anti-MCM2 Antibody from antibodies-online

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antibodies-online for
anti-MCM2 Antibody

Description

Product Characteristics: This antibody is designed, produced, and is suitable for Cancer, Immunology and Nuclear Signaling research. MCM2, also called DNA replication licensing factor MCM2, Minichromosome maintenance protein 2 homolog or Nuclear Protein BM28) is one of the highly conserved mini-chromosome maintenance proteins (MCM) that are involved in the initiation of eukaryotic genome replication. The hexameric protein complex formed by MCM proteins is a key component of the pre-replication complex (pre-RC) and may be involved in the formation of replication forks and in the recruitment of other DNA replication related proteins. This protein forms a complex with MCM4, 6, and 7, and has been shown to regulate the helicase activity of the complex. This protein is phosphorylated, and thus regulated by protein kinases CDC2 and CDC7. Double serines at positions 26 and 27 are conserved in rat and mouse. High homology >88% to similar proteins from several other species. Expected broad reactivity to various lysates.
Synonyms: BM28 antibody, CCNL 1 antibody, CCNL1 antibody, CDC like 1 antibody, Minichromosome maintenance complex component 2 antibody
Target Information: The protein encoded by this gene is one of the highly conserved mini-chromosome maintenance proteins (MCM) that are involved in the initiation of eukaryotic genome replication. The hexameric protein complex formed by MCM proteins is a key component of the pre-replication complex (pre_RC) and may be involved in the formation of replication forks and in the recruitment of other DNA replication related proteins. This protein forms a complex with MCM4, 6, and 7, and has been shown to regulate the helicase activity of the complex. This protein is phosphorylated, and thus regulated by, protein kinases CDC2 and CDC7. Multiple alternatively spliced transcript variants have been found, but the full-length nature of some variants has not been defined. [provided by RefSeq, Oct 2012]