Cell Signaling Technology

Product Pathways - Cell Cycle / Checkpoint

MCM4 Antibody #3228

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Mk Endogenous 96 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

MCM4 Antibody recognizes endogenous levels of total MCM4 protein. This antibody cross-reacts with a 250 kDa protein of unknown origin.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly431 of human MCM4 protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using MCM4 Antibody.

Background

The minichromosome maintenance (MCM) 2-7 proteins are a family of six related proteins required for initiation and elongation of DNA replication. MCM2-7 bind together to form the heterohexameric MCM complex that is thought to act as a replicative helicase at the DNA replication fork (1-5). This complex is a key component of the pre-replication complex (pre-RC) (reviewed in 1). Cdc6 and CDT1 recruit the MCM complex to the origin recognition complex (ORC) during late mitosis/early G1 phase forming the pre-RC and licensing the DNA for replication (reviewed in 2). Licensing of the chromatin permits the DNA to replicate only once per cell cycle, thereby helping to ensure that genetic alterations and malignant cell growth do not occur (reviewed in 3). Phosphorylation of the MCM2, MCM3, MCM4, and MCM6 subunits appears to regulate MCM complex activity and the initiation of DNA synthesis (6-8). MCM proteins are removed during DNA replication, causing chromatin to become unlicensed through inhibition of pre-RC reformation. Studies have shown that the MCM complex is involved in checkpoint control by protecting the structure of the replication fork and assisting in restarting replication by recruiting checkpoint proteins after arrest (reviewed in 3,9).

  1. Lei, M. and Tye, B.K. (2001) J Cell Sci 114, 1447-54.
  2. Lygerou, Z. and Nurse, P. (2000) Science 290, 2271-3.
  3. Forsburg, S.L. (2004) Microbiol Mol Biol Rev 68, 109-31.
  4. Tye, B.K. and Sawyer, S. (2000) J Biol Chem 275, 34833-6.
  5. Labib, K. et al. (2000) Science 288, 1643-7.
  6. Charych, D.H. et al. (2008) J Cell Biochem 104, 1075-86.
  7. Masai, H. et al. (2006) J Biol Chem 281, 39249-61.
  8. Lin, D.I. et al. (2008) Proc Natl Acad Sci USA 105, 8079-84.
  9. Bailis, J.M. et al. (2008) Mol Cell Biol 28, 1724-38.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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