Product Pathways - Metabolism
Mitofusin-1 (D6E2S) Rabbit mAb #14739
|14739S||100 µl ( 10 western blots )||￥3,250.00||现货查询 购买询价 防伪查询|
|14739||carrier free & custom formulation / quantity||email request|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation, IF-IC=Immunofluorescence (Immunocytochemistry),
Specificity / Sensitivity
Mitofusin-1 (D6E2S) Rabbit mAb recognizes endogenous levels of total mitofusin-1 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro551 of human mitofusin-1 protein.
Western blot analysis of extracts from various cell lines using Mitofusin-1 (D6E2S) Rabbit mAb (upper) and β-Actin (D6A8) Rabbit mAb #8457 (lower).
Western blot analysis of extracts from HeLa cells, transfected with SignalSilence® Control siRNA (unconjugated) #6568 (-), or SignalSilence® Mitofusin-1 siRNA I #13274 (+), using Mitofusin-1 (D6E2S) Rabbit mAb (upper) and β-Actin (D6A8) Rabbit mAb #8457 (lower). The Mitofusin-1 (D6E2S) Rabbit mAb confirms silencing of mitofusin-1 expression, while the β-Actin (D6A8) Rabbit mAb is used as a loading control.
Immunoprecipitation of mitofusin-1 protein from HeLa cell extracts using Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (lane 2) or Mitofusin-1 (D6E2S) Rabbit mAb (lane 3). Lane 1 is 10% input. Western blot analysis was performed using Mitofusin-1 (D6E2S) Rabbit mAb.
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).
- 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.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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XP is a registered trademark of Cell Signaling Technology, Inc.
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