抗人 MICA 抗体对
01AB01530
MHC class I polypeptide-related sequence A (MICA) is a highly polymorphic, membrane-bound glycoprotein that serves as a stress-inducible ligand for the activating receptor NKG2D (KLRK1). Although structurally similar to classical MHC class I molecules, MICA does not associate with beta-2-microglobulin or present peptides. It is primarily expressed on epithelial cells, fibroblasts, and endothelial cells, with significant upregulation occurring during infection, tissue injury, or malignant transformation. Engagement of MICA by NKG2D on NK cells, gamma-delta T cells, and CD8+ alpha-beta T cells triggers potent cytotoxicity and cytokine release, facilitating immune surveillance. However, proteolytic shedding of MICA from the cell surface can generate soluble forms that down-modulate NKG2D expression, representing a key mechanism for tumor immune evasion.
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技术参数
- 靶点基因名
- MICA
- 基因别名
- PERB11.1
- 蛋白别名
- MHC class I polypeptide-related sequence A; MICA
- UniProt
- Q29983
- 物种
- Human
产品详情
- 靶点名称
- MICA
- 蛋白名称
- MHC class I polypeptide-related sequence A
- 蛋白别名
- MHC class I polypeptide-related sequence A; MIC-A
- 靶点基因名
- MICA
- 基因别名
- PERB11.1
- UniProt
- Q29983
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
MHC class I polypeptide-related sequence A (MICA) is a highly polymorphic, membrane-bound glycoprotein that serves as a stress-inducible ligand for the activating receptor NKG2D (KLRK1). Although structurally similar to classical MHC class I molecules, MICA does not associate with beta-2-microglobulin or present peptides. It is primarily expressed on epithelial cells, fibroblasts, and endothelial cells, with significant upregulation occurring during infection, tissue injury, or malignant transformation. Engagement of MICA by NKG2D on NK cells, gamma-delta T cells, and CD8+ alpha-beta T cells triggers potent cytotoxicity and cytokine release, facilitating immune surveillance. However, proteolytic shedding of MICA from the cell surface can generate soluble forms that down-modulate NKG2D expression, representing a key mechanism for tumor immune evasion.