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M6444

Sigma-Aldrich

Anti-Mitofusin 2 antibody produced in rabbit

~1 mg/mL, affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-CMT2A, Anti-CMT2A2, Anti-CPRP1, Anti-KIAA0214, Anti-MARF, Anti-Mfn2

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~86 kDa

species reactivity

human, mouse, rat

concentration

~1 mg/mL

technique(s)

immunoprecipitation (IP): 5-10 μg using HeLa human epitheloid carcinoma cell lysate
western blot (chemiluminescent): 0.5-1 μg/mL using extract of mouse and rat brain mitochondria

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

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

General description

Anti-Mitofusin 2 is produced in rabbit using as immunogen a synthetic peptide corresponding to human mitofusin 2 with an N-terminal added cysteine, conjugated to KLH. Mitofusins (Mfn1 and Mfn2) form homotypic and heterotypic complexes for fusion in mitochondria.
Mitofusin-2 (MFN2) is an outer mitochondrial membrane protein.

Immunogen

synthetic peptide corresponding to amino acid residues 557-576 of human mitofusin 2 with an N-terminal added cysteine, conjugated to KLH. The corresponding sequence differs by one and two amino acids in rat and mouse mitofusin 2, respectively.

Application

Anti-Mitofusin 2 antibody has been used in immunoblotting. It may also be used in immunoprecipitation.
Anti-Mitofusin 2 antibody produced in rabbit has been used for Western blotting.
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Western Blotting (1 paper)

Biochem/physiol Actions

MFN2 is essential for the maintenance of mitochondrial network and controls mitochondrial metabolism. Mfn2-dependent regulatory mechanism is disturbed in obesity by reduced Mfn2 expression. Mutations in MFN2 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 participates in 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.

Physical form

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

Disclaimer

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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Storage Class Code

10 - Combustible liquids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Yuan Zhang et al.
American journal of physiology. Cell physiology, 305(5), C502-C511 (2013-06-21)
The function Bax and/or Bak in constituting a gateway for mitochondrial apoptosis in response to apoptotic stimuli has been unequivocally demonstrated. However, recent work has suggested that Bax/Bak may have unrecognized nonapoptotic functions related to mitochondrial function in nonstressful environments.
Ee Phie Tan et al.
The Journal of biological chemistry, 292(36), 14940-14962 (2017-07-26)
Dysfunctional mitochondria and generation of reactive oxygen species (ROS) promote chronic diseases, which have spurred interest in the molecular mechanisms underlying these conditions. Previously, we have demonstrated that disruption of post-translational modification of proteins with β-linked N-acetylglucosamine (O-GlcNAcylation) via overexpression
Mfn2 is critical for brown adipose tissue thermogenic function
Boutant M,et al.
The Embo Journal, 36(11), 1543-1558 (2017)
Ashley J Smuder et al.
Free radical biology & medicine, 115, 179-190 (2017-12-05)
Mechanical ventilation (MV) results in the rapid development of ventilator-induced diaphragm dysfunction (VIDD). While the mechanisms responsible for VIDD are not fully understood, recent data reveal that prolonged MV activates autophagy in the diaphragm, which may occur as a result
Dysregulation of mitochondrial quality control processes contribute to sarcopenia in a mouse model of premature aging
Joseph A M,et al.
Testing, 8(7), e69327-e69327 (2013)

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