
抗人 CELF4 抗体对
01AB02806
CUGBP Elav-like family member 4 (CELF4) is a neuron-enriched, cytoplasmic RNA-binding protein that regulates the stability, localization, and translation of target mRNAs. It preferentially binds to U/GU-rich elements in the 3′UTRs of transcripts and also influences the alternative splicing of genes such as MAPT and TNNT2. CELF4 targets a significant portion of the excitatory neuron transcriptome, particularly mRNAs encoding synaptic and excitability-related proteins, thereby shaping synaptic transmission and plasticity. Functionally, it acts as a potent negative regulator of neuronal excitability and a translational repressor of synaptic development programs. Clinically, CELF4 dysfunction is implicated in epilepsy and neurodevelopmental disorders. Loss of CELF4 in models leads to a complex neurological phenotype characterized by epileptic seizures, hyperexcitability, and abnormal sensory processing, underscoring its critical role in maintaining neuronal homeostasis.
| 规格 | 起售价 |
|---|---|
| 登录后可查看 | |
技术参数
- 靶点基因名
- CELF4
- 基因别名
- BRUNOL4
- 蛋白别名
- CUGBP Elav-like family member 4; CELF4
- UniProt
- Q9BZC1
- 物种
- Human
产品详情
- 靶点名称
- CELF4
- 蛋白名称
- CUGBP Elav-like family member 4
- 蛋白别名
- CUGBP Elav-like family member 4; CELF-4; Bruno-like protein 4; CUG-BP- and ETR-3-like factor 4; RNA-binding protein BRUNOL-4
- 靶点基因名
- CELF4
- 基因别名
- BRUNOL4
- UniProt
- Q9BZC1
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
CUGBP Elav-like family member 4 (CELF4) is a neuron-enriched, cytoplasmic RNA-binding protein that regulates the stability, localization, and translation of target mRNAs. It preferentially binds to U/GU-rich elements in the 3′UTRs of transcripts and also influences the alternative splicing of genes such as MAPT and TNNT2. CELF4 targets a significant portion of the excitatory neuron transcriptome, particularly mRNAs encoding synaptic and excitability-related proteins, thereby shaping synaptic transmission and plasticity. Functionally, it acts as a potent negative regulator of neuronal excitability and a translational repressor of synaptic development programs. Clinically, CELF4 dysfunction is implicated in epilepsy and neurodevelopmental disorders. Loss of CELF4 in models leads to a complex neurological phenotype characterized by epileptic seizures, hyperexcitability, and abnormal sensory processing, underscoring its critical role in maintaining neuronal homeostasis.