癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
EphA7 Antibody (N-term)
Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| IHC-P, FC, E |
|---|---|
| Primary Accession | Q15375 |
| Other Accession | P54759, Q61772 |
| Reactivity | Human, Rat, Mouse |
| Predicted | Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 112097 Da |
| Antigen Region | 11-41 aa |
| Gene ID | 2045 |
|---|---|
| Other Names | Ephrin type-A receptor 7, EPH homology kinase 3, EHK-3, EPH-like kinase 11, EK11, hEK11, EPHA7, EHK3, HEK11 |
| Target/Specificity | This EphA7 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 11-41 amino acids from the N-terminal region of human EphA7. |
| Dilution | IHC-P~~1:100~500 FC~~1:10~50 E~~Use at an assay dependent concentration. |
| Format | Purified monoclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein G column, followed by dialysis against PBS. |
| 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 | EphA7 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | EPHA7 |
|---|---|
| Synonyms | EHK3, HEK11 |
| Function | Receptor tyrosine kinase which binds promiscuously GPI- anchored ephrin-A family ligands residing on adjacent cells, leading to contact-dependent bidirectional signaling into neighboring cells. The signaling pathway downstream of the receptor is referred to as forward signaling while the signaling pathway downstream of the ephrin ligand is referred to as reverse signaling. Among GPI-anchored ephrin-A ligands, EFNA5 is a cognate/functional ligand for EPHA7 and their interaction regulates brain development modulating cell-cell adhesion and repulsion. Has a repellent activity on axons and is for instance involved in the guidance of corticothalamic axons and in the proper topographic mapping of retinal axons to the colliculus. May also regulate brain development through a caspase(CASP3)-dependent proapoptotic activity. Forward signaling may result in activation of components of the ERK signaling pathway including MAP2K1, MAP2K2, MAPK1 and MAPK3 which are phosphorylated upon activation of EPHA7. |
| Cellular Location | Cell membrane; Single-pass type I membrane protein |
| Tissue Location | Widely expressed. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Protein kinases are enzymes that transfer a phosphate group from a phosphate donor, generally the g phosphate of ATP, onto an acceptor amino acid in a substrate protein. By this basic mechanism, protein kinases mediate most of the signal transduction in eukaryotic cells, regulating cellular metabolism, transcription, cell cycle progression, cytoskeletal rearrangement and cell movement, apoptosis, and differentiation. With more than 500 gene products, the protein kinase family is one of the largest families of proteins in eukaryotes. The family has been classified in 8 major groups based on sequence comparison of their tyrosine (PTK) or serine/threonine (STK) kinase catalytic domains. The tyrosine kinase (TK) group is mainly involved in the regulation of cell-cell interactions such as differentiation, adhesion, motility and death. There are currently about 90 TK genes sequenced, 58 are of receptor protein TK (e.g. EGFR, EPH, FGFR, PDGFR, TRK, and VEGFR families), and 32 of cytosolic TK (e.g. ABL, FAK, JAK, and SRC families).
REFERENCES
Wilkinson, D.G., Nat Rev Neurosci 2(3):155-164 (2001).
Xu, Q., et al., Philos. Trans. R. Soc. Lond., B, Biol. Sci. 355(1399):993-1002 (2000).
Holder, N., et al., Development 126(10):2033-2044 (1999).
Zhou, R., Pharmacol. Ther. 77(3):151-181 (1998).
Fox, G.M., et al., Oncogene 10(5):897-905 (1995).
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