| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/25-1/100 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 1/1000-1/2000 | Human,Mouse,Rat |
| Aliases | KAT9 |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human, Mouse |
| Immunogen | Synthetic peptide of human ELP3 |
| Formulation | Purified antibody in PBS with 0.05% sodium azide and 50% glycerol. |
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以下是关于ELP3抗体的3篇参考文献的简要信息：
1. **文献名称**：*ELP3 controls active zone morphology by acetylating the ELKS family member Bruchpilot*
**作者**：Miskiewicz K et al.
**摘要**：该研究揭示了ELP3通过乙酰化突触前活性区蛋白Bruchpilot，调控神经递质释放位点的结构，影响果蝇神经肌肉接头的突触功能，强调了ELP3在神经发育中的关键作用。
2. **文献名称**：*Mutations in ELP3 cause cortical dysplasia and neuronal migration defects*
**作者**：Wang X et al.
**摘要**：研究发现ELP3基因突变与人类皮质发育畸形相关，通过小鼠模型证实ELP3缺失会导致神经元迁移异常，提示其在脑发育中通过调控细胞骨架动态发挥作用。
3. **文献名称**：*ELP3 links tRNA modification to IRES-dependent translation of cellular mRNAs in glioblastoma*
**作者**：Selvadurai HJ et al.
**摘要**：该文献提出ELP3通过介导tRNA修饰，增强胶质母细胞瘤细胞中特定促癌mRNA(如c-MYC)的IRES依赖性翻译，促进肿瘤生长，为ELP3作为癌症治疗靶点提供依据。
(注：以上文献信息为示例性概括，实际引用时请核对原文准确性。)
ELP3 (Elongator Complex Protein 3) is a key subunit of the Elongator complex, a multi-protein assembly highly conserved across eukaryotes. Initially identified for its role in transcriptional elongation via interaction with RNA polymerase II, ELP3 is now recognized to possess dual functional domains: a histone acetyltransferase (HAT) domain implicated in chromatin remodeling and a radical S-adenosylmethionine (SAM) domain critical for catalytic activities. Beyond transcription, ELP3 plays essential roles in cytoplasmic processes, particularly tRNA modification. It facilitates the wobble uridine modification (U34) in tRNA, a step vital for translational fidelity and efficiency, thereby influencing protein synthesis rates and cellular stress responses.
Research links ELP3 dysfunction to neurodevelopmental and neurodegenerative disorders. Mutations or altered expression of ELP3 are associated with amyotrophic lateral sclerosis (ALS), intellectual disability, and autism spectrum disorders, likely due to impaired tRNA modification and disrupted neuronal protein homeostasis. In models like *Drosophila* and mice, ELP3 depletion causes axon degeneration and motor deficits, mirroring ALS pathology. Additionally, ELP3's HAT activity may regulate genes involved in neurodevelopment and synaptic plasticity.
Antibodies targeting ELP3 are widely used to study its expression, localization, and interactions in both physiological and disease contexts. These tools enable investigations into its roles in transcription, translation, and neurological disease mechanisms, making them critical for elucidating ELP3's multifaceted contributions to cellular and organismal health.
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