blot: 2-4 μg/mL using A431 cell extract

isotype

IgG1

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

200

Gene Information

human ... SMN1(6606), SMN2(6607)
mouse ... Smn1(20595)

Application

Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Enzyme-linked immunosorbent assay (1 paper)

Mouse monoclonal clone 2B1 anti-SMN antibody is an important tool for studying the role of the survival of motor neurons protein in nuclear processes and spinal muscular atrophy (SMA). It may be used in immunoblotting (~35 kDa), immunoprecipitation, and immunocytochemistry.

Biochem/physiol Actions

Survival of Motor Neurons (SMN) complex is important in various biological processes, such as assembly and restructuring of spliceosomal small nuclear ribonucleoproteins (snRNPs), pre mRNA splicing and transcription. Spinal muscular atrophy (SMA) is caused by reduced expression or mutations in the survival of motor neurons (SMN) protein. Deletion or mutation in the telomeric copy (SMN1) causes the SMA phenotype. The severity of SMA is in direct correlation with the expression level of the SMN protein, either from the SMN1 gene or a different spliced form of SMN from the SMN2 gene. The SMN complex interacts with various protein substrates such as Sm and Lsm proteins of the spliceosomal snRNPs, fibrillarin, GAR1, RNA helicase A, the human hnRNP proteins (hnRNPQ, U and R), coilin and p53.

The antibody recognizes human, mouse, and Xenopus SMN.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

General description

Mouse monoclonal clone 2B1 anti-SMN antibody recognizes human, mouse, and Xenopus survival of motor neurons proteins.

Immunogen

recombinant human SMN

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15mM sodium azide.

Preparation Note

For continuous use, store at 2-8 °C for up to one month. For extended storage, freeze in working aliquots. Repeated freezing and thawing, or storage in "frostfree" freezers, is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilution samples should be discarded if not used within 12 hours.

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Storage Class

12 - Non Combustible Liquids

wgk

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable

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Utility of survival motor neuron ELISA for spinal muscular atrophy clinical and preclinical analyses.

Dione T Kobayashi et al.

PloS one, 6(8), e24269-e24269 (2011-09-10)

Genetic defects leading to the reduction of the survival motor neuron protein (SMN) are a causal factor for Spinal Muscular Atrophy (SMA). While there are a number of therapies under evaluation as potential treatments for SMA, there is a critical

Spinal muscular atrophy: why do low levels of survival motor neuron protein make motor neurons sick?

Burghes AHM and Beattie CE

Nature Reviews. Neuroscience, 10(8), 597-597 (2009)

Evaluation of SMN protein, transcript, and copy number in the biomarkers for spinal muscular atrophy (BforSMA) clinical study.

Thomas O Crawford et al.

PloS one, 7(4), e33572-e33572 (2012-05-05)

The universal presence of a gene (SMN2) nearly identical to the mutated SMN1 gene responsible for Spinal Muscular Atrophy (SMA) has proved an enticing incentive to therapeutics development. Early disappointments from putative SMN-enhancing agent clinical trials have increased interest in

Animal models of systemic lupus erythematosus (SLE) and ex vivo assay design for drug discovery.

Matthew M Seavey et al.

Current protocols in pharmacology, Chapter 5, Unit 5-Unit 5 (2011-09-22)

Systemic Lupus Erythematosus (SLE) is a debilitating and often fatal autoimmune disease that involves multiple organ systems. It can develop for years before being diagnosed. Current treatments for SLE usually involve the use of cytotoxic or immunosuppressive agents that can

Erin G Conlon et al.

eLife, 7 (2018-07-14)

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) represent two ends of a disease spectrum with shared clinical, genetic and pathological features. These include near ubiquitous pathological inclusions of the RNA-binding protein (RBP) TDP-43, and often the presence of a

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