Render Target: STATIC
Render Timestamp: 2024-12-20T11:51:24.849Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-30 01:53:10.675
Product last modified at: 2024-12-17T18:46:49.176Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Mitofusin-2 (D1E9) Rabbit mAb #11925

Filter:
  • WB
  • IP
  • IF

    Supporting Data

    REACTIVITY H Hm Mk
    SENSITIVITY Endogenous
    MW (kDa) 80
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • Hm-Hamster 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:200
    Immunofluorescence (Immunocytochemistry) 1:100 - 1:200

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Mitofusin-2 (D1E9) Rabbit mAb recognizes endogenous levels of total mitofusin-2 protein.

    Species Reactivity:

    Human, Hamster, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val573 of human mitofusin-2 protein.

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