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MFN2 Monoclonal antibody
MFN2 Monoclonal Antibody for IF, IHC, WB, ELISA
Cat no : 67487-1-Ig
|Positive WB detected in
|HEK-293 cells, HeLa cells, HepG2 cells, Jurkat cells, K-562 cells, HSC-T6 cells, LNCaP cells
|Positive IHC detected in
|human heart tissue
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Positive IF detected in
|Western Blot (WB)
|WB : 1:5000-1:50000
|IHC : 1:1000-1:4000
|IF : 1:400-1:1600
|It is recommended that this reagent should be titrated in each testing system to obtain optimal results.
|Sample-dependent, check data in validation data gallery
67487-1-Ig targets MFN2 in WB, IHC, IF, ELISA applications and shows reactivity with Human, Mouse, Rat samples.
|Human, Mouse, Rat
|human, mouse, rat, fish
|Host / Isotype
|Mouse / IgG2a
|MFN2 fusion protein Ag29873
|Calculated molecular weight
|757 aa, 86 kDa
|Observed molecular weight
|GenBank accession number
|Gene ID (NCBI)
|Protein A purification
|PBS with 0.02% sodium azide and 50% glycerol pH 7.3.
|Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage. 20ul sizes contain 0.1% BSA.
MFN2, also named as CPRP1 and KIAA0214, belongs to the mitofusin family. It is an Essential transmembrane GTPase, which mediates mitochondrial fusion. 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 of MFN2 induces the formation of mitochondrial networks. It plays an important role in the regulation of vascular smooth muscle cell proliferation. Defects in MFN2 are the cause of Charcot-Marie-Tooth disease type 2A2 (CMT2A2). Defects in MFN2 are the cause of Charcot-Marie-Tooth disease type 6 (CMT6). Ubiquitinated forms of Mfn2 (mono- and polyubiquitinated) are present during mitophagy.
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Roles of HIF-1α/BNIP3 mediated mitophagy in mitochondrial dysfunction of letrozole-induced PCOS rats
Diosgenin Ameliorated Type II Diabetes-Associated Nonalcoholic Fatty Liver Disease through Inhibiting De Novo Lipogenesis and Improving Fatty Acid Oxidation and Mitochondrial Function in Rats
Hypoxia-induced GPCPD1 depalmitoylation triggers mitophagy via regulating PRKN-mediated ubiquitination of VDAC1
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