Human PI 3-Kinase p55 gamma (NP_003620.3) VersaClone cDNA

Name: Human PI 3-Kinase p55 gamma (NP_003620.3) VersaClone cDNA
Brand: R&D Systems
SKU: RDC3487
Price: 270 USD
Availability: InStock

R&D Systems | Catalog # RDC3487

Submit a review

Product Documents

100% Guarantee

Preparation & Storage
Background
Product Documents
Specific Notices
Research Areas

Key Product Details

Species

Human

Accession Number

NP_003620.3

Formulation, Preparation, and Storage

Shipping

The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.

Storage

Store the unopened product at -20 to -70 °C. Use a manual defrost freezer and avoid repeated freeze-thaw cycles. Do not use past expiration date.

Background: PI 3-Kinase p55 gamma

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