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Target intelligence / Profile preview
Late cornified envelope protein 3B (LCE3B)
- Target
- LCE3B
- Molecular classification
- Structural protein, Antimicrobial peptide (defensin-like), Other (cornified envelope protein)
01
Overview
Late cornified envelope protein 3B (LCE3B) is a structural and antimicrobial protein exclusively expressed in the epidermis, especially during the terminal differentiation of keratinocytes. It helps form the cornified envelope in the stratum corneum, providing both a physical and an antimicrobial barrier against pathogens. LCE3B and its family members possess defensin-like antibacterial activity effective against both Gram-positive and Gram-negative bacteria. Genetic deletion involving LCE3B (and LCE3C) increases susceptibility to psoriasis, likely by altering epidermal defense mechanisms and related inflammatory pathways. Despite its role in innate host defense, there is no evidence of LCE3B being directly targeted by any approved drugs, nor are there established therapeutic agents presently in clinical use for modulating LCE3B activity.
- Other names
- LCE3BLate cornified envelope 3BLate cornified envelope protein 3B
02
Mechanism of action
Not applicable (no current drugs with direct known action)
03
Biological functions
Innate cutaneous host defensePhysical barrier function of the stratum corneum (skin)Defense response to Gram-negative bacteriumDefense response to Gram-positive bacteriumAntibacterial activity (membrane permeabilization, killing)Terminal differentiation of keratinocytes
04
Disease associations
Psoriasis (risk factor via deletion of LCE3B/C)Inflammation (potentially through altered host defense regulation)Other skin diseases with altered barrier function (speculative/association)
05
Safety considerations
No notable safety concerns reported for targeting or modulating LCE3B.Therapeutic challenges are unknown due to lack of drug development.
06
Biomarkers
Genetic deletion of LCE3B and LCE3C (LCE3B/C-del) is a biomarker of psoriasis riskExpression level of LCE3A (which is regulated by LCE3B/C status) may correlate with disease activity in psoriasis
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