Mitofusin-1 (D5A17) Rabbit mAb

Catalog No.: F3771

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:30
    Application
    WB, IP
    Reactivity
    Mouse, Rat
    Source
    Rabbit
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW Observed MW
    84 kDa 84 kDa
    *Why do the predicted and actual molecular weights differ?
    The following reasons may explain differences between the predicted and actual protein molecular weight.

    Datasheet & SDS

    Biological Description

    Specificity

    Mitofusin-1 (D5A17) Rabbit mAb detects endogenous levels of total Mitofusin-1 protein.

    Clone
    D5A17
    Synonym(s)
    Mitofusin-1, Transmembrane GTPase MFN1, Mfn1
    Background

    Mitofusin 1 (MFN1) is a key member of the dynamin-related GTPase family located on the outer mitochondrial membrane, where it is essential for mitochondrial fusion, a process vital for maintaining mitochondrial network integrity, energy homeostasis, and cell survival. MFN1 contains an N-terminal GTPase domain enabling GTP binding and hydrolysis, two heptad repeat regions (HR1 and HR2) that form coiled-coil structures mediating dimerization and tethering between adjacent mitochondria, and two transmembrane helices anchoring the protein within the outer membrane. The extended HR2 facilitates direct interaction with MFN1 or MFN2 on neighboring mitochondria to drive efficient fusion. MFN1 works closely with MFN2 and OPA1 to preserve mitochondrial morphology, stabilize mitochondrial DNA (mtDNA), regulate ATP production, support apoptosis pathways, and allow metabolic adaptation under stress. It also promotes mitophagy, preventing accumulation of dysfunctional mitochondria, and is important for embryogenesis and neuronal development. Loss or dysfunction of MFN1 impairs mitochondrial dynamics, causing energy deficits, neurodegeneration, and metabolic disease. Although MFN1 mutations are less common than those in MFN2, deficiency exacerbates Charcot–Marie–Tooth type 2A–like neuropathy, muscle atrophy, and neuroinflammatory conditions; altered MFN1 expression is observed in diseases such as Parkinson’s, Alzheimer’s, and some cancers.

    References
    • https://pubmed.ncbi.nlm.nih.gov/30647902/
    • https://pubmed.ncbi.nlm.nih.gov/27920125/

    Tech Support

    Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

    Handling Instructions

    Tel: +1-832-582-8158 Ext:3
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