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。
PI3KCA Antibody (C-term)
Purified Rabbit Polyclonal Antibody (Pab)
- 产品详情
- 文献引用 : 3
- 实验流程
- 背景知识
Application 
| WB, FC, IHC-P, E |
|---|---|
| Primary Accession | P42336 |
| Other Accession | P32871 |
| Reactivity | Human |
| Predicted | Bovine |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 124284 Da |
| Antigen Region | 1019-1050 aa |
| Gene ID | 5290 |
|---|---|
| Other Names | Phosphatidylinositol 4, 5-bisphosphate 3-kinase catalytic subunit alpha isoform, PI3-kinase subunit alpha, PI3K-alpha, PI3Kalpha, PtdIns-3-kinase subunit alpha, Phosphatidylinositol 4, 5-bisphosphate 3-kinase 110 kDa catalytic subunit alpha, PtdIns-3-kinase subunit p110-alpha, p110alpha, Phosphoinositide-3-kinase catalytic alpha polypeptide, Serine/threonine protein kinase PIK3CA, PIK3CA |
| Target/Specificity | This PI3KCA antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1019-1050 amino acids from the C-terminal region of human PI3KCA. |
| Dilution | WB~~1:1000 FC~~1:10~50 IHC-P~~1:100~500 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation 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 | PI3KCA Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | PIK3CA |
|---|---|
| Function | Phosphoinositide-3-kinase (PI3K) phosphorylates phosphatidylinositol (PI) and its phosphorylated derivatives at position 3 of the inositol ring to produce 3-phosphoinositides (PubMed:15135396, PubMed:23936502, PubMed:28676499). Uses ATP and PtdIns(4,5)P2 (phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3) (PubMed:15135396, PubMed:28676499). PIP3 plays a key role by recruiting PH domain- containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Participates in cellular signaling in response to various growth factors. Involved in the activation of AKT1 upon stimulation by receptor tyrosine kinases ligands such as EGF, insulin, IGF1, VEGFA and PDGF. Involved in signaling via insulin-receptor substrate (IRS) proteins. Essential in endothelial cell migration during vascular development through VEGFA signaling, possibly by regulating RhoA activity. Required for lymphatic vasculature development, possibly by binding to RAS and by activation by EGF and FGF2, but not by PDGF. Regulates invadopodia formation through the PDPK1-AKT1 pathway. Participates in cardiomyogenesis in embryonic stem cells through a AKT1 pathway. Participates in vasculogenesis in embryonic stem cells through PDK1 and protein kinase C pathway. In addition to its lipid kinase activity, it displays a serine-protein kinase activity that results in the autophosphorylation of the p85alpha regulatory subunit as well as phosphorylation of other proteins such as 4EBP1, H-Ras, the IL-3 beta c receptor and possibly others (PubMed:23936502, PubMed:28676499). Plays a role in the positive regulation of phagocytosis and pinocytosis (By similarity). |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Phosphatidylinositol 3-kinase is composed of an 85 kDa regulatory subunit and a 110 kDa catalytic subunit. This protein represents the catalytic subunit, which uses ATP to phosphorylate PtdIns, PtdIns4P and PtdIns(4,5)P2. PI3KCA has been found to be oncogenic and has been implicated in cervical cancers.
REFERENCES
Tiwari, S. Nat Immunol. August; 10(8): 907?17 (2009).
Ballou, L.M., et al., J. Biol. Chem. 278(26):23472-23479 (2003).
Singh, B., et al., Genes Dev. 16(8):984-993 (2002).
Shayesteh, L., et al., Nat. Genet. 21(1):99-102 (1999).
Volinia, S., et al., Genomics 24(3):472-477 (1994).
Hiles, I.D., et al., Cell 70(3):419-429 (1992).
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