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Documentos Principais

M9073

Sigma-Aldrich

Anti-Mitofusin 2 antibody,Mouse monoclonal

clone Mito-2, purified from hybridoma cell culture

Sinônimo(s):

Anti-CMT2A, Anti-CMT2A2, Anti-CPRP1, Anti-HSG, Anti-Hyperplasia suppressor, Anti-KIAA0214, Anti-MARF, Anti-MFN2, Anti-Mitochondrial assembly regulatory factor, Anti-Transmembrane GTPase MFN2

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About This Item

Número MDL:
Código UNSPSC:
12352203
NACRES:
NA.41

fonte biológica

mouse

conjugado

unconjugated

forma do anticorpo

purified from hybridoma cell culture

tipo de produto de anticorpo

primary antibodies

clone

Mito-2, monoclonal

forma

buffered aqueous solution

peso molecular

antigen ~86 kDa

reatividade de espécies

mouse, rat

concentração

~1.0 mg/mL

técnica(s)

western blot: 2-5 μg/mL using whole extract of rat brain mitochondria

Isotipo

IgG1

nº de adesão UniProt

Condições de expedição

dry ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... MFN2(9927)

Descrição geral

Mitofusin-2 (MFN2) is an outer mitochondrial membrane protein.
Monoclonal Anti-Mitofusin 2 (mouse IgG1 isotype) is derived from the hybridoma Mito-2 produced by the fusion of mouse myeloma cells and splenocytes from BALB/c mice immunized with a synthetic peptide corresponding to a fragment of human Mitofusin 2 conjugated to KLH. Mitofusin 2ismammalian homolog of the Drosophila protein fuzzy onion (Fzo). It is a transmembrane GTPases embedded in the outer membrane of mitochondria. Mitofusin 2 is broadly expressed, with highest expression in heart and skeletal muscle and is induced during myogenesis.

Aplicação

Anti-Mitofusin 2 antibody,Mouse monoclonal has been used in western blotting.

Ações bioquímicas/fisiológicas

Mitofusin 2 (Mfn2) mutant embryos have a specific and severe disruption of a layer of the placenta. Repression of Mfn2 causes morphological and functional fragmentation of the mitochondrial network into independent clusters and reduces mitochondrial membrane potential and glucose oxidation. Thus, this Mfn2-dependent regulatory mechanism is disturbed in obesity by reduced Mfn2 expression. Mutations in Mitofusin 2 cause Charcot-Marie-Tooth neuropathy type 2A, a neurological disorder that results from degeneration of axons in peripheral nerves.
Mitofusin-2 (MFN2) plays an important role as a mitochondrial fusion protein and controls many cell processes. It is mainly involved in regulating metabolic processes in the mitochondria. MFN2 prevents the formation of reactive oxygen species and controls endoplasmic reticulum stress. Mutations in the gene encoding this protein have been linked to diabetes and obesity.

forma física

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

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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Short-duration swimming exercise after myocardial infarction attenuates cardiac dysfunction and regulates mitochondrial quality control in aged mice
Zhao D, et al.
Oxidative Medicine and Cellular Longevity, 2018 (2018)
Mutations in the mitochondrial GTPase mitofusin 2 cause Charcot-Marie-Tooth neuropathy type 2A
Zuchner S, et al.
Nature Genetics, 36(5), 449-449 (2004)
Mitofusin-2 determines mitochondrial network architecture and mitochondrial metabolism A novel regulatory mechanism altered in obesity
Bach D, et al.
The Journal of Biological Chemistry, 278(19), 17190-17197 (2003)
Membrane topology and mitochondrial targeting of mitofusins, ubiquitous mammalian homologs of the transmembrane GTPase Fzo
Rojo M, et al.
Journal of Cell Science, 115(8), 1663-1674 (2002)
The dynamics of cardiolipin synthesis post-mitochondrial fusion
Xu FY, et al.
Biochimica et Biophysica Acta - Biomembranes, 1798(8), 1577-1585 (2010)

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