Flightless-I Antibody #14189
- 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
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).
Limited Uses
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