|Application ||WB, IHC|
|Calculated MW||48551 Da|
|Other Names||Cyclin-A2, Cyclin-A, CCNA2, CCN1, CCNA|
|Target/Specificity||A synthetic peptide corresponding to residues near the N-term of human Cyclin A2 was used as immunogen.|
|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||Cyclin-A2 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Cyclin which controls both the G1/S and the G2/M transition phases of the cell cycle. Functions through the formation of specific serine/threonine protein kinase holoenzyme complexes with the cyclin-dependent protein kinases CDK1 or CDK2. The cyclin subunit confers the substrate specificity of these complexes and differentially interacts with and activates CDK1 and CDK2 throughout the cell cycle.|
|Cellular Location||Nucleus. Cytoplasm Note=Exclusively nuclear during interphase (PubMed:1312467) Detected in the nucleus and the cytoplasm at prophase (PubMed:1312467). Cytoplasmic when associated with SCAPER (PubMed:17698606).|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Cyclin A is a member of the Cyclin A family that can bind and activate Cdc2 and Cdk2 and is involved in the control of mitosis and S phase (1). During S phase, cyclin A forms a complex with Cdk2, the pRB-related protein p107 and E2F (2). Additionally, deregulation of cyclin A expression might contribute to tumor formation (3). The cyclin A family consist of two members, cyclin A1 and cyclin A2, to which cyclin A2 promotes both G1/S and G2/M transition (4).
1. Pines, J. & Hunter, T. (1990) Nature ( London) 346, 760-762.
2. Devoto, S. H., Mudryj, M., Pines, J., Hunter, T. & Nevins, J. R. (1992) Cell 68, 167-176.
3. Wang, J., Zindy, F., Chenivesse, X., Lamas, E., Henglein, B. & Brechot, C. (1992) Oncogene 7, 1653-1656.
4. Pagano, M.; Pepperkok, R.; Verde, F.; Ansorge, W.; Draetta, G. EMBO J. 11: 961-971, 1992.
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