Product Pathways - Metabolism
Mitofusin-2 (D1E9) Rabbit mAb #11925
|11925S||100 µl (10 western blots)||---||In Stock||---|
|11925||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Hamster, Monkey||Endogenous||80||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation, IF-IC=Immunofluorescence (Immunocytochemistry)
Specificity / Sensitivity
Mitofusin-2 (D1E9) Rabbit mAb recognizes endogenous levels of total mitofusin-2 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val573 of human mitofusin-2 protein.
Western blot analysis of extracts from various cell lines using Mitofusin-2 (D1E9) Rabbit mAb.
Confocal immunofluorescent analysis of HeLa cells using Mitofusin-2 (D1E9) Rabbit mAb (green). Actin filaments were labeled with DY-554 phalloidin (red). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye).
Immunoprecipitation of Mitofusin-2 from PANC-1 cell extracts using Normal Rabbit IgG #2729 (lane 2) or Mitofusin-2 (D1E9) Rabbit mAb (lane 3). Lane 1 is 10% input. Western blot analysis was performed using Mitofusin-2 (D2D10) Rabbit mAb #9482.
Mitofusins are mitochondrial transmembrane GTPases that function to regulate mitochondrial fusion, a process that occurs in concert with mitochondrial division and is necessary for the maintenance of structural and genetic mitochondrial integrity (1,2). Two mitofusins have been described in mammals, mitofusin-1 and -2, which share 60% amino acid identity and appear to function coordinately to regulate mitochondrial fusion (3). Mitochondrial fusion is widely recognized as important for normal cell growth and development (4), and may have evolved as a mechanism to offset the deleterious effects of mtDNA mutations (3). Null mutations in either mitofusin are embryonic lethal in mice, whereas conditional knockout studies have shown that combined deletion of mitofusin-1 and mitofusin-2 in skeletal muscle results in severe mitochondrial dysfunction (3).
Research studies have revealed that mutations in mitofusin-2 are linked to Charcot-Marie-Tooth disease, an inherited neurodegenerative disease characterized by a progressive loss of muscle tissue and sensory perception (5,6).
- Zhang, Y. and Chan, D.C. (2007) FEBS Lett 581, 2168-73.
- Chan, D.C. (2006) Annu Rev Cell Dev Biol 22, 79-99.
- Chen, H. et al. (2010) Cell 141, 280-9.
- Bereiter-Hahn, J. and Vöth, M. (1994) Microsc Res Tech 27, 198-219.
- Kijima, K. et al. (2005) Hum Genet 116, 23-7.
- Züchner, S. et al. (2004) Nat Genet 36, 449-51.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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