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Cat.No.: F2786
| Dilution |
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| Application |
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| WB, IHC, ELISA |
| Reactivity |
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| Human |
| Source |
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| Mouse Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Positive Control | Human kidney |
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| Negative Control |
| Specificity |
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| β-defensin 1 Antibody [K23F18] detects endogenous levels of total β-defensin 1 protein. |
| Clone |
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| K23F18 |
| Synonym(s) |
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| BD1, HBD1, DEFB1, Beta-defensin 1, BD-1, hBD-1 |
| Background |
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| β-defensin 1 (DEFB1) is a constitutively secreted, 4.8 kDa cationic antimicrobial peptide produced by epithelial cells lining the respiratory, urogenital, gastrointestinal, and skin mucosa. It adopts a compact β-hairpin structure stabilized by three invariant disulfide bonds (Cys5–Cys31, Cys10–Cys30, Cys19–Cys28), forming a rigid scaffold with an exposed cationic face, comprising residues Arg7, Lys20, and Lys27, that facilitates electrostatic attraction to anionic bacterial membranes, while a hydrophobic N-terminal tip (Phe2, Val3, Ile5) enables bilayer insertion. Reduced β-defensin 1^red with free Cys15/Cys43 thiols self-assembles into amyloid-like fibrils that create stable, bacteria-entrapping nets through cysteine crosslinking, immobilizing both Gram-positive and Gram-negative pathogens, including resistant strains, whereas oxidized β-defensin 1^ox selectively destabilizes Gram-negative LPS outer membranes. Both forms independently trigger platelet α-granule exocytosis, enhancing bacterial containment by 50–80% against S. aureus, and act as chemoattractants for neutrophils via CCR6, mimicking IL-8 to promote NET deployment, thus bridging immediate physical entrapment to adaptive immune activation without inducing resistance. Expressed as a monomer across barrier tissues, β-defensin 1 maintains microbiota homeostasis by exerting selective microbial pressure; its deficiency leads to Crohn’s disease dysbiosis through Paneth cell dysfunction, cystic fibrosis mucus overgrowth via CFTR interaction, and increased skin infections. |
| References |
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