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SAB1406464

Sigma-Aldrich

Anti-SOD1 antibody produced in mouse

purified immunoglobulin, buffered aqueous solution

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About This Item

Código UNSPSC:
12352203
NACRES:
NA.41

fonte biológica

mouse

conjugado

unconjugated

forma do anticorpo

purified immunoglobulin

tipo de produto de anticorpo

primary antibodies

clone

polyclonal

forma

buffered aqueous solution

peso molecular

antigen ~15.9 kDa

reatividade de espécies

human

técnica(s)

western blot: 1 μg/mL

nº de adesão NCBI

nº de adesão UniProt

Condições de expedição

dry ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... SOD1(6647)

Descrição geral

Superoxide Dismutase (SOD) or CuZn-SOD (SOD1), a cytoplasmic and mitochondrial intermembrane space protein, is located on human chromosome 21q22. It belongs to superoxide dismutase multigene family.
The protein encoded by this gene binds copper and zinc ions and is one of two isozymes responsible for destroying free superoxide radicals in the body. The encoded isozyme is a soluble cytoplasmic protein, acting as a homodimer to convert naturally-occuring but harmful superoxide radicals to molecular oxygen and hydrogen peroxide. The other isozyme is a mitochondrial protein. Mutations in this gene have been implicated as causes of familial amyotrophic lateral sclerosis. Rare transcript variants have been reported for this gene. (provided by RefSeq)

Imunogênio

SOD1 (NP_000445.1, 1 a.a. ~ 154 a.a) full-length human protein.

Sequence
MATKAVCVLKGDGPVQGIINFEQKESNGPVKVWGSIKGLTEGLHGFHVHEFGDNTAGCTSAGPHFNPLSRKHGGPKDEERHVGDLGNVTADKDGVADVSIEDSVISLSGDHCIIGRTLVVHEKADDLGKGGNEESTKTGNAGSRLACGVIGIAQ

Ações bioquímicas/fisiológicas

Superoxide Dismutase (SOD) or CuZn-SOD (SOD1) mutations results in amyotrophic lateral sclerosis. It acts as a mediator of the HMF (hypomagnetic field) effect.

forma física

Solution in phosphate buffered saline, pH 7.4

Exoneração de responsabilidade

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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Código de classe de armazenamento

10 - Combustible liquids

Classe de risco de água (WGK)

WGK 1

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


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Shielding of the geomagnetic field reduces hydrogen peroxide production in human neuroblastoma cell and inhibits the activity of CuZn superoxide dismutase
Zhang HT, et al.
Protein & cell, 8(7), 527-537 (2017)
Jianzhu Luo et al.
Frontiers in physiology, 4, 295-295 (2013-11-07)
ecSOD function has prototypically been associated with the extracellular space due to its secretion and localization to the extracellular matrix. A myocyte-specific ecSOD transgenic mouse has shown that it can also be localized to the myocyte intracellular compartment and is
An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria
Wong PC, et al.
Neuron, 14(6), 1105-1116 (1995)
A review of asthma genetics: gene expression studies and recent candidates
Malerba G1 and Pignatti PF
Journal of applied genetics, 46(1), 93-104 (2005)
Xuan Xu et al.
Cardiovascular diagnosis and therapy, 10(3), 453-469 (2020-07-23)
Myocardial mitochondrial dysfunction is the leading cause of chronic heart failure (CHF). Increased reactive oxygen species (ROS) levels, disruption of mitochondrial biogenesis and mitochondrial Ca2+([Ca2+]m) homeostasis and reduction of the mitochondrial membrane potential (ΔΨm) cause myocardial mitochondrial dysfunction. Therefore, treating

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