|Other Names||Methyl-CpG-binding domain protein 4, 322-, Methyl-CpG-binding endonuclease 1, Methyl-CpG-binding protein MBD4, Mismatch-specific DNA N-glycosylase, MBD4, MED1|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP1039c was selected from the C-term region of human MBD4. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Mismatch-specific DNA N-glycosylase involved in DNA repair. Has thymine glycosylase activity and is specific for G:T mismatches within methylated and unmethylated CpG sites. Can also remove uracil or 5-fluorouracil in G:U mismatches. Has no lyase activity. Was first identified as methyl-CpG-binding protein.|
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DNA methylation is the major modification of eukaryotic genomes and plays an essential role in mammalian development. Human proteins MECP2, MBD1, MBD2, MBD3, and MBD4 comprise a family of nuclear proteins related by the presence in each of a methyl-CpG binding domain (MBD). Each of these proteins, with the exception of MBD3, is capable of binding specifically to methylated DNA. MBD4 may function to mediate the biological consequences of the methylation signal. In addition, MBD4 has protein sequence similarity to bacterial DNA repair enzymes and thus may have some function in DNA repair. Further, MBD4 gene mutations are detected in tumors with primary microsatellite-instability (MSI), a form of genomic instability associated with defective DNA mismatch repair, and the MBD4 gene meets 4 of 5 criteria of a bona fide MIS target gene.
Evertson, S., et al., Anticancer Res. 23(4):3569-3574 (2003).Yamada, T., et al., Cancer Lett. 181(1):115-120 (2002).Schlegel, J., et al., Oncol. Rep. 9(2):393-395 (2002).Petronzelli, F., et al., J. Biol. Chem. 275(42):32422-32429 (2000).Petronzelli, F., et al., J. Cell. Physiol. 185(3):473-480 (2000).
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