PI 3-Kinase p55 gamma Antibody [PerCP] Summary
Immunogen |
E. coli-derived recombinant human PI 3-Kinase p55 gamma Lys251-Gly378 Accession # Q92569 |
Specificity |
Detects endogenous human, mouse and rat PI 3-Kinase p55 gamma in Western blots. |
Isotype |
IgG |
Clonality |
Polyclonal |
Host |
Goat |
Gene |
PIK3R3 |
Purity |
Antigen Affinity-purified |
Innovator's Reward |
Test in a species/application not listed above to receive a full credit towards a future purchase. |
Applications/Dilutions
Dilutions |
|
Application Notes |
Optimal dilution of this antibody should be experimentally determined. |
Packaging, Storage & Formulations
Storage |
Store at 4C in the dark. |
Buffer |
PBS |
Preservative |
0.05% Sodium Azide |
Purity |
Antigen Affinity-purified |
Alternate Names for PI 3-Kinase p55 gamma Antibody [PerCP]
Background
PI 3-Kinase p55 gamma, also referred to as PI3Kp55 gamma or p55gamma, is a regulatory subunit of phosphatidylinositol 3-kinase (PI 3-Kinase / PI3K) (1). Class 1A PI 3-Kinases are heterodimers consisting of one 110 kDa catalytic subunit (p110 alpha, beta, or delta) and one regulatory subunit (p85 alpha, p85 beta, p55 alpha, p50 alpha, or p55 gamma) (1). The p55 gamma regulatory subunit is encoded by the PIK3R3 gene and is predominantly expressed in the brain (2). Human PI 3 Kinase p55 gamma protein is 461 amino acids (aa) in length with a theoretical molecular weight of ~54 kDa (3). Structurally, PI 3-Kinase p55 gamma contains a proline rich domain (aa 34 - 44) and two Src homology domains (SH2, aa 65 - 160 and 358 - 452) (1,3). In general, Class 1A PI 3-Kinases are activated through the binding of membrane-bound tyrosine kinase receptors, such as insulin-like growth factor 1 (IGF-1) (1,2,4). Activation of PI 3-Kinase results in the phosphorylation of phosphatidyl inositol and a downstream signaling cascade of the AKT/mTOR pathway (2,4). PI 3-Kinase pathway activation results in a number of cellular responses including proliferation, survival, growth, migration, membrane trafficking, and metabolism (2). The PI3-Kinase/AKT/mTOR pathway has been shown to be dysregulated in a number of cancers, largely through loss or inactivation of the tumor suppressor PTEN (4). Furthermore, one study found that anaplastic lymphoma kinase (ALK) promoted cell migration during brain development specifically through the p55 gamma regulatory subunit of PI 3-Kinase (5).
References
1. Backer J. M. (2010). The regulation of class IA PI 3-kinases by inter-subunit interactions. Current Topics in Microbiology and Immunology. https://doi.org/10.1007/82_2010_52
2. Hirsch, E., Costa, C., & Ciraolo, E. (2007). Phosphoinositide 3-kinases as a common platform for multi-hormone signaling. The Journal of Endocrinology. https://doi.org/10.1677/JOE-07-0097
3. Uniprot (Q92569)
4. Yang, J., Nie, J., Ma, X., Wei, Y., Peng, Y., & Wei, X. (2019). Targeting PI3K in cancer: mechanisms and advances in clinical trials. Molecular Cancer. https://doi.org/10.1186/s12943-019-0954-x
5. Seo, M., Kim, J. H., & Suk, K. (2017). Role of the p55-gamma subunit of PI3K in ALK-induced cell migration: RNAi-based selection of cell migration regulators. Cell Adhesion & Migration. https://doi.org/10.1080/19336918.2016.1202385
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are
guaranteed for 1 year from date of receipt.
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