
抗人 TGIF1 抗体对
01AB01380
TGFB-induced factor homeobox 1 (TGIF1), is a member of the three-amino acid loop extension (TALE) superclass of atypical homeodomain transcription factors. It binds specifically to retinoid X receptor (RXR) responsive elements, such as those in the cellular retinol-binding protein II promoter, and acts as a transcriptional corepressor by inhibiting 9-cis-retinoic acid-dependent RXR alpha activation. TGIF1 also functions as a transcriptional corepressor of SMAD2, linking it to the TGF-β signaling pathway, and plays a critical role in embryonic development by regulating gene expression involved in forebrain patterning and ventral midline structure formation. The protein is produced in multiple isoforms via alternative splicing and participates in chromatin binding and sequence-specific DNA binding activities essential for its regulatory functions. Mutations in TGIF1 impair TGIF1’s DNA binding or protein interactions, leading to abnormal forebrain and facial development.
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技术参数
- 靶点基因名
- TGIF1
- 基因别名
- TGIF
- 蛋白别名
- TGFB induced factor homeobox 1; TGIF1
- UniProt
- Q15583
- 物种
- Human
产品详情
- 靶点名称
- TGIF1
- 蛋白名称
- TGFB induced factor homeobox 1
- 蛋白别名
- Homeobox protein TGIF1; 5'-TG-3'-interacting factor 1
- 靶点基因名
- TGIF1
- 基因别名
- TGIF
- UniProt
- Q15583
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
TGFB-induced factor homeobox 1 (TGIF1), is a member of the three-amino acid loop extension (TALE) superclass of atypical homeodomain transcription factors. It binds specifically to retinoid X receptor (RXR) responsive elements, such as those in the cellular retinol-binding protein II promoter, and acts as a transcriptional corepressor by inhibiting 9-cis-retinoic acid-dependent RXR alpha activation. TGIF1 also functions as a transcriptional corepressor of SMAD2, linking it to the TGF-β signaling pathway, and plays a critical role in embryonic development by regulating gene expression involved in forebrain patterning and ventral midline structure formation. The protein is produced in multiple isoforms via alternative splicing and participates in chromatin binding and sequence-specific DNA binding activities essential for its regulatory functions. Mutations in TGIF1 impair TGIF1’s DNA binding or protein interactions, leading to abnormal forebrain and facial development.