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Render Timestamp: 2024-07-26T10:08:12.919Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Flightless-I Antibody #14189

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 145
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:200

    Storage

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

    Protocol

    Specificity / Sensitivity

    Flightless-1 Antibody recognizes endogenous levels of total Flightless-I protein.


    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human Flightless-I protein. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    The flightless-I (fliI) gene was first identified in Drosophila mutant screens for genes involved in flight behavior. Homozygous mutant alleles at the fliI locus are embryonic lethal, whereas heterozygous mutations yield a "flightless" phenotype resulting from defects in flight muscle fiber development (1). The encoded protein (flightless-I, FLII) is a highly conserved member of the gelsolin superfamily, defined by the presence of C-terminal gelsolin motifs that function as actin-binding domains (2). Genetic knock-out studies in mice and worms confirmed that Flightless-I plays a critical and highly conserved role in embryonic development, likely through its effects on actin remodeling of the cytoskeleton (3,4). Postnatally, Flightless-I is recognized to play an important role in wound repair (5). Flightless-I protein levels are increased in many wound types, and depletion of Flightless-I protein levels has been shown to accelerate wound repair by promoting fibroblast proliferation and epithelial migration (6-8). Studies in animal models suggest that Flightless-I may inhibit the wound repair process by modulating TGF-β signaling dynamics in the wound environment (9).

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