Key features and details
- Rabbit polyclonal to Mitofusin 2
- Suitable for: WB
- Reacts with: Mouse, Rat, Human, Duck, Penguin
- Isotype: IgG
Product nameAnti-Mitofusin 2 antibody
See all Mitofusin 2 primary antibodies
DescriptionRabbit polyclonal to Mitofusin 2
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Mouse, Rat, Human, Duck, Penguin
Predicted to work with: Cynomolgus monkey, Orangutan
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Storage bufferpH: 7.40
Preservative: 0.097% Sodium azide
Constituent: 0.0268% PBS
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab50838 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 0.5 - 1 µg/ml. Detects a band of approximately 86 kDa (predicted molecular weight: 86 kDa).|
FunctionEssential transmembrane GTPase, which mediates mitochondrial fusion. Fusion of mitochondria occurs in many cell types and constitutes an important step in mitochondria morphology, which is balanced between fusion and fission. MFN2 acts independently of the cytoskeleton. It therefore plays a central role in mitochondrial metabolism and may be associated with obesity and/or apoptosis processes. Overexpression induces the formation of mitochondrial networks. Plays an important role in the regulation of vascular smooth muscle cell proliferation. Involved in the clearance of damaged mitochondria via selective autophagy (mitophagy). Is required for PARK2 recruitment to dysfunctional mitochondria. Involved in the control of unfolded protein response (UPR) upon ER stress including activation of apoptosis and autophagy during ER stress. Acts as an upstream regulator of EIF2AK3 and suppresses EIF2AK3 activation under basal conditions.
Tissue specificityUbiquitous; expressed at low level. Highly expressed in heart and kidney.
Involvement in diseaseCharcot-Marie-Tooth disease 2A2
Neuropathy, hereditary motor and sensory, 6A
Sequence similaritiesBelongs to the TRAFAC class dynamin-like GTPase superfamily. Dynamin/Fzo/YdjA family. Mitofusin subfamily.
Contains 1 dynamin-type G (guanine nucleotide-binding) domain.
modificationsPhosphorylated by PINK1.
Ubiquitinated by non-degradative ubiquitin by PARK2, promoting mitochondrial fusion; deubiquitination by USP30 inhibits mitochondrial fusion.
Cellular localizationMitochondrion outer membrane. Colocalizes with BAX during apoptosis.
- Information by UniProt
- CMT2A antibody
- CMT2A2 antibody
- CPRP 1 antibody
Lane 1 : Anti-Mitofusin 2 antibody (ab50838) at 0.5 µg/ml
Lanes 2-3 : Anti-Mitofusin 2 antibody (ab50838) at 1 µg/ml
Lane 4 : Anti-Mitofusin 2 antibody (ab50838) at 2 µg/ml
Lanes 1-2 & 4 : rat brain mitochondria extract
Lane 3 : rat brain mitochondria extract with Mitofusin 2 immunizing peptide at 5 µg/ml
All lanes : Goat Anti-Rabbit IgG, Peroxidase conjugate and a chemiluminescent substrate
Developed using the ECL technique.
Predicted band size: 86 kDa
Observed band size: 86 kDa
ab50838 has been referenced in 38 publications.
- Sprenger HG et al. Loss of the mitochondrial i-AAA protease YME1L leads to ocular dysfunction and spinal axonopathy. EMBO Mol Med 11:N/A (2019). PubMed: 30389680
- Gu Y et al. Inhibitory effect of mabuterol on proliferation of rat ASMCs induced by PDGF-BB via regulating [Ca2+]i and mitochondrial fission/fusion. Chem Biol Interact 307:63-72 (2019). PubMed: 31009640
- Yuan Y et al. Mitochondrial ROS-induced lysosomal dysfunction impairs autophagic flux and contributes to M1 macrophage polarization in a diabetic condition. Clin Sci (Lond) 133:1759-1777 (2019). PubMed: 31383716
- Larrea D et al. MFN2 mutations in Charcot-Marie-Tooth disease alter mitochondria-associated ER membrane function but do not impair bioenergetics. Hum Mol Genet 28:1782-1800 (2019). PubMed: 30649465
- Darwesh AM et al. Genetic Deletion or Pharmacological Inhibition of Soluble Epoxide Hydrolase Ameliorates Cardiac Ischemia/Reperfusion Injury by Attenuating NLRP3 Inflammasome Activation. Int J Mol Sci 20:N/A (2019). PubMed: 31319469