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MABN834

Sigma-Aldrich

Anti-SOD1 Antibody (ALS mutant), clone MS785

clone MS785, from rat

Sinónimos:

Superoxide dismutase [Cu-Zn], Superoxide dismutase 1, hSod1, SOD1

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rat

Quality Level

antibody form

purified antibody

antibody product type

primary antibodies

clone

MS785, monoclonal

species reactivity

human

technique(s)

immunocytochemistry: suitable
immunohistochemistry: suitable
immunoprecipitation (IP): suitable
western blot: suitable

isotype

IgG2bκ

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... SOD1(6647)

General description

SOD1 or Superoxide dismutase 1 is a critical enzyme for free radical metabolism and serves as a major detoxifier in cellular metabolism. SOD1 mutations are associated with disease and in particular with Amyotrophic lateral sclerosis 1, or ALS, often referred to as “Lou Gehrig’s Disease.” Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that is characterized by the selective loss of upper and lower motor neurons. There are >100 mutations in SOD1 in humans but not all appear to be pathogenic. The clone MS785 is a monoclonal antibody generated against the Derlin-1-binding region of SOD1 (DBR), and it distinguished most ALS-causative SOD1 mutants from both wild-type and nontoxic mutants. Moreover, MS785 recognized endogenous SOD1 in B lymphocytes derived from 14 ALS patients carrying SOD1 mutations but not from 11 healthy controls, thus MS785 appears to selectively recognize all Derlin-1–interactive SOD1 mutants but not WT SOD1.

Immunogen

Epitope: N-terminus
KLH-conjugated linear peptide corresponding to the N-terminus of human SOD1.

Application

Detect Anti-SOD1 Antibody (ALS mutant ), clone MS785 using this Anti-SOD1 Antibody (ALS mutant ), clone MS785 validated for use in Western Blotting
and Immunoprecipitation.
Immunoprecipitation Analysis: A representative lot immunoprecipitated SOD1 in transfected HEK293 cells (Fujisawa, T., et al. (2012). Ann Neurol. 72: 739–749).
Western Blotting Analysis: A representative lot SOD1 in transfected HEK293 cells (Fujisawa, T., et al. (2012). Ann Neurol. 72: 739–749).
Immunoprecipitation Analysis: A representative lot immunoprecipitated SOD1 in transfected HEK293 cells (Homma, K., et al. (2013). Ann Neurol. Cell. 52:1-12).
Immunocytochemistry (ICC): A representative lot of this antibody detected SOD1-G93A in HEK293 cells overexpressing G93A, but not the wild-type SOD1. (Fujisawa, T., et al. 2015. Neurobiol. Dis. 82; 486-487).
Immunohistochemistry (IHC): A representative lot of this antibody detected SOD1-G93A in the anterior horns of spinal cord tissue sections of SOD1G93A-transgenic mice, but not non-transgenic mice. ((Fujisawa, T., et al. 2015. Neurobiol. Dis. 82; 486-487).
Research Category
Neuroscience
Research Sub Category
Developmental Signaling

Quality

Evaluated by Western Blotting in transfected HEK293 with SOD1 mutant and HEK293 control lysates.

Western Blotting Analysis: 0.5 µg/mL of this antibody detected SOD1 in 1 µg of transfected HEK293 with SOD1 mutant and HEK293 control lysates.

Target description

~16 kDa observed

Physical form

Format: Purified
Protein G Purified
Purified rat monoclonal IgG2bκ in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Storage and Stability

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

Other Notes

Concentration: Please refer to lot specific datasheet.

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.

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Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Rafael López-Blanch et al.
Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 21(1), e00301-e00301 (2024-01-19)
Oxidative stress and neuroinflammation are major contributors to the pathophysiology of ALS. Nicotinamide riboside (a NAD+ precursor) and pterostilbene (a natural antioxidant) were efficacious in a human pilot study of ALS patients and in ALS SOD1G93A transgenic mice. Ibudilast targets
Yuko Kobayakawa et al.
Frontiers in neuroscience, 12, 894-894 (2018-12-14)
Connexin36 (Cx36) forms gap junctions between neurons, which are called electrical synapses, enabling adjacent neurons to communicate directly. The participation of chemical synapses in neurodegeneration in amyotrophic lateral sclerosis (ALS) has long been indicated, but it remains unclear whether electrical

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