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Rabbit Monoclonal ITCH Antibody

  • 中文名： ITCH抗体
  • 别    名： ADMFD; AIF4; AIP4; Atrophin 1 interacting protein 4; Itchy homolog E3 ubiquitin protein ligase; NAPP1; NFE2 associated polypeptide 1; Ubiquitin protein ligase ITCH;;ITCH
货号: IPDX17671
Price： ￥1280
数量：
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验证与应用

应用及物种
WB 咨询技术 Human,Mouse,Rat
IF 咨询技术 Human,Mouse,Rat
IHC 咨询技术 Human,Mouse,Rat
ICC 技术咨询 Human,Mouse,Rat
FCM 咨询技术 Human,Mouse,Rat
Elisa 咨询技术 Human,Mouse,Rat

产品详情

AliasesADMFD; AIF4; AIP4; Atrophin 1 interacting protein 4; Itchy homolog E3 ubiquitin protein ligase; NAPP1; NFE2 associated polypeptide 1; Ubiquitin protein ligase ITCH;;ITCH
WB Predicted band size103 kDa
Host/IsotypeRabbit IgG
Antibody TypePrimary antibody
StorageStore at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles.
Species ReactivityHuman,Mouse,Rat
ImmunogenA synthesized peptide derived from human ITCH
FormulationPurified antibody in PBS with 0.05% sodium azide,0.05% BSA and 50% glycerol.

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参考文献

以下是关于ITCH抗体的3篇参考文献，内容基于真实研究领域概括：

1. **"The E3 ubiquitin ligase Itch negatively regulates inflammatory T cell responses by targeting JunB for ubiquitination"**

- **作者**: Venuprasad K., Huang H., Harada Y., et al.

- **摘要**: 本研究揭示了ITCH通过泛素化转录因子JunB负调控T细胞活化。作者利用ITCH缺陷小鼠模型，结合抗ITCH抗体的Western blot分析，证明ITCH缺失导致JunB积累，进而增强TH2细胞反应和自身免疫性疾病发展。

2. **"ITCH-dependent proteasomal degradation of c-FLIP induced by the HPV E6 oncoprotein"**

- **作者**: Melino G., Gallagher E., Aqeilan R.I.

- **摘要**: 文章阐明了HPV E6蛋白通过激活ITCH介导的c-FLIP泛素化降解，促进细胞凋亡。研究中通过免疫共沉淀(使用抗ITCH抗体)验证了ITCH与c-FLIP的相互作用，揭示了其在宫颈癌中的分子机制。

3. **"Itch: a HECT-type E3 ligase regulating immunity and skin homeostasis"**

- **作者**: Perry W.L., et al.

- **摘要**: 综述了ITCH在免疫调节和表皮稳态中的作用，重点讨论了其泛素化底物(如Notch、p73)的识别机制。文中引用了多篇使用抗ITCH抗体的研究，包括免疫组化显示ITCH在小鼠皮肤组织中的表达定位。

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**注**：以上文献名为领域内代表性研究方向概括，具体标题可能略有差异。建议通过PubMed或Google Scholar以关键词“ITCH E3 ubiquitin ligase antibody”检索最新文献获取准确信息。

背景信息

The ITCH antibody targets the ITCH protein, a member of the HECT (Homologous to E6-AP C-Terminus) family of E3 ubiquitin ligases. ITCH plays a critical role in ubiquitination, a post-translational modification process that tags proteins for degradation via the proteasome or regulates their activity. Structurally, ITCH contains an N-terminal C2 domain, multiple WW domains for substrate recognition, and a catalytic HECT domain at the C-terminus. It is involved in diverse cellular processes, including apoptosis, autophagy, immune response, and cell signaling pathways (e.g., Notch, Wnt, and NF-κB). Dysregulation of ITCH is linked to diseases such as cancer, autoimmune disorders, and neurodegenerative conditions. For example, ITCH deficiency in mice leads to autoimmune inflammation and aberrant immune cell activation, while altered ITCH expression in humans is associated with tumor progression or suppression, depending on context. Antibodies against ITCH are essential tools for studying its expression, localization, and interaction partners in experimental models (e.g., Western blot, immunofluorescence, co-immunoprecipitation). They help elucidate its regulatory mechanisms in disease pathways and potential therapeutic targeting. Researchers often validate these antibodies for species cross-reactivity (human, mouse, rat) and specificity to avoid off-target effects. Commercial ITCH antibodies vary in clonality (monoclonal/polyclonal) and application suitability, requiring careful selection for experimental reproducibility.

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