Cell Signaling Technology

Product Pathways - PI3K / Akt Signaling

PI3 Kinase p110β (C33D4) Rabbit mAb #3011

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H Endogenous 110 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

PI3 Kinase p110β (C33D4) Rabbit mAb detects endogenous levels of total PI3K p110β protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide of human PI3K p110β.

Western Blotting

Western Blotting

Western blot analysis of extracts from MCF-7 and K-562 cells using PI3 Kinase p110β (C33D4) Rabbit mAb.

Background

Phosphoinositide 3-kinase (PI3K) catalyzes the production of phosphatidylinositol-3,4,5-triphosphate by phosphorylating phosphatidylinositol (PI), phosphatidylinositol-4-phosphate (PIP), and phosphatidylinositol-4,5-bisphosphate (PIP2). Growth factors and hormones trigger this phosphorylation event, which in turn coordinates cell growth, cell cycle entry, cell migration, and cell survival (1). PTEN reverses this process, and research studies have shown that the PI3K signaling pathway is constitutively activated in human cancers that have loss of function of PTEN (2). PI3Ks are composed of a catalytic subunit (p110) and a regulatory subunit. Various isoforms of the catalytic subunit (p110α, p110β, p110γ, and p110δ) have been isolated, and the regulatory subunits that associate with p110α, p110β, and p110δ are p85α and p85β (3). In contrast, p110γ associates with a p101 regulatory subunit that is unrelated to p85. Furthermore, p110γ is activated by βγ subunits of heterotrimeric G proteins (4).

p110ß is widely distributed in tissue and plays an essential role in early embryonic development (5). p110ß stimulates cell proliferation, invasive cell growth, and expression is increased in a number of tumors including glioblastomas (6-8).

  1. Cantley, L.C. (2002) Science 296, 1655-7.
  2. Simpson, L. and Parsons, R. (2001) Exp Cell Res 264, 29-41.
  3. Neri, L.M. et al. (2002) Biochim Biophys Acta 1584, 73-80.
  4. Stoyanov, B. et al. (1995) Science 269, 690-3.
  5. Okkenhaug, K. and Vanhaesebroeck, B. (2003) Nat Rev Immunol 3, 317-30.
  6. Czauderna, F. et al. (2003) Nucleic Acids Res 31, 670-82.
  7. Bénistant, C. et al. (2000) Oncogene 19, 5083-90.
  8. Knobbe, C.B. and Reifenberger, G. (2003) Brain Pathol 13, 507-18.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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