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PI3-kinase (p110) Antibody (subunit alpha)Rabbit Monoclonal Antibody

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United States
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Ordering Information
Catalog # Size Availability Price  
AJ1607a 100ul 400 ul 2-3 days $ 315.00 Add to cart
  • Specification
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PI3-kinase (p110) Antibody (subunit alpha) - Product info

ApplicationWB, IF
  • Applications Legend:
  • W=Western Blotting
  • IP=Immunoprecipitation
  • IHC-P=Immunohistochemistry (Paraffin)
  • IF-IC=Immunofluorescence (Immunocytochemistry)
  • F=Flow Cytometry
Primary AccessionP42336
ReactivityHuman
Clone NamesEP383Y
Calculated MW124284 Da
Gene ID 5290
Other Names
PIK3CA, Phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit alpha isoform, PI3-kinase p110 subunit alpha;PtdIns-3-kinase p110
Target/Specificity
A synthetic peptide of human near the C-term of PI3-K p110 alpha was used as an immunogen.
Dilution
WB~~1:5000~20000
Format
50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.
Storage
Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
Precautions
PI3-kinase (p110) Antibody (subunit alpha) is for research use only and not for use in diagnostic or therapeutic procedures.

PI3-kinase (p110) Antibody (subunit alpha) - Protein Information

Name PIK3CA
Function
Phosphoinositide-3-kinase (PI3K) that phosphorylates PtdIns (Phosphatidylinositol), PtdIns4P (Phosphatidylinositol 4- phosphate) and PtdIns(4,5)P2 (Phosphatidylinositol 4,5- bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). 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 in breast cancer cells 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 Has also serine-protein kinase activity: phosphorylates PIK3R1 (p85alpha regulatory subunit), EIF4EBP1 and HRAS

PI3-kinase (p110) Antibody (subunit alpha) - Related products

AP8016c: PI3KCA Antibody (Center)

AP3558a: Phospho-PK3CA-pY317 Antibody

AP7860a: PK3CA Antibody (Y317)

AP8016a: PI3KCA Antibody (N-term)

AP8016b: PI3KCA Antibody (C-term)

RI13994: PIK3CA predesign siRNA

BP3558a: Phospho-PK3CA-pY317 Antibody Blocking Peptide

BP7860a: PK3CA Antibody (Y317) Blocking Peptide

BP8016a: PI3KCA Antibody (N-term) Blocking Peptide

BP8016b: PI3KCA Antibody (C-term) Blocking Peptide

BP8016c: PI3KCA Antibody (Center) Blocking Peptide

AJ1607a: PI3-kinase (p110) Antibody (subunit alpha)

AF1827a: PIK3CA / P110alpha Antibody

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Provided below are standard protocols that you may find useful for product applications.

BACKGROUND

PI3-Kinases (PI3-Ks) are a family of lipid kinases that are implicated in signal transduction. PI3-K consists of two subunits; p85 and p10. The p85 subunit localize PI3-K activity to the plasma membrane while the p110 subunit contains the catalytic domain of PI3-K (1-2). Four isoforms of p110 has been found; α, β, γ, and the Δ subunit. The alpha isoform, also known as PI3KCA, is a transforming oncogene (3) that was shown to have activating mutations in nine types of cancers such as colon, brain, breast and stomach (4-5). Three hot spot mutations (E542K and E545K; and H1047R) make p110α a potential drug target.

REFERENCES

1. Otsu et al. (1992) Cell 65, 91-104
2. Hiles et al. (1991) Cell 70, 419-429
3. Chang HW, Aoki M, Fruman D, et al. Science 1997;276:1848
4. Depowski PL, Rosenthal SI, Ross JS. Mod Pathol 2001;14:672
5. Bose S, Crane A, Hibshoosh H, Mansukhani M, Sandweis L, Parsons R, Hum Pathol 2002;33:405