Cell Signaling Technology

Product Pathways - Metabolism

Mitofusin-2 (D1E9) Rabbit mAb #11925

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP IF-IC H Hm Mk Endogenous 80 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IF-IC=Immunofluorescence (Immunocytochemistry)
Reactivity Key:  H=Human  Hm=Hamster  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

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 Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using Mitofusin-2 (D1E9) Rabbit mAb.

IP

IP

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.

IF-IC

IF-IC

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).


Background

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).

  1. Zhang, Y. and Chan, D.C. (2007) FEBS Lett 581, 2168-73.
  2. Chan, D.C. (2006) Annu Rev Cell Dev Biol 22, 79-99.
  3. Chen, H. et al. (2010) Cell 141, 280-9.
  4. Bereiter-Hahn, J. and Vöth, M. (1994) Microsc Res Tech 27, 198-219.
  5. Kijima, K. et al. (2005) Hum Genet 116, 23-7.
  6. Züchner, S. et al. (2004) Nat Genet 36, 449-51.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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