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Merck
CN

AB10346

Anti-SOD2 Antibody

serum, Chemicon®

别名:

Superoxide Dismutase 2 (SOD2)

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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
polyclonal
Application:
WB
Citations:
7
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biological source

rabbit

conjugate

unconjugated

antibody form

serum

antibody product type

primary antibodies

clone

polyclonal

species reactivity

mouse, human, rat

manufacturer/tradename

Chemicon®

technique(s)

western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

mouse ... Sod2(20656)

General description

28 kDa
This gene is a member of the iron/manganese superoxide dismutase family. It encodes a mitochondrial protein that forms a homotetramer and binds one manganese ion per subunit. This protein binds to the superoxide byproducts of oxidative phosphorylation and converts them to hydrogen peroxide and diatomic oxygen. Mutations in this gene have been associated with idiopathic cardiomyopathy (IDC), premature aging, sporadic motor neuron disease, and cancer. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.

Immunogen

Epitope: AA G93 – Y217
Recombinant human SOD2

Application

This Anti-SOD2 Antibody is validated for use in WB for the detection of SOD2.

Analysis Note

Routinely evaluated by immunoblot.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany


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存储类别

10 - Combustible liquids

wgk

WGK 1



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相关内容

"Aging: getting older, exhibiting the signs of age, the decline in the physical (and mental) well-being over time, leading to death. Since the beginning of time, man has been obsessed with trying to slow down, stop, or even reverse the signs of aging. Many have gone as far as experimenting with nutritional regimens, eccentric exercises, fantastic rituals, and naturally occurring or synthetic wonder-elements to evade the signs of normal aging. Biologically speaking, what is aging? And what does the latest research tell us about the possibility of discovering the elusive “fountain of youth”? Many advances in our understanding of aging have come from systematic scientific research, and perhaps it holds the key to immortality. Scientifically, aging can be defined as a systems-wide decline in organismal function that occurs over time. This decline occurs as a result of numerous events in the organism, and these events can be classified into nine “hallmarks” of aging, as proposed by López-Otin et al. (2013). Several of the pathologies associated with aging are a direct result of these events going to extremes and may also involve aberrant activation of proliferation signals or hyperactivity. The hallmarks of aging have been defined based on their fulfillment of specific aging related criteria, such as manifestation during normal aging, acceleration of aging if experimentally induced or aggravated, and retardation of aging if prevented or blocked, resulting in increased lifespan. The nine hallmarks of aging are genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. The biological processes underlying aging are complex. By understanding the hallmarks in greater detail, we can get closer to developing intervention strategies that can make the aging process less of a decline, and more of a recline."

"Redox reactions are powerful chemical processes that involve the reduction and oxidation of proteins and metabolites found in living things. The mechanisms that regulate them are key to maintaining homeostasis and the balance between good health and disease pathology. Oxidative stress is the state where the delicate balance of redox biology is upset, and the pathology of oxidative stress are the cellular consequences to such an imbalance."


Yukio Shimasaki et al.
Circulation research, 113(7), 891-901 (2013-07-04)
Mitochondria, although required for cellular ATP production, are also known to have other important functions that may include modulating cellular responses to environmental stimuli. However, the mechanisms whereby mitochondria impact cellular phenotype are not yet clear. To determine how mitochondria
Loss of LRPPRC causes ATP synthase deficiency.
Mourier, A; Ruzzenente, B; Brandt, T; Kuhlbrandt, W; Larsson, NG
Human Molecular Genetics null
Anthony R Cyr et al.
Redox biology, 1, 172-177 (2013-09-12)
Manganese superoxide dismutase, encoded by the Sod2 gene, is a ubiquitously expressed mitochondrial antioxidant enzyme that is essential for mammalian life. Mice born with constitutive genetic knockout of Sod2 do not survive the neonatal stage, which renders the longitudinal study