- CITATIONS: 1
|Application ||DB, E|
|Other Accession||Q00566, Q9Z2D6, Q95LG8|
|Predicted||Monkey, Mouse, Rat|
|Calculated MW||52441 Da|
|Other Names||Methyl-CpG-binding protein 2, MeCp-2 protein, MeCp2, MECP2|
|Target/Specificity||This MeCP2 Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding S80 of human MeCP2.|
|Precautions||Phospho-MeCP2(S80) Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Chromosomal protein that binds to methylated DNA. It can bind specifically to a single methyl-CpG pair. It is not influenced by sequences flanking the methyl-CpGs. Mediates transcriptional repression through interaction with histone deacetylase and the corepressor SIN3A. Binds both 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC)-containing DNA, with a preference for 5-methylcytosine (5mC).|
|Cellular Location||Nucleus. Note=Colocalized with methyl-CpG in the genome|
|Tissue Location||Present in all adult somatic tissues tested.|
Provided below are standard protocols that you may find useful for product applications.
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. MECP2, MBD1 and MBD2 can also repress transcription from methylated gene promoters. In contrast to other MBD family members, MECP2 is X-linked and subject to X inactivation. MECP2 is dispensible in stem cells, but is essential for embryonic development. MECP2 gene mutations are the cause of some cases of Rett syndrome, a progressive neurologic developmental disorder and one of the most common causes of mental retardation in females.
Mnatzakanian, G.N., et al., Nat. Genet. 36(4):339-341 (2004).
Laccone, F., et al., Hum. Mutat. 23(3):234-244 (2004).
Suzuki, M., et al., Oncogene 22(54):8688-8698 (2003).
Balmer, D., et al., J. Mol. Med. 81(1):61-68 (2003).
Hagberg, B., et al., Eur. J. Paediatr. Neurol. 7(6):417-421 (2003).
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