Merck
Wszystkie zdjęcia(6)

M6319

Sigma-Aldrich

Anti-Mitofusin-2 (N-Terminal) antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

Synonim(y):
Anti-MARF, Mitofusin 2 Antibody, Mitofusin 2 Antibody - Anti-Mitofusin-2 (N-Terminal) antibody produced in rabbit, Anti-Mfn2, Anti-KIAA0214, Anti-CMT2A2, Anti-CMT2A, Anti-CPRP1
Numer MDL:
NACRES:
NA.41

pochodzenie biologiczne

rabbit

Poziom jakości

200

białko sprzężone

unconjugated

forma przeciwciała

affinity isolated antibody

antibody product type

primary antibodies

klon

polyclonal

forma

buffered aqueous solution

masa cząsteczkowa

antigen ~86 kDa

species reactivity

rat, mouse, human

technique(s)

immunoprecipitation (IP): 5-10 μg using HeLa human epitheloid carcinoma cell lysate
indirect immunofluorescence: 20-30 μg/mL using differentiated mouse C2 cells
western blot (chemiluminescent): 0.5-1 μg/mL using extracts of rat or mouse brain mitochondria

numer dostępu UniProt

transport

dry ice

temp. przechowywania

−20°C

Gene Information

human ... MFN2(9927)
mouse ... Mfn2(170731)
rat ... Mfn2(64476)

Opis ogólny

Mitofusins (Mfn1 and Mfn2) are the mammalian homologs of the Drosophila protein fuzzy onion (Fzo). They are transmembrane GTPases embedded in the outer membrane of mitochondria, essential for fusion of mitochondria in mammalian cells. Mfn1 and Mfn2 form homotypic and heterotypic complexes that are functional for fusion. Mitochondrial fusion is also important for cell growth, mitochondrial membrane potential, respiration, and embryonic development. Mice deficient in either Mfn1 or Mfn2 die in mid-gestation. Mfn2 mutant embryos have a specific and severe disruption of a layer of the placenta. Mitofusin 2 is broadly expressed, with highest expression in heart and skeletal muscle and is induced during myogenesis. Repression of Mfn2 causes morphological and functional fragmentation of the mitochondrial network into independent clusters and reduces mitochondrial membrane potential and glucose oxidation. Thus, Mfn2 is essential for the maintenance of mitochondrial network and controls mitochondrial metabolism. 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.

Specyficzność

Anti-Mitofusin 2 (N-terminal) antibody recognizes human, rat, and mouse mitofusin 2. Detection of the mitofusin 2 band by immunoblotting is specifically inhibited with the immunizing peptide.
The antibody is specific for N-terminal of mitofusin 2 (~86 kDa)

Immunogen

synthetic peptide corresponding to amino acid residues 38-55 of human mitofusin 2 with C-terminal added cysteine, conjugated to KLH. The corresponding sequence differs by one amino acid in both rat and mouse mitofusin 2.

Zastosowanie

Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Western Blotting (1 paper)
Anti-mitofusion 2 antibody may be used for immunoprecipitation in HeLa cells; immunoblotting in mouse and rat brain mitochondia and immunoflurescence in mouse C2 cells
Anti-Mitofusin 2 (N-terminal) antibody is suitable for immunoblotting (~86 kDa), immunoprecipitation, and immunofluorescence applications.
By immunoblotting, a working antibody concentration of 0.5-1 mg/mL is recommended using an extracts of rat and mouse brain mitochondria and a chemiluminescent detection reagent.
By indirect immunofluorescence, a working antibody concentration of 20-30 mg/mL is recommended using differentiated mouse C2 cells.
5-10 mg of the antibody immunoprecipitates mitofusin 2 from HeLa human epithelioid carcinoma cell lysate.

Postać fizyczna

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

Oświadczenie o zrzeczeniu się odpowiedzialności

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.

Kod klasy składowania

12 - Non Combustible Liquids

WGK

WGK 1

Temperatura zapłonu °F

Not applicable

Temperatura zapłonu °C

Not applicable

Certyfikat analizy

Wprowadź numer partii, aby wyszukać certyfikat analizy (COA).

Świadectwo pochodzenia

Wprowadź numer partii, aby wyszukać świadectwo pochodzenia (COO).

Quotes and Ordering

Short mitochondrial ARF triggers Parkin/PINK1-dependent mitophagy
Grenier K, et al.
The Journal of Biological Chemistry (2014)
Jonathan P Little et al.
Journal of applied physiology (Bethesda, Md. : 1985), 111(6), 1554-1560 (2011-08-27)
Low-volume high-intensity interval training (HIT) is emerging as a time-efficient exercise strategy for improving health and fitness. This form of exercise has not been tested in type 2 diabetes and thus we examined the effects of low-volume HIT on glucose
Cecília García-Pérez et al.
American journal of physiology. Heart and circulatory physiology, 301(5), H1907-H1915 (2011-08-23)
Propagation of ryanodine receptor (RyR2)-derived Ca(2+) signals to the mitochondrial matrix supports oxidative ATP production or facilitates mitochondrial apoptosis in cardiac muscle. Ca(2+) transfer likely occurs locally at focal associations of the sarcoplasmic reticulum (SR) and mitochondria, which are secured
Kensuke Tsushima et al.
Circulation research, 122(1), 58-73 (2017-11-03)
Cardiac lipotoxicity, characterized by increased uptake, oxidation, and accumulation of lipid intermediates, contributes to cardiac dysfunction in obesity and diabetes mellitus. However, mechanisms linking lipid overload and mitochondrial dysfunction are incompletely understood. To elucidate the mechanisms for mitochondrial adaptations to
Robert H Baloh et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 27(2), 422-430 (2007-01-12)
Mutations in the mitochondrial fusion protein mitofusin 2 (MFN2) are the most commonly identified cause of Charcot-Marie-Tooth type 2 (CMT2), a dominantly inherited disease characterized by degeneration of peripheral sensory and motor axons. However, the mechanism by which mutations in

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