人 IKZF2 抗体对
01AB00276
IKAROS family zinc finger 2 (IKZF2), also known as Helios, is a DNA-binding protein belonging to the Ikaros transcription factor family. It contains multiple C2H2-type zinc finger domains that mediate sequence-specific DNA binding and protein-protein interactions, playing a critical role in immune regulation. Primarily expressed in hematopoietic cells, IKZF2 regulates lymphocyte development, including T-cell differentiation and function, and modulates immune tolerance by influencing regulatory T (Treg) cells. Structurally, IKZF2 forms homo- or heterodimers with other Ikaros family members to regulate gene expression. Dysregulation of IKZF2 is linked to autoimmune diseases, such as systemic lupus erythematosus (SLE), and hematologic malignancies, including T-cell acute lymphoblastic leukemia (T-ALL), where mutations or altered expression disrupt immune homeostasis or promote oncogenesis.
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技术参数
- 靶点基因名
- IKZF2
- 基因别名
- HELIOS; ZNFN1A2
- 蛋白别名
- IKAROS family zinc finger 2; IKZF2
- UniProt
- Q9UKS7
- 物种
- Human
产品详情
- 靶点名称
- IKZF2
- 蛋白名称
- IKAROS family zinc finger 2
- 蛋白别名
- Zinc finger protein Helios; Ikaros family zinc finger protein 2
- 靶点基因名
- IKZF2
- 基因别名
- HELIOS; ZNFN1A2
- UniProt
- Q9UKS7
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
IKAROS family zinc finger 2 (IKZF2), also known as Helios, is a DNA-binding protein belonging to the Ikaros transcription factor family. It contains multiple C2H2-type zinc finger domains that mediate sequence-specific DNA binding and protein-protein interactions, playing a critical role in immune regulation. Primarily expressed in hematopoietic cells, IKZF2 regulates lymphocyte development, including T-cell differentiation and function, and modulates immune tolerance by influencing regulatory T (Treg) cells. Structurally, IKZF2 forms homo- or heterodimers with other Ikaros family members to regulate gene expression. Dysregulation of IKZF2 is linked to autoimmune diseases, such as systemic lupus erythematosus (SLE), and hematologic malignancies, including T-cell acute lymphoblastic leukemia (T-ALL), where mutations or altered expression disrupt immune homeostasis or promote oncogenesis.