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Product Name
MFN2 antibody
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Description
MFN2 Rabbit Polyclonal antibody. Positive IHC detected in human heart tissue, human colon cancer tissue, human kidney tissue. Positive WB detected in mouse testis tissue, HEK-293 cells, human heart tissue, human liver tissue, mouse kidney tissue, mouse liver tissue, mouse lung tissue. Positive IP detected in mouse kidney tissue. Observed molecular weight by Western-blot: 86kd
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Tested applications
ELISA, WB, IP, IHC
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Species reactivity
Human,Mouse,Rat; other species not tested.
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Alternative names
CMT2A antibody; CMT2A2 antibody; CPRP1 antibody; HSG antibody; KIAA0214 antibody; MARF antibody; MFN2 antibody; Mitofusin 2 antibody; Transmembrane GTPase MFN2 antibody
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Isotype
Rabbit IgG
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Preparation
This antibody was obtained by immunization of MFN2 recombinant protein (Accession Number: XM_005263548). Purification method: Antigen affinity purified.
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Clonality
Polyclonal
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Formulation
PBS with 0.1% sodium azide and 50% glycerol pH 7.3.
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Storage instructions
Store at -20℃. DO NOT ALIQUOT
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Applications
Recommended Dilution:
WB: 1:500-1:5000
IP: 1:500-1:5000
IHC: 1:20-1:200
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Validations
mouse testis tissue were subjected to SDS PAGE followed by western blot with Catalog No:112530(MFN2 antibody) at dilution of 1:400
IP Result of anti-MFN2 (IP:Catalog No:112530, 3ug; Detection:Catalog No:112530 1:1000) with mouse kidney tissue lysate 8000ug.
Immunohistochemical of paraffin-embedded human heart using Catalog No:112530(MFN2 antibody) at dilution of 1:50 (under 40x lens)
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Background
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).
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References
- Kar R, Mishra N, Singha PK, Venkatachalam MA, Saikumar P. Mitochondrial remodeling following fission inhibition by 15d-PGJ2 involves molecular changes in mitochondrial fusion protein OPA1. Biochemical and biophysical research communications. 399(4):548-54. 2010.
- Rehman J, Zhang HJ, Toth PT. Inhibition of mitochondrial fission prevents cell cycle progression in lung cancer. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 26(5):2175-86. 2012.
- Ota K, Obayashi M, Ozaki K. Relocation of p25α/tubulin polymerization promoting protein from the nucleus to the perinuclear cytoplasm in the oligodendroglia of sporadic and COQ2 mutant multiple system atrophy. Acta neuropathologica communications. 2:136. 2014.
- Deng J, Yang M, Chen Y. FUS Interacts with HSP60 to Promote Mitochondrial Damage. PLoS genetics. 11(9):e1005357. 2015.
- Li H, Ruan Y, Zhang K. Mic60/Mitofilin determines MICOS assembly essential for mitochondrial dynamics and mtDNA nucleoid organization. Cell death and differentiation. 23(3):380-92. 2016.
- Sharoar MG, Shi Q, Ge Y. Dysfunctional tubular endoplasmic reticulum constitutes a pathological feature of Alzheimer's disease. Molecular psychiatry. 2015.
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