|Positive WB detected in||mouse brain tissue, HeLa cells, COLO 320 cells, mouse liver tissue, rat brain tissue, rat heart tissue|
|Positive IP detected in||mouse kidney tissue|
|Positive IHC detected in||human heart tissue, human colon cancer tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Western Blot (WB)||WB : 1:2000-1:10000|
|Immunoprecipitation (IP)||IP : 0.5-4.0 ug for IP and 1:200-1:1000 for WB|
|Immunohistochemistry (IHC)||IHC : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
12186-1-AP targets MFN2 in WB, IP, IHC, IF applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||bovine, chicken, human, mouse, rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||MFN2 fusion protein Ag2845|
|Full Name||mitofusin 2|
|Calculated molecular weight||757 aa, 86 kDa|
|Observed molecular weight||86 kDa|
|GenBank accession number||BC017061|
|Gene ID (NCBI)||9927|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
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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Julia (Verified Customer) (11-16-2018)