AIDA Antibody (C-term) 精选
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- 产品详情
- 实验流程
- 背景知识
Application
| WB, E |
|---|---|
| Primary Accession | Q96BJ3 |
| Other Accession | Q8C4Q6, Q4R8C7, Q6PBN2, NP_073742.2 |
| Reactivity | Human |
| Predicted | Zebrafish, Monkey, Mouse, Rat, Bovine, Canine, Rabbit, Chicken |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 35023 Da |
| Antigen Region | 255-283 aa |
| Gene ID | 64853 |
|---|---|
| Other Names | Axin interactor, dorsalization-associated protein, Axin interaction partner and dorsalization antagonist, AIDA, C1orf80 |
| Target/Specificity | This AIDA antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 255-283 amino acids from the C-terminal region of human AIDA. |
| Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | AIDA Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | AIDA |
|---|---|
| Synonyms | C1orf80 |
| Function | Acts as a ventralizing factor during embryogenesis. Inhibits axin-mediated JNK activation by binding axin and disrupting axin homodimerization. This in turn antagonizes a Wnt/beta-catenin- independent dorsalization pathway activated by AXIN/JNK-signaling (By similarity). |
| Tissue Location | Widely expressed in adult tissues, with highest expression in the heart and skeletal muscle |
Research Areas
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
AIDA acts as a ventralizing factor during embryogenesis. Inhibits axin-mediated JNK activation by binding axin and disrupting axin homodimerization. This in turn antagonizes a Wnt/beta-catenin-independent dorsalization pathway activated by AXIN/JNK-signaling (By similarity).
REFERENCES
Rui, Y., et al. Dev. Cell 13(2):268-282(2007)
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