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Key Documents

06-984

Sigma-Aldrich

Anti-Mn-SOD Antibody

Upstate®, from rabbit

Synonyme(s) :

Mn superoxide dismutase, indophenoloxidase B, manganese superoxide dismutase, manganese-containing superoxide dismutase, mangano-superoxide dismutase, superoxide dismutase 2, mitochondrial

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About This Item

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

Source biologique

rabbit

Niveau de qualité

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

polyclonal

Espèces réactives

mouse, bovine, human, rat

Ne doit pas réagir avec

canine

Conditionnement

antibody small pack of 25 μg

Fabricant/nom de marque

Upstate®

Technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
western blot: suitable

Isotype

IgG

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

ambient

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... SOD2(6648)

Description générale

Superoxide dismutase (SOD) is an antioxidant enzyme involved in the defense system against reactive oxygen species (ROS). SOD catalyzes the dismutation reaction of superoxide radical anion (O2-) to hydrogen peroxide, which is then catalyzed to innocuous O2 and H2O by glutathione peroxidase and catalase. Several classes of SOD have been identified. These include intracellular copper, zinc SOD (Cu, Zn SOD/SOD1), mitochondrial manganese SOD (Mn SOD/SOD2) and extracellular Cu, Zn SOD (EC SOD/SOD3). The manganese containing 80 kDa tetrameric enzyme SOD2 is located in the mitochondrial matrix in close proximity to a primary endogenous source of superoxide, the mitochondrial respiratory chain.

Spécificité

Recognizes MnSOD, Mr 24 kDa.

Immunogène

Recombinant human MnSOD (manganous superoxide dismutase).

Application

Anti-Mn-SOD Antibody is an antibody against Mn-SOD for use in IH, IH(P) & WB.
Immunohistochemistry (Paraffin):
10 μg/mL of a previous lot detected MnSOD in paraffin embedded rat brain tissue sections.

Qualité

Evaluated by western blot on RIPA lysates of MCF-7, A431 or rat L6 RIPA cells.

Western Blot Analysis:
0.5-2 μg/mL of this antibody detected MnSOD in RIPA lysates of rat L6 RIPA cells. 1-4 μg/mL of a previous lot detected MnSOD in RIPA lysates of human MCF-7, A431 and rat L6 RIPA cells.

Description de la cible

~24 kDa

Forme physique

Format: Purified
Purified rabbit polyclonal in buffer containing 70% storage buffer 0.1 M Tris-glycine, pH 7.4, 0.15 M NaCl, 0.05% sodium azide and 30% glycerol.

Remarque sur l'analyse

Control
L6 cell lysate, rat brain tissue extract.

Autres remarques

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Informations légales

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

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Consulter la Bibliothèque de documents

Metabolic utilization of exogenous pyruvate by mutant p53 (R175H) human melanoma cells promotes survival under glucose depletion.
Valery A Chavez-Perez,Mary Strasberg-Rieber,Manuel Rieber
Cancer Biology & Therapy null
Low concentrations of methamphetamine can protect dopaminergic cells against a larger oxidative stress injury: mechanistic study.
El Ayadi, A; Zigmond, MJ
Testing null
Manganese superoxide dismutase expression in human cancer cells: a possible role of mRNA processing.
St Clair, D K and Oberley, L W
Free Radical Research Communications, 12-13 Pt 2, 771-778 (1991)
Michael K Jones et al.
American journal of physiology. Gastrointestinal and liver physiology, 301(3), G537-G546 (2011-07-02)
Mitochondrial superoxide dismutase (SOD2) prevents accumulation of the superoxide that arises as a consequence of oxidative phosphorylation. However, SOD2 is a target of oxidative/nitrosative inactivation, and reduced SOD2 activity has been demonstrated to contribute to portal hypertensive gastropathy. We investigated
Julia S Schlehe et al.
Neurobiology of disease, 58, 57-67 (2013-05-25)
Deficiency in human mitochondrial Complex-1 has been linked to a wide variety of neurological disorders. Homozygous deletion of the Complex-1 associated protein, Ndufaf2, leads to a severe juvenile onset encephalopathy involving degeneration of the substantia nigra and other sub-cortical regions

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