抗人 LCE3C 抗体对
01AB03376
Late cornified envelope 3C (LCE3C) is a small, cationic structural protein essential for the formation of the cornified envelope within the stratum corneum. Characterized by an exceptionally high cysteine content, LCE3C functions as a key component of the innate cutaneous host defense system. It exhibits potent defensin-like antimicrobial activity against a broad range of commensal and pathogenic bacteria at low micromolar concentrations, utilizing a mechanism similar to human beta-defensins. Clinically, the deletion of the LCE3B and LCE3C genes is a well-established genetic risk factor for psoriasis. This deficiency leads to disrupted host defense mechanisms and altered epidermal antimicrobial responses rather than a simple failure of the physical skin barrier. Understanding LCE3C's role in maintaining skin homeostasis is vital for addressing inflammatory skin conditions and enhancing the protective capacity of the epidermal barrier.
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技术参数
- 靶点基因名
- LCE3C
- 基因别名
- LEP15; SPRL3A
- 蛋白别名
- late cornified envelope 3C; LCE3C
- UniProt
- Q5T5A8
- 物种
- Human
产品详情
- 靶点名称
- LCE3C
- 蛋白名称
- late cornified envelope 3C
- 蛋白别名
- Late cornified envelope protein 3C; Late envelope protein 15; Small proline-rich-like epidermal differentiation complex protein 3A
- 靶点基因名
- LCE3C
- 基因别名
- LEP15; SPRL3A
- UniProt
- Q5T5A8
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Late cornified envelope 3C (LCE3C) is a small, cationic structural protein essential for the formation of the cornified envelope within the stratum corneum. Characterized by an exceptionally high cysteine content, LCE3C functions as a key component of the innate cutaneous host defense system. It exhibits potent defensin-like antimicrobial activity against a broad range of commensal and pathogenic bacteria at low micromolar concentrations, utilizing a mechanism similar to human beta-defensins. Clinically, the deletion of the LCE3B and LCE3C genes is a well-established genetic risk factor for psoriasis. This deficiency leads to disrupted host defense mechanisms and altered epidermal antimicrobial responses rather than a simple failure of the physical skin barrier. Understanding LCE3C's role in maintaining skin homeostasis is vital for addressing inflammatory skin conditions and enhancing the protective capacity of the epidermal barrier.