人 TUT7 抗体对
01AB01864
Terminal uridylyl transferase 7 (TUT7) is a cytoplasmic and nucleoplasmic RNA uridylyltransferase that regulates global RNA turnover. It catalyzes the addition of uridine residues to the 3' ends of RNAs with short poly(A) tails, thereby promoting deadenylation-dependent mRNA decay. TUT7 also plays a critical role in microRNA processing, specifically the mono- or oligo-uridylylation of pre-let-7 miRNA, where it acts as either a positive or negative regulator of let-7 biogenesis depending on the presence of LIN28A. Through these mechanisms, it influences cell fate, oncogenic pathways, and the silencing of transposable elements like LINE-1. Clinically, variants in the TUT7 gene are associated with Wilms’ tumor and spastic ataxia 4. Furthermore, its essential role in germ cell development is evidenced by mouse models where the combined loss of TUT7 and its paralog TUT4 results in female infertility.
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技术参数
- 靶点基因名
- TUT7
- 基因别名
- HS2; KIAA1711; ZCCHC6
- 蛋白别名
- terminal uridylyl transferase 7; TUT7
- UniProt
- Q5VYS8
- 物种
- Human
产品详情
- 靶点名称
- TUT7
- 蛋白名称
- terminal uridylyl transferase 7
- 蛋白别名
- Terminal uridylyltransferase 7; TUTase 7; Zinc finger CCHC domain-containing protein 6
- 靶点基因名
- TUT7
- 基因别名
- HS2; KIAA1711; ZCCHC6
- UniProt
- Q5VYS8
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Terminal uridylyl transferase 7 (TUT7) is a cytoplasmic and nucleoplasmic RNA uridylyltransferase that regulates global RNA turnover. It catalyzes the addition of uridine residues to the 3' ends of RNAs with short poly(A) tails, thereby promoting deadenylation-dependent mRNA decay. TUT7 also plays a critical role in microRNA processing, specifically the mono- or oligo-uridylylation of pre-let-7 miRNA, where it acts as either a positive or negative regulator of let-7 biogenesis depending on the presence of LIN28A. Through these mechanisms, it influences cell fate, oncogenic pathways, and the silencing of transposable elements like LINE-1. Clinically, variants in the TUT7 gene are associated with Wilms’ tumor and spastic ataxia 4. Furthermore, its essential role in germ cell development is evidenced by mouse models where the combined loss of TUT7 and its paralog TUT4 results in female infertility.