MECP2 / Unconjugated / 5B-9H

Product Details

Description	Methylation of DNA contributes to the regulation of gene transcription in both mammalian and invertebrate systems. DNA methylation predominates on cytosine residues that are present in dinucleotide motifs consisting of a 5' cytosine followed by guanosine (CpG), and it requires the enzymatic activity of DNA methyltransferase, which results in transcriptional repression of the methylated gene. Several proteins have been identified that associate with the methyl-CpG sites, and they include methyl-CpG binding protein-1 (MBD1), MBD2, MBD3 and MeCP2. Expression of the MBD proteins is highest in somatic tissues. MBD1 binds in a context specific manner to methyl-CpG rich domains and, in turn, mediates the transcriptional inhibition that is commonly observed with DNA methylation. Similarly, MBD2 inhibits transcription of methylated genes by associating with histone deacetylase (HDAC1) within the MeCP1 repressor complex. In addition, MBD4, which is also designated MED1, associates with the mismatch repair protein MLH1 and preferentially binds to methylated cytosine residues in mismatched base pairs. MeCP2 binds tightly to chromosomes in a methylation-dependent manner and associates with a corepressor complex containing the transcriptional repressor mSin3A and histone deacetylases.
Conjugate	Unconjugated
Clone	5B-9H
Target Species	Human
Applications	FC, ICC, WB, IHC
Supplier	HuaBio
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About MECP2
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 most cases of Rett syndrome, a progressive neurologic developmental disorder and one of the most common causes of cognitive disability in females. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Oct 2015]

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