|Application ||WB, IHC|
|Calculated MW||174385 Da|
|Other Names||DNA topoisomerase 2-alpha, DNA topoisomerase II, alpha isozyme, TOP2A, TOP2|
|Target/Specificity||A synthetic peptide corresponding to C-terminal residues of human Topo IIα was used as an 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||Topoisomerase-II Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Control of topological states of DNA by transient breakage and subsequent rejoining of DNA strands. Topoisomerase II makes double-strand breaks. Essential during mitosis and meiosis for proper segregation of daughter chromosomes. May play a role in regulating the period length of ARNTL/BMAL1 transcriptional oscillation (By similarity).|
|Cellular Location||Cytoplasm. Nucleus, nucleoplasm. Note=Generally located in the nucleoplasm|
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Provided below are standard protocols that you may find useful for product applications.
DNA topoisomerase II alpha (Topo IIα) is a 170 kDa ubiquitous nuclear enzyme belonging to the topo family, which regulates the topological states of DNA. Topo II is required in chromatin condensation and segregation during mitosis. Topo II α is cell cycle regulated and its level peaks between G2 to M phase. It has been linked to cell proliferation and it may be the main isoform of Topo II involved mitotic processes (1). Topo II α passes one strand of DBA through a reversible break in a second DNA strand, which catalyzes the topological isomerisation of DNA during cell cycle (2). Topo II α overexpression has been linked to a number of human maligenacies and is the target for many chemotherapeutic agents. The majority of anticancer drugs targeting Topo IIα initiate apoptosis by stabilizing the convalent complex formed between DNA and Topo IIα (3).
1. Ohasi Y, et al. Anticancer Res, 19:1873
2. Sakaguchi A, et al. J Cell Sci 117:1047-104, 2004.
3. Zhou Z, et al. Mol Cancer Res 3:271-275, 2005.
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